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

This Article Abstract Full Text (PDF) 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): Hans Meisner Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Massoudy, P. Articles by Meisner, H. Search for Related Content PubMed PubMed Citation Articles by Massoudy, P. Articles by Meisner, H.

Ann Thorac Surg 1999;67:1059-1064
© 1999 The Society of Thoracic Surgeons

---

Original Article

Sodium nitroprusside during coronary artery bypass grafting: evidence for an antiinflammatory action

^a Departments of Department of Cardiovascular Surgery, German Heart Center Munich, Munich, Germany
^b Department of Anesthesiology, German Heart Center Munich, Munich, Germany
^c Department of Physiology, University of Munich, Munich, Germany

Accepted for publication October 14, 1998.

Address reprint requests to Dr Massoudy, Department of Cardiovascular Surgery, German Heart Center Munich, Lazarettstr 36, 80636 Munich, Germany
e-mail: massoudy{at}dhm.mhn.de

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. It was the aim of the present study to investigate whether a nitric oxide donor can reduce systemic inflammation and the cardiac inflammatory response during coronary artery bypass grafting with cardiopulmonary bypass.

Methods. Patients undergoing elective coronary artery bypass grafting (n = 22) were randomly assigned to treatment with either sodium nitroprusside (0.5 µg · kg^-1 · min^-1) or placebo (controls), both for the first 20 minutes of reperfusion. Interleukin-6 and interleukin-8 levels, the adhesion molecules CD41 and CD62 on platelets and CD41 on monocytes and PMN (as markers for coaggregate formation), CD11b on monocytes and PMN, as well as platelet and leukocyte counts were determined in radial artery and coronary sinus blood before cardiopulmonary bypass and during reperfusion (1, 5, 10, 25, and 35 minutes).

Results. A reduction of systemic interleukin-6 levels (15.4 ± 3.5 pg/mL, 36.7 ± 5.9 pg/mL, and 46.8 ± 8.0 pg/mL versus 33.4 ± 7.7 pg/mL, 76.7 ± 13.2 pg/mL, and 106.0 ± 26.5 pg/mL, respectively, at 1, 25, and 35 minutes of reperfusion) and interleukin-8 (29.6 ± 4.5 pg/mL versus 54.0 ± 9.4, pg/mL, resp., at 35 minutes of reperfusion) resulted from treatment with sodium nitroprusside. No intracardiac production of interleukin-8 in sodium nitroprusside-treated patients (-1.1 ± 0.4 pg/mL and -2.8 ± 2.2 pg/mL, resp., for the coronary sinus–radial artery difference at 5 and 25 minutes of reperfusion) was observed, whereas cardiac production of interleukin-8 was present in controls (2.5 ± 1.5 pg/mL and 5.5 ± 2.8 pg/mL, resp.). Retention of platelet/leukocyte coaggregates occurred during coronary passage in controls (coronary sinus–radial artery difference for CD41-positive monocytes at 1 and 10 minutes of reperfusion, -16.3% ± 8.5% and -8.8% ± 2.6%, resp.). This was reduced in sodium nitroprusside-treated patients (with 5.8% ± 5.2% and 0.0% ± 3.2%). Retention of platelets in controls (ratio of coronary sinus to radial artery platelet count at 5 and 10 minutes of reperfusion, 88% ± 6% and 91% ± 5%) was compared to washout in treated patients (108% ± 6% and 113% ± 7%).

Conclusions. In patients undergoing routine coronary artery bypass grafting, administration of sodium nitroprusside during early reperfusion alleviates systemic inflammation and the cardiac inflammatory response.

	Introduction

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Reperfusion can aggravate the damage sustained by the heart during ischemia [1–3]. In experimental studies nitric oxide (NO) has been shown to reduce reperfusion injury and therefore, to act as a cardioprotective agent [4–6]. This action seems to be independent of vasodilatation, but may relate to the capacity of NO to act as an oxygen radical scavenger [4]. During cardiac operations with cardiopulmonary bypass (CPB) a systemic inflammatory reaction has been described that leads to the activation of white blood cells and their migration into the tissues [7, 8]. Moreover, the heart has been shown to be a site of inflammation during postischemic reperfusion in the clinical situation [9–11]. Experiments using canine models put on CPB and undergoing ischemia and reperfusion demonstrated a protective effect of endogenous nitric oxide [12]. However, studies of the clinical situation are lacking with the exception of a study in pediatric cardiac operations, where a reduction of complement activation during CPB was observed [13].

