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Ann Thorac Surg 1996;61:1714-1720
© 1996 The Society of Thoracic Surgeons
Department of Thoracic and Cardiovascular Surgery, Hannover Medical School, Hannover, Germany
Accepted for publication January 6, 1996.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. Ten patients with postoperative hyperdynamic circulatory dysregulation (group I) requiring application of 
-constrictors and 10 patients with routine cardiac procedures and stable postoperative hemodynamic indices (group II) were analyzed for mediator release and metabolic and hemodynamic changes until the third postoperative day.
Results. Group I patients showed a significantly increased cardiac index and decreased systemic vascular resistance after bypass (cardiac index, group I: 5.2 ± 1.2 L•min-1•m-2, group II: 2.5 ± 1.6 L•min-1•m-2; systemic vascular resistance, group I: 495 ± 204 dyne • s • cm-5, group II: 1,356 ± 466 dyne•s•cm-5) and at 3 hours (cardiac index, group I: 4.4 ± 0.8 L•min-1•m-2, group II: 2.9 ± 0.6 L•min-1•m-2; systemic vascular resistance, group I: 567 ± 211 dyne•s•cm-5, group II: 1,053 ± 273 dyne•s•cm-5). Significantly higher serum levels of interleukin-6 were assessed in group I (post-bypass, group I: 6,812 ± 9,293 pg/mL, group II: 295 ± 303 pg/mL; 3 hours, group I: 3,474 ± 5,594 pg/mL, group II: 286 ± 296 pg/mL). Concentrations of elastase, tumor necrosis factor, soluble tumor necrosis factor receptor, and interleukin-8 were elevated in group I (not significant). Early postoperative levels of soluble E-selectin and soluble intercellular adhesion molecule were also higher in group I (not significant). Continuously increased levels of endotoxin could be detected in only 3 of 10 patients in group I. Severe lactic acidosis (
5 mmol/L) occurred in group I only.
Conclusions. Postoperative hyperdynamic instability after open heart operations appears to be associated with a certain pattern of mediator release. In particular, interleukin-6 appears to be involved in circulatory dysregulation and metabolic derangement.
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Introduction |
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For editorial comment, see page 1607.
The aim of our study was to clarify whether such inflammatory mechanisms are involved in the SIRS, which in our experience is observed predominantly in adult patients with complex cardiac interventions, but also occurs in a smaller proportion of routine cardiac procedures. Two subgroups of 10 patients each were investigated for mediator release (interleukin [IL]-6, IL-8, tumor necrosis factor [TNF]-, soluble TNF-receptor [sTNF-R], elastase, neopterin), soluble adhesion molecules (intercellular adhesion molecule [sICAM], sE-selectin), endotoxin levels, and white blood cell count, and their influence on hemodynamic stability and organ function as well as the occurrence of bacterial and fungal infections.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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-constrictor application were allocated to group I. Group II patients underwent routine coronary artery bypass grafting or aortic valve procedures with stable hemodynamic indices and served as controls. We excluded from the study patients with acute infections, insulin-dependent diabetes, acute or chronic renal failure requiring hemodialysis, and acute cardiogenic shock. Preoperative patient data are given in Table 1
. Informed patient consent was obtained in all control cases (group II), whereas invasive hemodynamic monitoring was necessary for treatment and was used routinely in all patients (group I) with substantial postoperative circulatory instability. In all group I cases, relatives agreed to additional blood sampling for the study.
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Postoperative Treatment
In case of postoperative hemodynamic instability, infusion of dopamine and adequate fluid replacement were initiated first. If patients could not be stabilized with these interventions, epinephrine and norepinephrine infusions were started depending on the cardiac output and the SVR. To prevent infections in patients with marked hyperdynamic circulatory derangement and prolonged intensive care unit stay, we expanded the antibiotic prophylaxis (tobramycin, flucloxacillin, cefotaxime).
In prospectively scheduled patients (group II), hemodynamic, serologic, and hematologic measurements were taken at the following times: before induction of anesthesia (preop), 10 minutes after CPB (post-CPB), until 3 hours postoperatively (
3h), and 19, 27, 43, and 67 hours postoperatively.
