HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Song Wan Jean-Louis Vincent Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wan, S. Articles by Vincent, J.-L. Search for Related Content PubMed PubMed Citation Articles by Wan, S. Articles by Vincent, J.-L.

Ann Thorac Surg 1997;63:269-276
© 1997 The Society of Thoracic Surgeons

---

Current Reviews

Cytokine Responses to Cardiopulmonary Bypass: Lessons Learned From Cardiac Transplantation

Departments of Cardiac Surgery and Intensive Care, University Hospital Erasme, Free University of Brussels, Brussels, Belgium

	Abstract

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
Background. A growing body of evidence relates the release during cardiopulmonary bypass (CPB) of proinflammatory cytokines, such as tumor necrosis factor-, interleukin (IL)-6, and IL-8, to the postoperative systemic inflammatory response syndrome. Antiinflammatory cytokines, such as IL-10, however, may also play an important role in limiting these complications.

Methods. The English-language literature was reviewed. Emphasis was placed on cytokine responses during clinical CPB for cardiac operations and, in particular, for heart and heart-lung transplantation.

Results. The recent data indicate that (1) although cytokine release can be triggered by many factors during CPB, ischemia-reperfusion may play the most important role; (2) the levels of tumor necrosis factor-, IL-6, and IL-8 are correlated with the duration of cardiac ischemia and the myocardium is a major source of these three cytokines during CPB; (3) IL-10 levels are correlated with the duration of CPB and the liver is a major source of IL-10 during CPB; and (4) steroid pretreatment is an effective intervention to inhibit the release of proinflammatory cytokines and enhance IL-10 production.

Conclusions. The improved knowledge of cytokine responses to CPB may help to develop interventions aimed at reducing postoperative morbidity and mortality.

	Introduction

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
Although cardiopulmonary bypass (CPB) is fundamental for cardiac operations, it is associated with substantial postoperative morbidity [1]. Complement activation has been incriminated for many years [2, 3], although recent studies question its involvement in the development of acute lung injury after CPB [4, 5]. Considerable interest has been recently focused on the involvement of cytokine network during and after CPB [6–19]. The release of proinflammatory cytokines, such as tumor necrosis factor- (TNF-) [12, 13], interleukin (IL)-1ß [13], and IL-8 [14–16], has been associated with the development of complications after CPB. Interestingly, the antiinflammatory cytokine IL-10 is also released during CPB [17–19]. Hence, the inflammatory response to CPB is an extremely complex phenomenon that is far from completely understood. Table 1 presents a brief overview of some recent clinical studies on cytokine response to CPB.

Once the release of cytokines during CPB has been described, it becomes important to explore the mechanisms involved. A better understanding of this process may lead us to consider some form of intervention. The aim of the present article is to review some important elements implicated in the cytokine response to CPB, with particular reference to patients undergoing cardiac transplantation.

	The Role of Endotoxin Release

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
Cardiopulmonary bypass can trigger the release of endotoxin [6, 27–30], which can act as a powerful trigger for release of cytokines such as TNF- [6, 30, 31]. Circulating endotoxin can appear immediately after the beginning of CPB [27] and the gut is its most likely source, as CPB has been shown to impair gut barrier function and lead to increase gut permeability [32, 33]. Although endotoxin is a potent trigger of the inflammatory cascade of mediators, the role of endotoxin in the release of cytokines during CPB is not straightforward. For instance, Dauber and associates [34] found that bypass-induced coronary and pulmonary vascular injury correlated with peak circulating TNF levels, but not with endotoxin levels, although both of them were associated with peripheral pump-oxygenator bypass.

	The Role of Complement Activation

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
Complement activation during CPB has also been suggested as contributing to the release of cytokines [9–11]. Complement is activated during CPB by blood-air interfaces or blood-material interaction and formation of heparin-protamine complexes, through either the alternate pathway (after the onset of CPB) or the classic pathway (after the administration of protamine). The degree of complement activation depends on the degree of surgical trauma and the duration of CPB [2, 3]. Ivey and co-workers [35] recently found that IL-8 generation during reperfusion of the ischemic myocardium may be indirectly dependent on complement fragment C5a production. However, IL-8 can be induced only after reperfusion of the ischemic myocardium in rabbits [35] and dogs [36], as well as in humans [37]. The precise role of complement activation as a trigger of cytokine release (including IL-8) under CPB conditions is still unclear.

	The Role of Ischemia-Reperfusion and the Relationship With Myocardial Injury

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
Most cases of CPB are associated with aortic cross-clamping, which results in global myocardial ischemia, whereas the release of the aortic cross-clamp results in myocardial reperfusion. Lindal and colleagues [38] recently showed in patients undergoing CPB that ischemia is associated with ultrastructural evidence of myocytic and microvascular injury, which seems to be reversible in nature, but subsequent reperfusion leads to more severe myocardial damage. Colletti and co-workers [39] clearly showed in a rat model that hepatic ischemia-reperfusion, in the absence of endotoxin, can induce TNF- production that further results in pulmonary and hepatic injury. Kukielka and associates [40] recently demonstrated that IL-6 synthesis by the canine myocardium is accelerated by reperfusion.

Jansen and colleagues [12] first reported that TNF concentration can be detected only after release of the aortic cross-clamp during clinical CPB. Consistently, the important role of ischemia-reperfusion is supported by some other observations relating the magnitude of proinflammatory cytokine response to the duration of ischemia [15, 16, 18]. Kawamura and co-workers [15] studied 11 patients undergoing valvular operations and found IL-6 and IL-8 levels to be correlated with the duration of aortic cross-clamping and the degree of myocardial injury as reflected by the creatine kinase-MB isoenzyme values. Hennein and colleagues [16] showed in 22 patients undergoing coronary artery bypass grafting (CABG) that the duration of aortic cross-clamping was the only independent predictor of postoperative TNF- and IL-6 levels. These investigators reported a direct relationship between IL-6 and IL-8 levels and the development of left ventricular wall dyskinesia in the postoperative period [16]. In 10 patients undergoing normothermic CPB, however, Frering and associates [41] failed to observe any significant correlation between IL-6 and IL-8 levels and either the CPB time or the aortic cross-clamping time.