The hypothesis of the present study was that the application of a NO donor reduces the systemic inflammatory reaction and the interaction of activated blood cells with the coronary endothelium during early reperfusion in patients undergoing routine coronary artery bypass grafting. The proinflammatory cytokines interleukin-6 (IL-6) and IL-8, leukocyte adhesion molecule CD11b, platelet adhesion molecules CD41 and CD62, as well as CD41 on leukocytes, which have all been shown to be upregulated by CPB [11], were determined in the present study.

	Material and methods

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Patients
The study was prospective and randomized. Inclusion criteria were (1) left ventricular ejection fraction 55% or more; (2) age 75 years or less; (3) no myocardial infarction (as defined by significant elevation of serum creatine-kinase levels or electrocardiographic signs for myocardial infarction) within 14 days before the operation; and (4) intraoperative aortic clamping time between 40 and 70 minutes. Exclusion criteria were known hypersensitivity to sodium nitroprusside (SNP) or any other nitro substances, inflammatory diseases, or currently taking immunosuppressive drugs. Every patient with a profile suitable for enrollment in the study was informed about the nature of the study and about potential side effects of the application of SNP and had to sign a written consent the day before the operation. The preoperative patient characteristics are shown in Table 1. The study was approved by the local ethics committee in August 1996. Sodium nitroprusside (Nipruss) was kindly donated by Schwarz Pharma (Mannheim, Germany).

Operation
All patients underwent coronary artery bypass grafting with CPB using roller pumps (Stöckert, Munich, Germany) and disposable bubble oxygenators (Dideco, Mirandola, Italy). The pump was primed with 1,500 mL of lactated Ringer’s solution to which 100 mmoles of sodium bicarbonate and 5,000 IU of heparin (Ratiopharm, Ulm, Germany) were added. The CPB was instituted at a flow rate of 2.4 L · min^-1 · m^-2 body surface area after systemic heparinization. The body temperature was cooled to 26° to 28°C (moderate hypothermia) and 1,000 mL of cold Bretschneider solution (Custodiol; Köhler Chemie, Alsbach-Hähnlein, Germany) was applied as antegrade cardioplegia after clamping of the aorta. The remaining blood of the CPB circuit was prepared using a cell-saver (Haemonetics, Munich, Germany) before retransfusion.

Intervention
After release of the aortic cross-clamp, patients received either SNP (0.5 µg · kg^-1 · min^-1) or 5% glucose solution (the solvent for Nipruss) as placebo, both infused into the arterial line of the heart–lung machine through a Luer lock (Braun, Melsungen, Germany). After 20 minutes the infusion was stopped. During infusion of SNP/placebo a tangential clamp (Lambert-Kay clamp, Johnson & Johnson, Nordersted, Germany) was fixed on the ascending aorta to allow for sewing of the proximal anastomoses of the venous bypasses. The Lambert-Kay clamp was released at approximately 25 minutes of reperfusion. Protamine (1 mg/kg) was given at approximately 35 minutes of reperfusion.

Blood samples
The blood for arterial measurements was drawn from a cannula in the radial artery. The coronary venous blood was withdrawn from a catheter (multipurpose, 6F, Cordis, Roden, the Netherlands), which was placed transcutaneously into the coronary sinus through the internal jugular vein under fluoroscopic control. The correct position of this catheter was monitored by registering the pressure curve and determining oxygen saturation (25% to 45%) of samples from coronary sinus blood. Samples were taken at the following time points: (1) after application of heparin; (2) 1, 5, and 10 minutes after release of the aortic cross-clamp; (3) after release of the Lambert-Kay clamp (approximately 25 minutes after release of the aortic cross-clamp); and (4) after application of protamine (approximately 35 minutes after release of the aortic cross-clamp). Blood was simultaneously drawn from the radial artery and the coronary sinus at all time points.

Immunoassays
An aliquot of the blood (2 mL) was stored on ice until centrifuged (2,000 g for 10 minutes) to obtain platelet-poor plasma, which was stored at -20°C until final processing within 1 to 14 days. Concentrations of IL-6 and IL-8 were determined by sandwich-type immunoassays (Endogen, Woburn, MA). In both cases standards covered a range from 0 to 1,000 pg/mL. Because of continuous hemodilution during the surgical intervention, all measured concentrations had to be corrected to the hematocrit of the arterial sample before heparin administration to ensure their comparability. Cardiac release of IL-6 and IL-8 was calculated from the coronary venoarterial differences at each time point.