Group I patients were identified early postoperatively by hemodynamic indices indicating high-output circulatory failure. These included increased cardiac index (CI) and reduced SVR of less than 800 dynes•s•cm-5, along with mandatory requirements for -constrictor application (norepinephrine) to maintain adequate arterial perfusion pressure. Measurements in group I patients were synchronized to the sampling protocol to make data acquisition comparable to the prospective protocol of group II patients, in the following way. Hemodynamic measurements at any time leading to patient assignment to group I were allocated to the previous time point of the prospective protocol (group II). All subsequent measurements in group I were then performed according to the regular schedule.
Hemodynamic Data
Arterial pressure, pulmonary artery pressure, right atrial pressure, left atrial pressure, SVR, and cardiac index (CI) were recorded or calculated at time points according to the protocol.
Serologic Indices
The following set of mediators and adhesion molecules was chosen to evaluate the extent of the systemic inflammatory response: IL-6, IL-8, TNF-, sTNF-R, elastase, endotoxin, sICAM, sE-selectin, and neopterin. Enzyme-linked immunosorbent assay techniques were applied to determine IL-6 [9], IL-8 [10], TNF- [11], sTNF-R [12], sICAM (Bender Diagnostics, Vienna, Austria), sE-selectin (Bender Diagnostics), and polymorphonuclear elastase (IMAC Merck, Darmstadt, Germany). Endotoxin was assessed using a modified limulus amebocyte lysate test (Kabi, Stockholm, Sweden) [13]. Neopterin was measured by radioimmunoassay RIA (Immutest; Henning, Berlin, Germany). For evaluation of organ function, routine laboratory indices including creatinine, urea, transaminases, and lactate were assessed according to the protocol.
Hematologic Indices
Cellular blood elements were counted according to the protocol without further immunologic or morphologic differentiation of white blood cells.
Microbiology
For assessment of potential bacterial involvement, blood, urine, and sputum cultures were taken daily.
Postoperative Follow-up
Complete postoperative follow-up was obtained in all patients. The duration of artificial ventilation was accepted as a gross evaluation of pulmonary function and functional rehabilitation in the absence of circulatory depression.
Statistical Analysis
Analysis was performed using Student's t test, and results were expressed as the mean ± standard deviation. Intragroup comparisons at different times were done with the Wilcoxon test. A p value less than 0.05 was regarded as statistically significant. A multiple variance analysis was tried, but conclusive results were not obtainable because of the small group size (n = 10).
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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) was observed after CPB and at 3 hours when compared with preoperative data. This increase was significantly different from values in control patients, which were more stable (post-CPB, group I: 5.2 ± 1.2 L•min-1•m-2, group II: 2.5 ± 0.64 L•min-1•m-2; 3h, group I: 4.4 ± 0.81 L•min-1•m-2, group II: 2.9 ± 0.63 L • min-1 • m-2). Concomitant with changes in CI, a decrease in SVR (Fig 2) occurred in group I that was most evident immediately after bypass (SVR post-CPB, group I: 495 ± 204 dynes•s•cm-5, group II: 1,356 ± 466 dynes•s•cm-5) and at 3 hours (SVR 3h, group I: 567 ± 211 dynes • s • cm-5, group II: 1,053 ± 273 dynes•s•cm-5). These values were significantly different from preoperative values in groups I and II. High-dose norepinephrine infusion was required in all group I patients to provide a mean arterial pressure of more than 60 mm Hg. Thus, a similar trend in changes of hemodynamic indices after CPB was found for both groups, with normalization of SVR and CI after 19 hours.
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). The highest values were measured at 67 hours (group I: 13.9 ± 11.9 pg/mL, group II: 4.2 ± 7.3 pg/mL) (Fig 3). Levels of sTNF-R were consistently higher in group I (not significant) throughout the postoperative period (see Table 2). The highest values were observed early after CPB in both groups (group I: 13.1 ± 8.4 ng/mL, group II: 6.5 ± 3.9 ng/mL).
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). In the later course, similar levels were found in both groups.
Interleukin-8
A high peak of IL-8 levels (see Table 2) was found in group I early after bypass (group I: 139 ± 456 pg/mL, group II: 35 ± 44 pg/mL; not significant). Later, IL-8 levels remained similar, with a steady decrease over time in both groups.