To further define the influence of the duration of myocardial ischemia on the degree of cytokine release after CPB, we compared the blood cytokine levels in patients undergoing CABG with those undergoing heart transplantation (HTx), in whom the duration of ischemia was much longer. Levels of TNF-, IL-6, and IL-8, which increased after reperfusion of the myocardium, were much higher in the HTx group than in the CABG group [18]. Moreover, we recently extended these findings to a larger population, including recipients of heart-lung transplantation (HLTx) who had had an even longer ischemic time. Blood sampling schedule, cytokine determination, and data analysis were the same as described previously [18]. Steroids were only given in the HTx and HLTx group, starting 90 minutes after declamping. In contrast to a previous report [16], TNF- levels did not correlate with the duration of ischemia in the current study at any time point. However, IL-6, IL-8, and IL-10 levels 1 to 2 hours after aortic declamping correlated significantly with the duration of ischemia. Figure 1 shows this correlation 90 minutes after declamping.

View larger version (15K): [in this window] [in a new window]   Fig 1. . Relationship between plasma interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-10 (IL-10) levels 90 minutes after aortic declamping and the ischemic duration in patients undergoing coronary artery bypass grafting (CABG, n = 20), heart transplantation (HTx, n = 11), or heart-lung transplantation (HLTx, n = 5).

View larger version (22K): [in this window] [in a new window]   Fig 2. . Relationship between peak creatine kinase-MB isoenzyme (CK-MB) values after operation and the ischemic duration in patients undergoing coronary artery bypass grafting (CABG, n = 20), heart transplantation (HTx, n = 11), or heart-lung transplantation (HLTx, n = 5).

	The Role of Interleukin-10 and the Organ Source of Cytokines

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

This begs the question of the source of these cytokines during CPB. Although it is logical to consider the myocardium as an important source, other organs also experience ischemia-reperfusion and therefore, may also release cytokines. To define the source of these cytokines, we recently introduced a coronary sinus catheter in patients undergoing CABG. Cytokine levels were simultaneously measured in arterial blood, coronary sinus blood, and mixed venous blood. We found that the myocardium, but not the lungs, is a major source of TNF- and IL-6 [23]. Furthermore, the heart may also release IL-8 during more severe injury [18, 23, 46]. In fact, Burns and colleagues [47] recently reported that activated local IL-8 gene expression in the myocardium is associated with pediatric CPB.

Neither the heart nor the lung, however, is the source of IL-10 [23]. We hypothesize that other organs such as the liver are primarily responsible for IL-10 release during CPB. Le Moine and colleagues [48] reported that the ischemic liver can be an important source of IL-8 and IL-10. In their study, IL-10 levels did not correlate with the duration of ischemia of the liver allografts [48]. Our previous study also found that IL-10 production was similar after HTx and CABG [18], suggesting the mechanism of IL-10 release is different with those proinflammatory cytokines. Accordingly, we recently measured IL-10 levels simultaneously in hepatic venous blood and arterial blood in steroid-pretreated patients undergoing CPB. We observed that the liver is a main source of IL-10 shortly after reperfusion during CPB [49]. By further including data from our previous study [50] of group II patients (6 HTx and 4 HLTx patients), who also received steroid pretreatment, arterial IL-10 levels 1 hour after aortic declamping in these patients were significantly correlated with the duration of CPB (Fig 3).

View larger version (21K): [in this window] [in a new window]   Fig 3. . Correlation between arterial interleukin-10 (IL-10) levels and the duration of cardiopulmonary bypass (CPB) 1 hour after aortic declamping in steroid-pretreated patients undergoing routine cardiac operations (coronary artery bypass grafting and aortic valve replacement [CABG+AVR]), heart transplantation (HTx), and heart-lung transplantation (HLTx).

	The Importance of Temperature

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

	Anticytokine Strategies During Cardiopulmonary Bypass

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
At least some of the anticytokine strategies developed in the sepsis syndrome [54] may also be considered under CPB conditions, with the aim to reduce postoperative complications. Millar and associates [55] noted that removal of TNF- and IL-6 by hemofiltration may have beneficial effects in children undergoing CPB. Steinberg and colleagues [56] found that heparin bonding of the bypass circuits can reduce the release of IL-6 and IL-8, but another Steinberg and associates [9] reported that heparin-coated CPB circuits have no effect on complement activation or cytokine production. Heparin-coated circuits with reduced doses of heparin are not likely to totally prevent the damaging effects of CPB [57]. It may be necessary, however, to maintain standardized systemic heparinization with the use of heparin-coated circuits. Such a protocol has been shown to decrease complement and TNF generation [58] and thereby improve the postoperative recovery of patients [59]. On the other hand, steroid administration has been a topic of intense investigation, which will be summarized in the next section. Aprotinin may present another option to reduce inflammatory response to CPB. Hill and co-workers [60] recently found that low-dose aprotinin was as effective as steroids in inhibiting CPB-induced release of TNF-.

	Steroid Administration Before Cardiopulmonary Bypass

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
Corticosteroids have been administered in cardiac operations for many years [61, 62], but their exact mechanism of action has not been well defined. Steroid administration before CPB has been found to reduce complement activation [29, 63], although this effect has not always been observed [12]. Steroids may also prevent cytokine release. Jansen and colleagues [12] reported that steroid administration before CPB can effectively reduce TNF- production after reperfusion. These effects were associated with a lower incidence of postoperative hemodynamic instability [12]. High TNF- levels have been recently related to an altered left ventricular performance in patients after CPB [30]. Engelman and co-workers [63] showed that steroid pretreatment can markedly inhibit the production of IL-1ß and IL-8. Tabardel and associates [17] reported that steroid administration before CPB can also increase the release of IL-10. Enhancing the production of IL-10 may bring some beneficial effects not only by inhibiting the release of other proinflammatory cytokines [42, 43], but also by diminishing the immunocyte hyperstimulation under CPB conditions [64]. By inhibition of TNF-, IL-6, and IL-8, steroid pretreatment can prevent peripheral vasodilation after warm heart operations [65]. However, it has been suggested that steroids may increase endotoxin release [29], which might counterbalance some of their effects.