Elastase
Leukocyte elastase revealed a maximum concentration after bypass (group I: 306 ± 141 ng/mL, group II: 201 ± 75 ng/mL) and remained elevated throughout the observation period when compared with the preoperative baseline values of group II (45 ± 26 ng/mL). Significant differences between the groups were not obtained, and maximal concentrations were followed by a steady decrease (see Table 2).
Endotoxin
In the majority of samples from both groups (71 of 90), endotoxin was not detectable. In only 17 of 50 samples in group I and 12 of 40 samples in group II, substantial amounts of endotoxin were noted (see Fig 3). In most cases with positive results, especially in 9 of 10 group II patients, only a single sample was found to be positive for endotoxin. One group II patient had multiple endotoxin-positive samples. In contrast, consistently elevated endotoxin levels throughout the observation period were found exclusively in 3 group I patients, varying between 17 and 30 pg/mL.
Soluble E-Selectin and Soluble Intercellular Adhesion Molecule
The plasma concentrations of both types of soluble adhesion molecules achieved higher levels in group I between post-bypass and 19 hours (not significant), with a maximum for sE-selectin (see Table 2) post-CPB of 74.4 ± 42.1 ng/mL, compared with 39.1 ± 17.9 ng/mL. Courses of sICAM levels appeared to be similar, varying between 309 ± 126 ng/mL and 691 ± 194 ng/mL.
Neopterin
Neopterin levels varied between 9.6 ± 4.8 µmol/L (preoperative, group II) and 38.8 ± 41.2 µmol/L (43 hours, group I), without a peak in either group. However, group I levels were higher at all intervals when compared with group II (see Table 2).
White Blood Cell Counts
Originating from baseline values of less than 8,000/µL, leukocytes increased postoperatively with higher values in group I for each time point, reaching a plateau between 19 and 43 hours (Fig 4). Group II levels were generally lower and were statistically different from group I values at 3 hours (group I: 18,500 ± 5,700/µL, group II: 13,300 ± 4,900/µL). After 27 hours, a steady decline of leukocyte counts occurred in both groups, but levels remained elevated above baseline until 67 hours (see Fig 4).
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3h, group I: 5.1 ± 1.8 mmol/L, group II: 2.9 ± 0.8 mmol/L). The difference between the groups was significant at these points. Elevated lactate levels in group II were not significantly different from baseline values (Fig 5).
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Organ Function
Impairment of organ function was more pronounced in group I, as evidenced by higher values of transaminases (aspartate aminotransferase, glutamic-pyruvic transaminase), urea, creatinine, and -amylase throughout the postoperative course. Preoperative values were normal and not significantly different between the groups excluding chronic preoperative organ dysfunction, especially in group I. The duration of respirator dependency was longer in group I (group I: 44.1 ± 27.9 hours, group II: 12.0 ± 3.5 hours; p < 0.05).
Postoperative Course
All control patients (group II) experienced an uneventful postoperative course without apparent organ dysfunction or infection. There were no deaths in group I, but postoperative morbidity was higher. As such, 2 patients required intraaortic balloon counterpulsation in addition to high-dose inotropic treatment. One reexploration was necessary for bleeding. Repeated hemodialysis for acute renal failure was required in another patient with normal renal function preoperatively, and 3 patients revealed substantial mental disturbances without evidence of persistent neurologic damage. In addition, the intensive care unit stay was significantly longer in group I patients (116.1 ± 118.9 hours) than in group II (29.8 ± 2.4 hours) (p < 0.05).