We [50] recently documented that administration of steroids before HTx and HLTx procedures, instead of as usual at the end of CPB, can significantly inhibit TNF- and IL-8 production but greatly increase the release of IL-10. These results are in agreement with previous studies stressing the crucial importance of the timing of anticytokine interventions [54]. Steroids have also been reported to negatively regulate IL-6 production [65]. Interleukin-6 levels are thought to reflect the degree of inflammatory injury after CPB [24]. Interestingly, IL-6 release is not significantly influenced by the timing of steroid administration [50]. Our study also included HLTx patients, and the lung allograft is able to release TNF-, IL-2, and interferon- [66, 67]. We noted that IL-8 levels increased much higher in HLTx patients than in HTx patients [50]. A possible explanation is that the longer duration of CPB and ischemia in HLTx than in HTx was associated with a higher cardiac, as well as pulmonary, release of cytokines.

The immunomodulating effects of steroids may have beneficial influences on allograft survival in HTx and HLTx patients. In particular, the release of IL-10 may provide benefits for prolonging allograft survival and induce tolerance [68], although a recent study suggested that IL-10 may serve a function in the immune regulation of the infiltrate at sites of inflammation, rather than in immune suppression of the rejection process [69]. Intragraft infusion of another important antiinflammatory cytokine IL-4, but not IL-10, may prolong graft survival [70]. It was recently suggested that steroid pretreatment can increase IL-4 production in vitro [71]. We observed, however, that IL-4 was not significantly released in steroid-pretreated patients during CPB [49]. Further investigations are certainly warranted to explore the pathophysiology involved and thereby improve therapy.

	Summary

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
The release of proinflammatory cytokines during and after CPB may play an important role in the deleterious effects of CPB to the heart and other organs. The mechanisms are primarily related to ischemia-reperfusion of the myocardium and also other organs, including the lung, the gut, and the liver. The production of proinflammatory cytokines is correlated with the duration of cardiac ischemia, as the myocardium is a main source of these cytokines during CPB. The production of antiinflammatory cytokine IL-10 is correlated with the duration of CPB and the liver was found to be a major source of IL-10 during CPB. There is also some association between the release of proinflammatory cytokines and the degree of myocardial injury after CPB. A number of anticytokine strategies, including procedures such as hemofiltration, heparin coating of the CPB circuits, or pharmacologic interventions, may be considered to reduce morbidity after CPB. Among these, steroid administration before both hypothermic or normothermic CPB may be a simple, safe, and effective intervention to influence the cytokine responses in open heart operations, not only by inhibiting proinflammatory cytokines TNF- and IL-8, but also by enhancing the release of antiinflammatory cytokine IL-10. A better understanding of the cytokine responses to CPB may lead to other interventions aimed at reducing the incidence and the severity of postoperative complications by modulating the inflammatory reactions associated with CPB.

	Acknowledgments

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
This study was supported by Fondation pour la Chirurgie Cardiaque, Belgium.

	Footnotes

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 
Address reprint requests to Dr Vincent, Department of Intensive Care, University Hospital Erasme, Free University of Brussels, Route de Lennik 808, B-1070, Brussels, Belgium.

	References

Top Footnotes Abstract Introduction The Role of Endotoxin... The Role of Complement... The Role of Ischemia-Reperfusion... The Role of Interleukin-10... The Importance of Temperature Anticytokine Strategies During... Steroid Administration Before... Summary Acknowledgments References

 

1. Kirklin JW. Technical and scientific advances in cardiac surgery over the past 25 years. Ann Thorac Surg 1990;49:26–31.[Medline]
2. Chenoweth DE, Cooper SW, Hugli TE, Stewart RW, Blackstone EH, Kirklin JW. Complement activation during cardiopulmonary bypass: evidence for generation of C3a and C5a anaphylatoxins. N Engl J Med 1981;304:497–503.[Abstract]
3. Kirklin JK, Westaby S, Blackstone EH, Kirklin JW, Chenoweth DE, Pacifico AD. Complement and the damaging effects of cardiopulmonary bypass. J Thorac Cardiovasc Surg 1983;86:845–57.[Abstract]
4. Tennenberg SD, Clardy CW, Bailey WW, Solomkin JS. Complement activation and lung permeability during cardiopulmonary bypass. Ann Thorac Surg 1990;50:597–601.[Abstract]
5. Bando K, Pillai R, Cameron DE, et al. Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1990;99:873–7.[Abstract]
6. Jansen NJG, van Oeveren W, Gu YJ, van Vliet MH, Eijsman L, Wildevuur CRH. Endotoxin release and tumor necrosis factor formation during cardiopulmonary bypass. Ann Thorac Surg 1992;54:744–8.[Abstract]
7. Jorens PG, de Jongh R, de Backer W, et al. Interleukin-8 production in patients undergoing cardiopulmonary bypass: the influence of pretreatment with methylprednisolone. Am Rev Respir Dis 1993;148:890–5.[Medline]
8. Butler J, Chong GL, Baigrie RJ, Pillai R, Westaby S, Rocker GM. Cytokine responses to cardiopulmonary bypass with membrane and bubble oxygenation. Ann Thorac Surg 1992;53:833–8.[Abstract]
9. Steinberg JB, Kapelanski DP, Olson JD, Weiler JM. Cytokine and complement levels in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1993;106:1008–16.[Abstract]
10. Kalfin RE, Engelman RM, Rousou JA, et al. Induction of interleukin-8 expression during cardiopulmonary bypass. Circulation 1993;88(Suppl 2):401–6.
11. Haeffner-Cavaillon N, Roussellier N, Ponzio O, et al. Induction of interleukin-1 production in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1989;98:1100–6.[Abstract]
12. Jansen NJG, van Oeveren W, v.d. Broek L, et al. Inhibition by dexamethasone of the reperfusion phenomena in cardiopulmonary bypass. J Thorac Cardiovasc Surg 1991;102:515–25.[Abstract]
13. Menasché P, Haydar S, Peynet J, et al. A potential mechanism of vasodilation after warm heart surgery: the temperature-dependent release of cytokines. J Thorac Cardiovasc Surg 1994;107:293–9.[Abstract/Free Full Text]
14. Finn A, Naik S, Klein N, Levinsky RJ, Strobel S, Elliott M. Interleukin-8 release and neutrophil degranulation after pediatric cardiopulmonary bypass. J Thorac Cardiovasc Surg 1993;105:234–41.[Abstract]
15. Kawamura T, Wakusawa R, Okada K, Inada S. Elevation of cytokines during open heart surgery with cardiopulmonary bypass: participation of interleukin 8 and 6 in reperfusion injury. Can J Anaesth 1993;40:1016–21.[Medline]
16. Hennein HA, Ebba H, Rodriguez JL, et al. Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization. J Thorac Cardiovasc Surg 1994;108:626–35.[Abstract/Free Full Text]
17. Tabardel Y, Duchateau J, Schmartz D, et al. Corticosteroids increase blood interleukin 10 levels during cardiopulmonary bypass in men. Surgery 1996;119:76–80.[Medline]
18. Wan S, Marchant A, DeSmet JM, et al. Human cytokine responses to cardiac transplantation and coronary artery bypass grafting. J Thorac Cardiovasc Surg 1996;111:469–77.[Abstract/Free Full Text]
19. Seghaye MC, Duchateau J, Bruniaux J, et al. Interleukin-10 release related to cardiopulmonary bypass in infants undergoing cardiac operations. J Thorac Cardiovasc Surg 1996;111:545–53.[Abstract/Free Full Text]
20. Barry WH. Mechanisms of immune-mediated myocyte injury. Circulation 1994;89:2421–32.[Abstract/Free Full Text]
21. Finkel MS, Oddis CV, Jacob TD, Watkins SC, Hattler BG, Simmons RL. Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 1992;257:387–9.[Abstract/Free Full Text]
22. Kapadia S, Lee J, Torre-Amione G, Birdsall HH, Ma TS, Mann DL. Tumor necrosis factor- gene and protein expression in adult feline myocardium after endotoxin administration. J Clin Invest 1995;96:1042–52.
23. Wan S, DeSmet JM, Barvais L, Goldstein M, Vincent JL, LeClerc JL. Myocardium is a major source of proinflammatory cytokines in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996;112:806–11.[Abstract/Free Full Text]
24. Casey LC. Role of cytokines in the pathogenesis of cardiopulmonary-induced multisystem organ failure. Ann Thorac Surg 1993;56:S92–6.
25. Ide H, Kakiuchi T, Furuta N, et al. The effect of cardiopulmonary bypass on T cells and their subpopulations. Ann Thorac Surg 1987;44:277–82.[Abstract]
26. DePalma L, Yu M, McIntosh CL, Swain JA, Davey RJ. Changes in lymphocyte subpopulations as a result of cardiopulmonary bypass: the effect of blood transfusion. J Thorac Cardiovasc Surg 1991;101:240–4.[Abstract]
27. Rocke DA, Gaffin SL, Wells MT, Koen Y, Brock-Utine JG. Endotoxemia associated with cardiopulmonary bypass. J Thorac Cardiovasc Surg 1987;93:832–7.[Abstract]
28. Kharazmi A, Andersen LW, Baek L, Valerius NH, Laub M, Rasmussen JP. Endotoxemia and enhanced generation of oxygen radicals by neutrophils from patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1989;98:381–5.[Abstract]
29. Andersen LW, Baek L, Thomsen BS, Rasmussen JP. Effect of methylprednisolone on endotoxemia and complement activation during cardiac surgery. J Cardiothorac Anesth 1989;3:544–9.[Medline]
30. Te Velthuis H, Jansen PGM, Oudemans-van Straaten HM, Sturk A, Eijsman L, Wildevuur CRH. Myocardial performance in elderly patients after cardiopulmonary bypass is suppressed by tumor necrosis factor. J Thorac Cardiovasc Surg 1995;110:1663–9.[Abstract/Free Full Text]
31. Michie HR, Manogue KR, Spriggs DR, et al. Detection of circulating tumor necrosis factor after endotoxin administration. N Engl J Med 1988;318:1481–6.[Abstract]
32. Ohri SK, Bjarnason I, Pathi V, et al. Cardiopulmonary bypass impairs small intestinal transport and increases gut permeability. Ann Thorac Surg 1993;55:1080–6.[Abstract]
33. Riddington DW, Venkatesh B, Boivin CM, et al. Intestinal permeability, gastric intramucosal pH, and systemic endotoxemia in patients undergoing cardiopulmonary bypass. JAMA 1996;275:1007–12.[Abstract/Free Full Text]
34. Dauber IM, Parsons PE, Welsh CH, et al. Peripheral bypass-induced pulmonary and coronary vascular injury: association with increased levels of tumor necrosis factor. Circulation 1993;88:726–35.[Abstract/Free Full Text]
35. Ivey CL, Williams FM, Collins PD, Jose PJ, Williams TJ. Neutrophil chemoattractants generated in two phases during reperfusion of ischmic myocardium in the rabbit: evidence for a role for C5a and interleukin-8. J Clin Invest 1995;95:2720–8.
36. Kukielka GL, Smith CW, LaRosa GJ, et al. Interleukin-8 gene induction in the myocardium after ischemia and reperfusion in vivo. J Clin Invest 1995;95:89–103.
37. Neumann F-J, Ott I, Gawaz M, et al. Cardiac release of cytokines and inflammatory responses in acute myocardial infarction. Circulation 1995;92:748–55.[Abstract/Free Full Text]