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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The most impressive difference in cytokine release was a significantly higher IL-6 release early postoperatively in patients with a hyperdynamic circulation (group I: post-CPB, 3h). Peak values of IL-6 occurred concurrent with the maximal circulatory derangement. However, a preceding TNF- release, reflecting a potential primary trigger for subsequent IL-6 release, as suggested by others [15], could not be found. This fact could be explained either by absent TNF release or by the presence of TNF-binding protein [16] and complex formation. A second reason for the lack of TNF peak level detection may be the sampling pattern in group I. These patients were identified only at the time of occurrence of a hyperdynamic circulatory state, possibly beyond the point of maximal TNF release. The soluble TNF receptor (sTNF-R), a large fragment of the TNF receptor, has been identified as a naturally occurring inhibitor of TNF. Therefore, TNF receptor shedding appears to be dependent on TNF liberation [17]. In concordance with elevated sTNF-R levels in group I, a higher preceding TNF release may be assumed, potentially explaining the missing TNF peak. Early and marked postoperative IL-6 release in group I therefore does not appear to conflict with the finding of low TNF values. The possibility of a pivotal TNF release initiating the acute-phase response thus cannot be ruled out from the results of our study.
The IL-6 levels obtained in group II patients, with maximal release early after bypass or up to 3 hours postoperatively, were similar to those reported by Butler and colleagues [4], who compared cytokine responses during the use of bubble and membrane oxygenators. However, IL-6 values in our group I patients were approximately tenfold higher, representing a strong argument for the hypothesis that involvement of inflammatory processes was the reason for circulatory derangement. In concordance with a similar pattern of IL-6 release by Butler and colleagues [4], changes in postbypass CI and SVR were also comparable to the hemodynamic indices of group II patients with a relatively stable course, whereas hemodynamic variables in group I were significantly more unstable.
By inclusion of sE-selectin and sICAM assessment, we tried to elucidate endothelial adhesion molecule involvement in this type of inflammatory response. Although a clear relation between cellular adhesion molecules and correlating soluble forms has not been proven, a similar behavior is widely assumed [18]. Consistently higher sE-selectin and sICAM levels in group I may indicate a contribution of endothelial activation to the generation of SIRS in patients undergoing open heart procedures. On the basis of our results, we can only speculate on the primary mechanisms initiating the inflammatory cascade. One initiating factor could be endotoxemia, but consistently elevated endotoxin levels were found only in 3 group I patients to support the hypothesis of bacterial or endotoxin translocation from the gut, as reported by other groups [6, 7, 14]. In endotoxin-negative patients, translocation processes may also be present, but neutralizing effects and fast clearance may prohibit the detection of endotoxins [13]. In contrast to other studies, the proportion of endotoxin-negative patients remains high and the absolute levels found appear to be relatively low. This discrepancy may be related to different techniques of sampling. In our study, we chose a special sampling kit free of endotoxin contamination.
Although neopterin has been shown to be a marker for septic complications [19], we could find neither high levels of neopterin release nor differences between the groups. The reason might be the rather slow kinetics of neopterin formation, which makes neopterin a less sensitive marker of transient septic processes than IL-6.
Our study as well as previous reports on SIRS after open heart operations supports a strong interest for preventive treatment options. Positive reports on steroid treatment in coronary bypass patients have been published [20], and a reduction of TNF and leukotriene B4 release as well as stabilization of hemodynamic indices and body temperature was reported. In contrast, elastase release was not influenced by dexamethasone treatment in such cases. These facts and our results demonstrating similar elastase levels in both groups may signify that the degree of elastase release may not be representative of the degree of inflammatory activation.
Finally, we consider this study to be an attempt to clarify the interrelation between the degree and pattern of inflammatory responses after open heart operations on the one hand and postoperative hemodynamic indices, organ function, and clinical outcome on the other hand. Our study suggests that a hyperdynamic circulatory derangement, especially occurring in more complex cardiac operations such as mitral or tricuspid valve procedures, is coincident with a marked inflammatory response.