38. Lindal S, Gunnes S, Lund I, Straume BK, Jørgensen L, Sørlie D. Myocardial and microvascular injury following coronary surgery and its attenuation by mode of reperfusion. Eur J Cardiothorac Surg 1995;9:83–9.[Abstract]
39. Colletti LM, Remick DG, Burtch GD, Kunkel SL, Strieter RM, Campbell DA Jr. Role of tumor necrosis factor- in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat. J Clin Invest 1990;85:1936–43.
40. Kukielka GL, Smith CW, Manning AM, Youker KA, Michael LH, Entman ML. Induction of interleukin-6 synthesis in the myocardium: potential role in postreperfusion inflammatory injury. Circulation 1995;92:1866–75.[Abstract/Free Full Text]
41. Frering B, Philip I, Dehoux M, Rolland C, Langlois JM, Desmonts JM. Circulating cytokines in patients undergoing normothermic cardiopulmonary bypass. J Thorac Cardiovasc Surg 1994;108:636–41.[Abstract/Free Full Text]
42. Gérard C, Bruyns C, Marchant A, et al. Interleukin-10 reduces the release of tumor necrosis factor and prevents lethality in experimental endotoxemia. J Exp Med 1993;177:547–50.[Abstract/Free Full Text]
43. Fiorentino DF, Zlotnik A, Mosmann TR, Howard M, O'Garra A. IL-10 inhibits cytokine production by activated macrophages. J Immunol 1991;147:3815–22.[Abstract]
44. McBride WT, Armstrong MA, Crockard AD, McMurray TJ, Rea JM. Cytokine balance and immunosuppressive changes at cardiac surgery: contrasting response between patients and isolated CPB circuits. Br J Anaesth 1995;75:724–33.[Abstract/Free Full Text]
45. Van der Poll T, Jansen J, Levi M, ten Cate H, ten Cate JW, van Deventer SJH. Regulation of interleukin 10 release by tumor necrosis factor in humans and chimpanzees. J Exp Med 1994;180:1985–8.[Abstract/Free Full Text]
46. Oz MC, Liao H, Naka Y, et al. Ischemia-induced interleukin-8 release after human heart transplantation: a potential role for endothelial cells. Circulation 1995;92(Suppl 2):428–32.[Abstract/Free Full Text]
47. Burns SA, Newburger JW, Xiao M, Mayer JE Jr, Walsh AZ, Neufeld EJ. Induction of interleukin-8 messenger RNA in heart and skeletal muscle during pediatric cardiopulmonary bypass. Circulation 1995;92(Suppl 2):315–21.[Abstract/Free Full Text]
48. Le Moine O, Marchant A, Durand F, et al. Systemic release of interleukin-10 during orthotopic liver transplantation. Hepatology 1994;20:889–92.[Medline]
49. Wan S, LeClerc JL, Schmartz D, et al. Hepatic release of interleukin-10 during cardiopulmonary bypass in steroid-pretreated patients. Am Heart J (in press).
50. Wan S, DeSmet JM, Antoine M, Goldman M, Vincent JL, LeClerc JL. Steroid administration in heart and heart-lung transplantation: is the timing adequate? Ann Thorac Surg 1996;61:674–8.[Abstract/Free Full Text]
51. Lichtenstein SV, Abel JG, Panos A, Slutsky AS, Salerno TA. Warm heart surgery: experience with long cross-clamp times. Ann Thorac Surg 1991; 52:1009–13.[Abstract]
52. Christakis GT, Koch JP, Deemar KA, et al. A randomized study of the systemic effects of warm heart surgery. Ann Thorac Surg 1992;54:449–59.[Abstract]
53. Menasché P, Peynet J, Haeffner-Cavaillon N, et al. Influence of temperature on neutrophil trafficking during clinical cardiopulmonary bypass. Circulation 1995;92(Suppl 2):334–40.[Abstract/Free Full Text]
54. Christman JW, Holden EP, Blackwell TS. Strategies for blocking the systemic effects of cytokines in the sepsis syndrome. Crit Care Med 1995;23:955–63.[Medline]
55. Millar AB, Armstrong L, van der Linden J, et al. Cytokine production and hemofiltration in children undergoing cardiopulmonary bypass. Ann Thorac Surg 1993;56:1499–502.[Abstract]
56. Steinberg BM, Grossi EA, Schwarz DS, et al. Heparin bonding of bypass circuits reduces cytokine release during cardiopulmonary bypass. Ann Thorac Surg 1995;60:525–9.[Abstract/Free Full Text]
57. Francalancia NA, Aeba R, Yousem SA, Griffith BP, Marrone GC. Deleterious effects of cardiopulmonary bypass on early graft function after single lung allotransplantation: evaluation of a heparin-coated bypass circuit. J Heart Lung Transplant 1994;13:498–507.[Medline]
58. Gu YJ, van Oeveren W, Akkerman C, Boonstra PW, Huyzen RJ, Wildevuur CRH. Heparin-coated circuits reduce the inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 1993;55:917–22.[Abstract]
59. Jansen PGM, te Velthuis H, Huybregts RAJM, et al. Reduced complement activation and improved postoperative performance after cardiopulmonary bypass with heparin-coated circuits. J Thorac Cardiovasc Surg 1995;110:829–34.[Abstract/Free Full Text]
60. Hill GE, Alonso A, Spurzem JR, Stammers AH, Robbins RA. Aprotinin and methylprednisolone equally blunt cardiopulmonary bypass-induced inflammation in humans. J Thorac Cardiovasc Surg 1995;110:1658–62.[Abstract/Free Full Text]
61. Replogle RL, Gazzaniga AB, Gross RE. Use of corticosteroids during cardiopulmonary bypass: possible lysosome stabilization. Circulation 1966;33(Suppl 1):86–91.
62. Niazi Z, Flodin P, Joyce L, Smith J, Mauer H, Lillehei RC. Effects of glucocorticosteroids in patients undergoing coronary artery bypass surgery. Chest 1979;76:262–8.[Abstract/Free Full Text]
63. Engelman RM, Rousou JA, Flack JE III, Deaton DW, Kalfin R, Das DK. Influence of steroids on complement and cytokine generation after cardiopulmonary bypass. Ann Thorac Surg 1995;60:801–4.[Abstract/Free Full Text]
64. Stefano GB, Rodriguez M, Glass R, Cesares F, Hughes TK, Bilfinger TV. Hyperstimulation of leukocytes by plasma from cardiopulmonary bypass patients is diminished by morphine and IL-10 pretreatment. J Cardiovasc Surg 1995;36:25–30.[Medline]
65. Teoh KHT, Bradley CA, Gauldie J, Burrows H. Steroid inhibition of cytokine-mediated vasodilation after warm heart surgery. Circulation 1995;92(Suppl 2):347–53.[Abstract/Free Full Text]
66. Sundaresan S, Alevy YG, Steward N, et al. Cytokine gene transcripts for tumor necrosis factor-, interleukin-2, and interferon- in human pulmonary allografts. J Heart Lung Transplant 1995;14:512–8.[Medline]
67. Serrick C, Adoumie R, Giaid A, Shennib H. The early release of interleukin-2, tumor necrosis factor- and interferon- after ischemia reperfusion injury in the lung allograft. Transplantation 1994;58:1158–62.[Medline]
68. Nickerson P, Steurer W, Steiger J, Zheng X, Steele AW, Strom TB. Cytokines and the TH1/TH2 paradigm in transplantation. Curr Opin Immunol 1994;6:757–64.[Medline]
69. Azzawi M, Hasleton PS, Grant SCD, Stewart JP, Hutchinson IV. Interleukin-10 in human heart transplantation: an in situ hybridization study. J Heart Lung Transplant 1995;14:519–28.[Medline]
70. Levy AE, Alexander JW. Administration of intragraft interleukin-4 prolongs cardiac allograft survival in rats treated with donor-specific transfusion/cyclosporine. Transplantation 1995;60:405–6.[Medline]
71. Ramírez F, Fowell DJ, Puklavec M, Simmonds S, Mason D. Glucocorticoids promote a Th2 cytokine response by CD4⁺ T cells in vitro. J Immunol 1996;156:2406–12.[Abstract]

This article has been cited by other articles:

				E. M. Carvalho, E. A Gabriel, and T. A Salerno Pulmonary Protection During Cardiac Surgery: Systematic Literature Review Asian Cardiovasc Thorac Ann, December 1, 2008; 16(6): 503 - 507. [Abstract] [Full Text] [PDF]

				C. S.H. Ng, A. A. Arifi, S. Wan, A. M.H. Ho, I. Y.P. Wan, E. M.C. Wong, and A. P.C. Yim Ventilation During Cardiopulmonary Bypass: Impact on Cytokine Response and Cardiopulmonary Function Ann. Thorac. Surg., January 1, 2008; 85(1): 154 - 162. [Abstract] [Full Text] [PDF]

				H. Heinze, C. Rosemann, C. Weber, G. Heinrichs, L. Bahlmann, M. Misfeld, M. Heringlake, and W. Eichler A single prophylactic dose of pentoxifylline reduces high dependency unit time in cardiac surgery -- a prospective randomized and controlled study Eur. J. Cardiothorac. Surg., July 1, 2007; 32(1): 83 - 89. [Abstract] [Full Text] [PDF]

				G. R. Stier and E. W. Verde The postoperative care of adult patients exposed to deep hypothermic circulatory arrest. Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2007; 11(1): 77 - 85. [Abstract] [PDF]

				T.B. Corcoran, A. Engel, H. Sakamoto, A. O'Shea, S. O'Callaghan-Enright, and G. D. Shorten The effects of propofol on neutrophil function, lipid peroxidation and inflammatory response during elective coronary artery bypass grafting in patients with impaired ventricular function Br. J. Anaesth., December 1, 2006; 97(6): 825 - 831. [Abstract] [Full Text] [PDF]

				X. Dong, Y. Liu, M. Du, Q. Wang, C. T. Yu, and X. Fan P38 mitogen-activated protein kinase inhibition attenuates pulmonary inflammatory response in a rat cardiopulmonary bypass model. Eur. J. Cardiothorac. Surg., July 1, 2006; 30(1): 77 - 84. [Abstract] [Full Text] [PDF]

				C.-H. Hsing, M.-Y. Hsieh, W.-Y. Chen, E. Cheung So, B.-C. Cheng, and M.-S. Chang Induction of Interleukin-19 and Interleukin-22 After Cardiac Surgery With Cardiopulmonary Bypass Ann. Thorac. Surg., June 1, 2006; 81(6): 2196 - 2201. [Abstract] [Full Text] [PDF]

				M. Westerberg, J. Gabel, A. Bengtsson, J. Sellgren, O. Eidem, and A. Jeppsson Hemodynamic effects of cardiotomy suction blood J. Thorac. Cardiovasc. Surg., June 1, 2006; 131(6): 1352 - 1357. [Abstract] [Full Text] [PDF]

				S. Rex, S. Brose, S. Metzelder, L. de Rossi, S. Schroth, R. Autschbach, R. Rossaint, and W. Buhre Normothermic Beating Heart Surgery with Assistance of Miniaturized Bypass Systems: The Effects on Intraoperative Hemodynamics and Inflammatory Response Anesth. Analg., February 1, 2006; 102(2): 352 - 362. [Abstract] [Full Text] [PDF]

				L. Gao, R. Taha, D. Gauvin, L. B. Othmen, Y. Wang, and G. Blaise Postoperative Cognitive Dysfunction After Cardiac Surgery Chest, November 1, 2005; 128(5): 3664 - 3670. [Abstract] [Full Text] [PDF]

				D. El Kebir, B. Hubert, R. Taha, E. Troncy, T. Wang, D. Gauvin, M. Gangal, and G. Blaise Effects of Inhaled Nitric Oxide on Inflammation and Apoptosis After Cardiopulmonary Bypass Chest, October 1, 2005; 128(4): 2910 - 2917. [Abstract] [Full Text] [PDF]

				K. Parekh, B. F. Meyers, G. A. Patterson, T. J. Guthrie, E. P. Trulock, R. J. Damiano Jr, and N. Moazami Outcome of lung transplantation for patients requiring concomitant cardiac surgery J. Thorac. Cardiovasc. Surg., September 1, 2005; 130(3): 859 - 863. [Abstract] [Full Text] [PDF]

				K. Prasongsukarn, J. G. Abel, W.R. E. Jamieson, A. Cheung, J. A. Russell, K. R. Walley, and S. V. Lichtenstein The effects of steroids on the occurrence of postoperative atrial fibrillation after coronary artery bypass grafting surgery: A prospective randomized trial J. Thorac. Cardiovasc. Surg., July 1, 2005; 130(1): 93 - 98. [Abstract] [Full Text] [PDF]

				N. Nesher, G. Uretzky, S. Insler, P. Nataf, I. Frolkis, E. Pineau, E. Cantoni, G. Bolotin, M. Vardi, D. Pevni, et al. Thermo-wrap technology preserves normothermia better than routine thermal care in patients undergoing off-pump coronary artery bypass and is associated with lower immune response and lesser myocardial damage J. Thorac. Cardiovasc. Surg., June 1, 2005; 129(6): 1371 - 1378. [Abstract] [Full Text] [PDF]