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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J. B. Celik, N. Gormus, S. Okesli, Z. I. Gormus, and H. Solak Methylprednisolone prevents inflammatory reaction occurring during cardiopulmonary bypass: effects on TNF-{alpha}, IL-6, IL-8, IL-10 Perfusion, May 1, 2004; 19(3): 185 - 191. [Abstract] [PDF]
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R. L. Levin, M. A. Degrange, G. F. Bruno, C. D. Del Mazo, D. J. Taborda, J. J. Griotti, and F. J. Boullon Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery Ann. Thorac. Surg., February 1, 2004; 77(2): 496 - 499. [Abstract] [Full Text] [PDF]
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A. J. Chong, C. R. Hampton, and E. D. Verrier Microvascular Inflammatory Response in Cardiac Surgery Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2003; 7(3): 333 - 354. [Abstract] [PDF]
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P. Gessler, J. Pfenninger, J.-P. Pfammatter, T. Carrel, O. Baenziger, and C. Dahinden Plasma levels of interleukin-8 and expression of interleukin-8 receptors on circulating neutrophils and monocytes after cardiopulmonary bypass in children J. Thorac. Cardiovasc. Surg., September 1, 2003; 126(3): 718 - 725. [Abstract] [Full Text] [PDF]
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G. M. Palatianos, C. N. Foroulis, M. I. Vassili, G. Astras, K. Triantafillou, E. Papadakis, A. A. Lidoriki, E. Iliopoulou, and E. N. Melissari A prospective, double-blind study on the efficacy of the bioline surface-heparinized extracorporeal perfusion circuit Ann. Thorac. Surg., July 1, 2003; 76(1): 129 - 135. [Abstract] [Full Text] [PDF]
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R. G. Leyh, T. Kofidis, M. Struber, S. Fischer, K. Knobloch, B. Wachsmann, C. Hagl, A. R. Simon, and A. Haverich Methylene blue: The drug of choice for catecholamine-refractory vasoplegia after cardiopulmonary bypass? J. Thorac. Cardiovasc. Surg., June 1, 2003; 125(6): 1426 - 1431. [Abstract] [Full Text] [PDF]
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S. M. Jakob Splanchnic Blood Flow in Low-Flow States Anesth. Analg., April 1, 2003; 96(4): 1129 - 1138. [Abstract] [Full Text] [PDF]
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P. Samankatiwat, I. Samartzis, P. Lertsithichai, D. Stefanou, P. P Punjabi, K. M Taylor, and T. Gourlay Leucocyte depletion in cardiopulmonary bypass: a comparison of four strategies Perfusion, March 1, 2003; 18(2): 95 - 105. [Abstract] [PDF]
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M. Czerny, D. Zimpfer, J. Kilo, R. Gottardi, D. Dunkler, E. Wolner, and M. Grimm Coronary reoperations: recurrence of angina and clinical outcome with and without cardiopulmonary bypass Ann. Thorac. Surg., March 1, 2003; 75(3): 847 - 852. [Abstract] [Full Text] [PDF]
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S. Schroeder, N. Borger, H. Wrigge, A. Welz, C. Putensen, A. Hoeft, and F. Stuber A tumor necrosis factor gene polymorphism influences the inflammatory response after cardiac operation Ann. Thorac. Surg., February 1, 2003; 75(2): 534 - 537. [Abstract] [Full Text] [PDF]
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R. Ascione, M. Caputo, and G. D. Angelini Off-pump coronary artery bypass grafting: not a flash in the pan Ann. Thorac. Surg., January 1, 2003; 75(1): 306 - 313. [Abstract] [Full Text] [PDF]
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Z. S. Meharwal, Y. K. Mishra, V. Kohli, R. Bapna, S. Singh, and N. Trehan Off-pump multivessel coronary artery surgery in high-risk patients Ann. Thorac. Surg., October 1, 2002; 74(4): S1353 - 1357. [Abstract] [Full Text] [PDF]
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A. Franke, W. Lante, V. Fackeldey, H. P. Becker, C. Thode, W. D. Kuhlmann, and A. Markewitz Proinflammatory and antiinflammatory cytokines after cardiac operation: different cellular sources at different times Ann. Thorac. Surg., August 1, 2002; 74(2): 363 - 370. [Abstract] [Full Text] [PDF]