				A. Bourbon, M. Vionnet, P. Leprince, E. Vaissier, J. Copeland, P. McDonagh, P. Debre, and I. Gandjbakhch The effect of methylprednisolone treatment on the cardiopulmonary bypass-induced systemic inflammatory response Eur. J. Cardiothorac. Surg., November 1, 2004; 26(5): 932 - 938. [Abstract] [Full Text] [PDF]

				M. Ryugo, Y. Sawa, M. Ono, Y. Miyamoto, A. N. Aleshin, and H. Matsuda Pharmacologic preconditioning of JTE-607, a novel cytokine inhibitor, attenuates ischemia-reperfusion injury in the myocardium J. Thorac. Cardiovasc. Surg., June 1, 2004; 127(6): 1723 - 1727. [Abstract] [Full Text] [PDF]

				E. J. Mullin, M. S. Metcalfe, and G. J. Maddern Artificial Liver Support: Potential to Retard Regeneration? Arch Surg, June 1, 2004; 139(6): 670 - 677. [Abstract] [Full Text] [PDF]

				R. J. Scheubel, H. Zorn, R.-E. Silber, O. Kuss, H. Morawietz, J. Holtz, and A. Simm Age-dependent depression in circulating endothelial progenitor cells inpatients undergoing coronary artery bypass grafting J. Am. Coll. Cardiol., December 17, 2003; 42(12): 2073 - 2080. [Abstract] [Full Text] [PDF]

				P. Giomarelli, S. Scolletta, E. Borrelli, and B. Biagioli Myocardial and lung injury after cardiopulmonary bypass: role of interleukin (IL)-10 Ann. Thorac. Surg., July 1, 2003; 76(1): 117 - 123. [Abstract] [Full Text] [PDF]

				C. S. Ng, A. A Arifi, S. Wan, T. W. Lee, and A. P. Yim Cardiac Operation With Associated Pulmonary Resection: a Word of Caution Asian Cardiovasc Thorac Ann, December 1, 2002; 10(4): 362 - 364. [Abstract] [Full Text] [PDF]

				L. Kubala, M. Ciz, J. Vondracek, J. Cerny, P. Nemec, P. Studenik, H. Cizova, and A. Lojek Perioperative and postoperative course of cytokines and the metabolic activity of neutrophils in human cardiac operations and heart transplantation J. Thorac. Cardiovasc. Surg., December 1, 2002; 124(6): 1122 - 1129. [Abstract] [Full Text]

				J. Borgermann, I. Friedrich, S. Flohe, J. Spillner, M. Majetschak, O. Kuss, A. Sablotzki, T. Feldt, J. C. Reidemeister, and F. U. Schade Tumor necrosis factor-{alpha} production in whole blood after cardiopulmonary bypass: Downregulation caused by circulating cytokine-inhibitory activities J. Thorac. Cardiovasc. Surg., September 1, 2002; 124(3): 608 - 617. [Abstract] [Full Text] [PDF]

				J. Butler, E. W. Murithi, V. L. Pathi, K. J.D. MacArthur, and G. A. Berg Duroflo II heparin bonding does not attenuate cytokine release or improve pulmonary function Ann. Thorac. Surg., July 1, 2002; 74(1): 139 - 142. [Abstract] [Full Text] [PDF]

				S. R. El Azab, P. M. J. Rosseel, J. J. de Lange, A. B. J Groeneveld, R. van Strik, E. M. van Wijk, and G. J. Scheffer Dexamethasone decreases the pro- to anti-inflammatory cytokine ratio during cardiac surgery Br. J. Anaesth., April 1, 2002; 88(4): 496 - 501. [Abstract] [Full Text] [PDF]

				C. S.H. Ng, S. Wan, A. P.C. Yim, and A. A. Arifi Pulmonary Dysfunction After Cardiac Surgery* Chest, April 1, 2002; 121(4): 1269 - 1277. [Abstract] [Full Text] [PDF]

				R. D Tallman, M. Dumond, and D. Brown Inflammatory mediator removal by zero-balance ultrafiltration during cardiopulmonary bypass Perfusion, March 1, 2002; 17(2): 111 - 115. [Abstract] [PDF]

				U. Joashi, S. M. Tibby, C. Turner, A. Mayer, C. Austin, D. Anderson, A. Durward, and I. A. Murdoch Soluble Fas may be a proinflammatory marker after cardiopulmonary bypass in children J. Thorac. Cardiovasc. Surg., January 1, 2002; 123(1): 137 - 144. [Abstract] [Full Text] [PDF]

				V. Stangl, G. Baumann, K. Stangl, and S. B Felix Negative inotropic mediators released from the heart after myocardial ischaemia-reperfusion Cardiovasc Res, January 1, 2002; 53(1): 12 - 30. [Abstract] [Full Text] [PDF]

				E. Tayama, N. Hayashida, S. Fukunaga, K. Tayama, T. Takaseya, R. Hiratsuka, and S. Aoyagi High-dose cimetidine reduces proinflammatory reaction after cardiac surgery with cardiopulmonary bypass Ann. Thorac. Surg., December 1, 2001; 72(6): 1945 - 1949. [Abstract] [Full Text] [PDF]

				M. Cugno, J. Nussberger, P. Biglioli, F. Alamanni, R. Coppola, and A. Agostoni Increase of Bradykinin in Plasma of Patients Undergoing Cardiopulmonary Bypass : The Importance of Lung Exclusion Chest, December 1, 2001; 120(6): 1776 - 1782. [Abstract] [Full Text] [PDF]

				D. Shum-Tim, C. I. Tchervenkov, A.-M. Jamal, T. Nimeh, C.-Y. Luo, E. Chedrawy, E. Laliberte, A. Philip, C. P. Rose, and J. Lavoie Systemic steroid pretreatment improves cerebral protection after circulatory arrest Ann. Thorac. Surg., November 1, 2001; 72(5): 1465 - 1472. [Abstract] [Full Text] [PDF]

				F.-U. Sack, B. Reidenbach, R. Dollner, A. Schledt, M. M. Gebhard, and S. Hagl Influence of steroids on microvascular perfusion injury of the bowel induced by extracorporeal circulation Ann. Thorac. Surg., October 1, 2001; 72(4): 1321 - 1326. [Abstract] [Full Text] [PDF]