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H. B. Bittner and M. A. Savitt Off-pump coronary artery bypass grafting decreases morbidity and mortality in a selected group of high-risk patients Ann. Thorac. Surg., July 1, 2002; 74(1): 115 - 118. [Abstract] [Full Text] [PDF]
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R. Ascione, S. Al-Ruzzeh, K. Amer, and G. D Angelini Subsystem organ function during coronary surgery Perfusion, July 1, 2002; 17(4): 295 - 303. [Abstract] [PDF]
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M. H. Chamberlain, R. Ascione, B. C. Reeves, and G. D. Angelini Evaluation of the effectiveness of off-pump coronary artery bypass grafting in high-risk patients: an observational study Ann. Thorac. Surg., June 1, 2002; 73(6): 1866 - 1873. [Abstract] [Full Text] [PDF]
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T. Ryan, J. Balding, E. M. McGovern, J. Hinchion, W. Livingstone, Z. Chughtai, and O. P. Smith Lactic acidosis after cardiac surgery is associated with polymorphisms in tumor necrosis factor and interleukin 10 genes Ann. Thorac. Surg., June 1, 2002; 73(6): 1905 - 1909. [Abstract] [Full Text] [PDF]
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A. Leins and J. Cremer Invited commentary Ann. Thorac. Surg., June 1, 2002; 73(6): 1910 - 1911. [Full Text] [PDF]
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A. Sablotzki, I. Friedrich, J. Muhling, M. G Dehne, J. Spillner, R. E Silber, and E. Czeslik The systemic inflammatory response syndrome following cardiac surgery: different expression of proinflammatory cytokines and procalcitonin in patients with and without multiorgan dysfunctions Perfusion, March 1, 2002; 17(2): 103 - 109. [Abstract] [PDF]
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 D J Brull, J Sanders, A Rumley, G D Lowe, S E Humphries, and H E Montgomery Impact of angiotensin converting enzyme inhibition on post-coronary artery bypass interleukin 6 release Heart, March 1, 2002; 87(3): 252 - 255. [Abstract] [Full Text] [PDF]
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V. R. Conti and C. McQuitty Vasodilation and Cardiopulmonary Bypass : The Role of Bradykinin and the Pulmonary Vascular Endothelium Chest, December 1, 2001; 120(6): 1759 - 1761. [Full Text] [PDF]
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U. P. Schurr, G. Zund, S. P. Hoerstrup, J. Grunenfelder, F. E. Maly, P. R. Vogt, and M. I. Turina Preoperative administration of steroids: influence on adhesion molecules and cytokines after cardiopulmonary bypass Ann. Thorac. Surg., October 1, 2001; 72(4): 1316 - 1320. [Abstract] [Full Text] [PDF]
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G. E. Hill The Inflammatory Response to Cardiopulmonary Bypass-- Should It Be Treated? Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2001; 5(3): 229 - 235. [Abstract] [PDF]
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S.R. Craig, H.A. Leaver, P.L. Yap, G.C. Pugh, and W.S. Walker Acute phase responses following minimal access and conventional thoracic surgery Eur. J. Cardiothorac. Surg., September 1, 2001; 20(3): 455 - 463. [Abstract] [Full Text] [PDF]
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 D.J. Brull, H.E. Montgomery, J. Sanders, S. Dhamrait, L. Luong, A. Rumley, G.D.O. Lowe, and S.E. Humphries Interleukin-6 Gene -174G>C and -572G>C Promoter Polymorphisms Are Strong Predictors of Plasma Interleukin-6 Levels After Coronary Artery Bypass Surgery Arterioscler Thromb Vasc Biol, September 1, 2001; 21(9): 1458 - 1463. [Abstract] [Full Text] [PDF]
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Y. Okazaki, K. Takarabe, J.-i. Murayama, E. Suenaga, K. Furukawa, K. Rikitake, M. Natsuaki, and T. Itoh Coronary endothelial damage during off-pump CABG related to coronary-clamping and gas insufflation Eur. J. Cardiothorac. Surg., June 1, 2001; 19(6): 834 - 839. [Abstract] [Full Text] [PDF]
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P. Demers, S. Elkouri, R. Martineau, A. Couturier, and R. Cartier Outcome with high blood lactate levels during cardiopulmonary bypass in adult cardiac operation Ann. Thorac. Surg., December 1, 2000; 70(6): 2082 - 2086. [Abstract] [Full Text] [PDF]
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H. Aebert, S. Kirchner, A. Keyser, D. E. Birnbaum, E. Holler, R. Andreesen, and G. Eissner Endothelial apoptosis is induced by serum of patients after cardiopulmonary bypass Eur. J. Cardiothorac. Surg., November 1, 2000; 18(5): 589 - 593. [Abstract] [Full Text] [PDF]
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T. Yokoyama, F. J. Baumgartner, A. Gheissari, E. R. Capouya, G. P. Panagiotides, and R. J. Declusin Off-pump versus on-pump coronary bypass in high-risk subgroups Ann. Thorac. Surg., November 1, 2000; 70(5): 1546 - 1550. [Abstract] [Full Text] [PDF]
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M. S. Ali, M. Harmer, and R. Vaughan Serum S100 protein as a marker of cerebral damage during cardiac surgery Br. J. Anaesth., August 1, 2000; 85(2): 287 - 298. [Abstract] [Full Text] [PDF]
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Y. Okazaki, Z.-L. Cao, S. Ohtsubo, M. Hamada, K. Naito, K. Rikitake, M. Natsuaki, and T. Itoh Leukocyte-depleted reperfusion after long cardioplegic arrest attenuates ischemia-reperfusion injury of the coronary endothelium and myocardium in rabbit hearts Eur. J. Cardiothorac. Surg., July 1, 2000; 18(1): 90 - 97. [Abstract] [Full Text] [PDF]
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M. Czerny, H. Baumer, J. Kilo, A. Lassnigg, A. Hamwi, T. Vukovich, E. Wolner, and M. Grimm Inflammatory response and myocardial injury following coronary artery bypass grafting with or without cardiopulmonary bypass Eur. J. Cardiothorac. Surg., June 1, 2000; 17(6): 737 - 742. [Abstract] [Full Text] [PDF]
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J. T. Cremer, T. Wittwer, A. Boning, M. B. Anssar, T. Kofidis, A. Mugge, and A. Haverich Minimally invasive coronary artery revascularization on the beating heart Ann. Thorac. Surg., June 1, 2000; 69(6): 1787 - 1791. [Abstract] [Full Text] [PDF]
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S. Pagni and E. H. Austin Use of intravenous methylene blue for the treatment of refractory hypotension after cardiopulmonary bypass J. Thorac. Cardiovasc. Surg., June 1, 2000; 119(6): 1297 - 1298. [Full Text]
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J.-P. Yared, N. J. Starr, F. K. Torres, C. A. Bashour, G. Bourdakos, M. Piedmonte, J. A. Michener, J. A. Davis, and T. E. Rosenberger Effects of single dose, postinduction dexamethasone on recovery after cardiac surgery Ann. Thorac. Surg., May 1, 2000; 69(5): 1420 - 1424. [Abstract] [Full Text] [PDF]
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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]
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M. Bog'a, F. Islamog'lu, I. Badak, M. Cikirikciog'lu, T. Bakalim, T. Yag'di, S. Buket, and A. Hamulu The effects of modified hemofiltration on inflammatory mediators and cardiac performance in coronary artery bypass grafting Perfusion, March 1, 2000; 15(2): 143 - 150. [Abstract] [PDF]
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T Wittwer, J Cremer, P Boonstra, J Grandjean, M Mariani, A Mugge, H Drexler, P den Heijer, E-R v Leitner, A Hepp, et al. Myocardial "hybrid" revascularisation with minimally invasive direct coronary artery bypass grafting combined with coronary angioplasty: preliminary results of a multicentre study Heart, January 1, 2000; 83(1): 58 - 63. [Abstract] [Full Text] [PDF]
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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]
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J. C. Kovacich, E. M. Boyle Jr, E. N. Morgan, T. G. Canty Jr, A. L. Farr, M. T. Caps, N. Frank, T. H. Pohlman, and E. D. Verrier INHIBITION OF THE TRANSCRIPTIONAL ACTIVATOR PROTEIN NUCLEAR FACTOR {kappa}BPREVENTS HEMODYNAMIC INSTABILITY ASSOCIATED WITH THE WHOLE-BODY INFLAMMATORYRESPONSE SYNDROME J. Thorac. Cardiovasc. Surg., July 1, 1999; 118(1): 154 - 162. [Abstract] [Full Text] [PDF]