				H. A. Hennein Inflammation After Cardiopulmonary Bypass: Therapy for the Postpump Syndrome Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2001; 5(3): 236 - 255. [Abstract] [PDF]

				E. Appachi and E. B. Mossad Inflammatory Mediators and S-100{beta} Protein Concentrations in Neonates and Infants With Congenital Heart Disease Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2001; 5(3): 256 - 261. [Abstract] [PDF]

				N. Drabe, G. Zund, J. Grunenfelder, M. Sprenger, S. P. Hoerstrup, L. Bestmann, F. E. Maly, and M. Turina Genetic predisposition in patients undergoing cardiopulmonary bypass surgery is associated with an increase of inflammatory cytokines Eur. J. Cardiothorac. Surg., September 1, 2001; 20(3): 609 - 613. [Abstract] [Full Text] [PDF]

				U. Kiziltepe, A. Uysalel, T. Corapcioglu, K. Dalva, H. Akan, and H. Akalin Effects of combined conventional and modified ultrafiltration in adult patients Ann. Thorac. Surg., February 1, 2001; 71(2): 684 - 693. [Abstract] [Full Text] [PDF]

				V. Gulielmos, M. Menschikowski, H.-M. Dill, M. Eller, S. Thiele, S. M. Tugtekin, W. Jaross, and S. Schueler Interleukin-1, interleukin-6 and myocardial enzyme response after coronary artery bypass grafting - a prospective randomized comparison of the conventional and three minimally invasive surgical techniques Eur. J. Cardiothorac. Surg., November 1, 2000; 18(5): 594 - 601. [Abstract] [Full Text] [PDF]

				A. P.C. Yim, S. Wan, T. W. Lee, and A. A. Arifi VATS lobectomy reduces cytokine responses compared with conventional surgery Ann. Thorac. Surg., July 1, 2000; 70(1): 243 - 247. [Abstract] [Full Text] [PDF]

				R. A. Bronicki, C. L. Backer, H. P. Baden, C. Mavroudis, S. E. Crawford, and T. P. Green Dexamethasone reduces the inflammatory response to cardiopulmonary bypass in children Ann. Thorac. Surg., May 1, 2000; 69(5): 1490 - 1495. [Abstract] [Full Text] [PDF]

				M. A. Weigand, H. Schmidt, Q. Zhao, K. Plaschke, E. Martin, and H. J. Bardenheuer Ketamine Modulates the Stimulated Adhesion Molecule Expression on Human Neutrophils In Vitro Anesth. Analg., January 1, 2000; 90(1): 206 - 206. [Abstract] [Full Text] [PDF]

				S. Wan, J.-L. LeClerc, M. Antoine, J.-M. DeSmet, A. P.C. Yim, and J.-L. Vincent Heparin-coated circuits reduce myocardial injury in heart or heart-lung transplantation: a prospective, randomized study Ann. Thorac. Surg., October 1, 1999; 68(4): 1230 - 1235. [Abstract] [Full Text] [PDF]

				M. Struber, J. T. Cremer, B. Gohrbandt, C. Hagl, M. Jankowski, B. Volker, H. Ruckoldt, M. Martin, and A. Haverich Human cytokine responses to coronary artery bypass grafting with and without cardiopulmonary bypass Ann. Thorac. Surg., October 1, 1999; 68(4): 1330 - 1335. [Abstract] [Full Text] [PDF]

				S. Wan and A. P.C. Yim Cytokines in myocardial injury: impact on cardiac surgical approach Eur. J. Cardiothorac. Surg., September 1, 1999; 16(suppl_1): S107 - S111. [Abstract] [Full Text] [PDF]

				S. Wan, M. B. Izzat, T. W. Lee, I. Y.P. Wan, N. L.S. Tang, and A. P.C. Yim Avoiding cardiopulmonary bypass in multivessel CABG reduces cytokine response and myocardial injury Ann. Thorac. Surg., July 1, 1999; 68(1): 52 - 56. [Abstract] [Full Text] [PDF]

				S. Wan, J.-L. LeClerc, C.-H. Huynh, D. Schmartz, J.-M. DeSmet, A. P.C. Yim, and J.-L. Vincent DOES STEROID PRETREATMENT INCREASE ENDOTOXIN RELEASE DURING CLINICAL CARDIOPULMONARY BYPASS? J. Thorac. Cardiovasc. Surg., May 1, 1999; 117(5): 1004 - 1008. [Abstract] [Full Text] [PDF]

				H. A. Hennein, U. Kiziltepe, S. Barst, K. A. Bocchieri, A. Hossain, D. R. Call, D. G. Remick, and J. P. Gold VENOVENOUS MODIFIED ULTRAFILTRATION AFTER CARDIOPULMONARY BYPASS IN CHILDREN: A PROSPECTIVE RANDOMIZED STUDY J. Thorac. Cardiovasc. Surg., March 1, 1999; 117(3): 496 - 505. [Abstract] [Full Text] [PDF]

				S. Wan, M. B. Izzat, and A. P.C. Yim Reducing inflammatory reactions by heparin-coated circuit Ann. Thorac. Surg., November 1, 1998; 66(5): 1868 - 1868. [Full Text] [PDF]

				K. Kawahito, Y. Misawa, and K. Fuse Extracorporeal membrane oxygenation support and cytokines. Ann. Thorac. Surg., April 1, 1998; 65(4): 1192 - 1193. [Full Text] [PDF]

				S. Wan, J.-M. DeSmet, and J.-L. Vincent Can Cardiopulmonary Bypass Be Less Aggressive? Asian Cardiovasc Thorac Ann, March 1, 1998; 6(1): 78 - 79. [Full Text] [PDF]

				A Sablotzki, M Dehne, I Welters, T Menges, N Lehmann, G Gorlach, C Osmer, and G Hempelmann Alterations of the cytokine network in patients undergoing cardiopulmonary bypass Perfusion, December 1, 1997; 12(6): 393 - 403. [Abstract] [PDF]

This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Song Wan Jean-Louis Vincent Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wan, S. Articles by Vincent, J.-L. Search for Related Content PubMed PubMed Citation Articles by Wan, S. Articles by Vincent, J.-L.