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F. J. Baumgartner, A. Gheissari, E. R. Capouya, G. P. Panagiotides, A. Katouzian, and T. Yokoyama Technical aspects of total revascularization in off-pump coronary bypass via sternotomy approach Ann. Thorac. Surg., June 1, 1999; 67(6): 1653 - 1658. [Abstract] [Full Text] [PDF]
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U. Boeken, P. Feindt, N. Zimmermann, G. Kalweit, T. Petzold, and E. Gams Increased preoperative C-reactive protein (CRP)-values without signs of an infection and complicated course after cardiopulmonary bypass (CPB) - operations Eur. J. Cardiothorac. Surg., May 1, 1999; 13(5): 541 - 545. [Abstract] [Full Text] [PDF]
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A. Liebold, C. Keyl, and D. E. Birnbaum The heart produces but the lungs consume proinflammatory cytokines following cardiopulmonary bypass Eur. J. Cardiothorac. Surg., March 1, 1999; 15(3): 340 - 345. [Abstract] [Full Text] [PDF]
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S. T Baksaas, H. I Flom-Halvorsen, E. Ovrum, V. Videm, T. E. Mollnes, F. Brosstad, and J. L Svennevig Leucocyte filtration during cardiopulmonary reperfusion in coronary artery bypass surgery Perfusion, March 1, 1999; 14(2): 107 - 117. [Abstract] [PDF]
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S T Baksaas, V Videm, T E Mollnes, S Tollofsrud, G Hetland, T Pedersen, and J L Svennevig Leucocyte filtration during cardiopulmonary bypass hardly changed leucocyte counts and did not influence myeloperoxidase, complement, cytokines or platelets Perfusion, December 1, 1998; 13(6): 429 - 436. [Abstract] [PDF]
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G. Asimakopoulos and K. M. Taylor Effects of cardiopulmonary bypass on leukocyte and endothelial adhesion molecules Ann. Thorac. Surg., December 1, 1998; 66(6): 2135 - 2144. [Abstract] [Full Text] [PDF]
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J. Bonatti, R. Ladurner, H. Antretter, C. Hormann, G. Friedrich, N. Moes, V. Muhlberger, and O. Dapunt Single coronary artery bypass grafting - a comparison between minimally invasive 'off pump' techniques and conventional procedures Eur. J. Cardiothorac. Surg., October 1, 1998; 14(suppl_1): S7 - S12. [Abstract] [Full Text] [PDF]
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W. Wang, H. M. Huang, De Ming Zhu, H. Chen, Z. K. Su, and W. X. Ding Modified ultrafiltration in paediatric cardiopulmonary bypass Perfusion, September 1, 1998; 13(5): 304 - 310. [Abstract] [PDF]
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L. Lindberg, A-K. Olsson, K. Anderson, and P. Jogi SERUM S-100 PROTEIN LEVELS AFTER PEDIATRIC CARDIAC OPERATIONS: A POSSIBLE NEW MARKER FOR POSTPERFUSION CEREBRAL INJURY J. Thorac. Cardiovasc. Surg., August 1, 1998; 116(2): 281 - 285. [Abstract] [Full Text] [PDF]
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R. D. Mainwaring, J. J. Lamberti, and T. E. Hugli Complement Activation and Cytokine Generation After Modified Fontan Procedure Ann. Thorac. Surg., June 1, 1998; 65(6): 1715 - 1720. [Abstract] [Full Text] [PDF]
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P. R. B. Evora, P. J. F. Ribeiro, J. C. S. de Andrade, and K. M. Taylor Methylene Blue Administration in SIRS After Cardiac Operations Ann. Thorac. Surg., April 1, 1997; 63(4): 1212 - 1213. [Full Text]
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K. M. Taylor SIRS-The Systemic Inflammatory Response Syndrome After Cardiac Operations Ann. Thorac. Surg., June 1, 1996; 61(6): 1607 - 1608. [Full Text]
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B. Dybdahl, A. Wahba, E. Lien, T. H. Flo, A. Waage, N. Qureshi, O. F.M. Sellevold, T. Espevik, and A. Sundan Inflammatory Response After Open Heart Surgery: Release of Heat-Shock Protein 70 and Signaling Through Toll-Like Receptor-4 Circulation, February 12, 2002; 105(6): 685 - 690. [Abstract] [Full Text] [PDF]
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