Flow cytometry
Flow cytometry for adhesion molecules on platelets and leukocytes was used as previously described [11]. In brief, for determination of leukocyte adhesion molecules, aliquots of the blood samples were mixed with 1 mL of FACS lysing solution (Becton Dickinson, Heidelberg, Germany) and double-stained with anti-CD41 antibodies (Serotec; Kidlington, Oxford, Great Britain) and anti-CD11b antibodies (Exalpha, Boston, MA). For analysis of platelets, 100 µL of blood and 1 mL of Cellfix (Becton Dickinson) were mixed and incubated with antibodies against CD41 (Serotec) and CD62 (Harlan Seralab; Crawley Down, Sussex, Great Britain).

Flow cytometry was performed with a FACScan and Lysis II software (Becton Dickinson). The mean fluorescence intensity was taken as a measure of antibody binding. The nonspecific background was quantified by measurement of the fluorescence intensity of samples labeled with nonbinding isotype-matched antibodies, and subsequently subtracted. Results are given in relative fluorescence units.

Statistical analysis
All results are expressed as mean ± standard error of the mean. Student’s t test for paired samples was used to evaluate differences between the groups with SPSS for Windows version 7.0 software (SPSS Inc, Chicago, IL). A difference on a two-tailed test was considered as statistically significant for p value less than 0.05.

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Interleukins, adhesion molecules, and quantitative cell counts
Systemic levels of IL-6 and IL-8 are shown in Figures 1 and 2 . The SNP effect on IL-6-levels was obvious right after the beginning of the SNP infusion. The effect on IL-8 levels became significant after the application of SNP had already been stopped. No effect of SNP application was observed on IL-6 levels during coronary passage (Table 2 ). In contrast, cardiac IL-8 production was significantly less in hearts of SNP-treated patients at 5 and 25 minutes of reperfusion compared to nontreated patients (Fig 3 ).

View larger version (14K): [in this window] [in a new window]   Fig 1. Systemic (= arterial) interleukin-6 concentration. Values are means, bars represent standard error of the mean. n = 8 to 11 patients, *p < 0.05 as compared to the respective value in controls. (CPB = cardiopulmonary bypass.)

View larger version (15K): [in this window] [in a new window]   Fig 2. Systemic (= arterial) interleukin-8 concentration. Values are means, bars represent standard error of the mean. n = 8 to 9 patients, *p < 0.05 as compared to the respective value in controls. (CPB = cardiopulmonary bypass.)

View larger version (17K): [in this window] [in a new window]   Fig 3. Coronary venoarterial difference of interleukin-8 concentration. Symbols are means, bars represent standard error of the mean. n = 8 to 9 patients, *p < 0.05 as compared to the respective value in controls. (CPB = cardiopulmonary bypass.)

View larger version (20K): [in this window] [in a new window]   Fig 4. Coronary venoarterial difference of CD41-positive monocytes. Values are means, bars represent standard error of the mean. n = 8 to 9 patients, *p < 0.05 as compared to the respective value in controls. (CPB = cardiopulmonary bypass.)

View larger version (19K): [in this window] [in a new window]   Fig 5. Coronary venoarterial difference of CD41-positive PMN. Values are means, bars represent standard error of the mean. n = 9 to 10 patients, *p < 0.05 as compared to the respective value in controls. (CPB = cardiopulmonary bypass.)

View larger version (18K): [in this window] [in a new window]   Fig 6. Coronary venoarterial ratio of platelet count. Values are means, bars represent standard error of the mean. n = 8 patients, *p < 0.05 as compared to the respective value in controls. (CPB = cardiopulmonary bypass.)

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
In the present study, the administration of SNP for only the first 20 minutes of reperfusion to patients undergoing coronary artery bypass grafting led to a reduction of the acute inflammatory response. In addition to lower systemic levels of IL-6 and IL-8 and less cardiac production of IL-8, the retention of platelet-bearing leukocytes and of platelets during coronary passage is ameliorated in SNP-treated patients.

In the present study, the effect was achieved without observing systemic hemodynamic changes. Coronary vascular resistance and flow rate, which were not measured in this study, theoretically, could have been altered by low-dose SNP. However, in the presence of preexisting ischemic vasodilation, such an effect seems rather unlikely.

Interleukins, adhesion molecules, and quantitative cell counts
The continuous increase in systemic IL-6 concentrations after release of aortic cross-clamp is in accordance with other studies. Maximum levels for IL-6 and IL-8 have been reported to occur between 2 and 4 hours after declamping of the aorta [14, 15]. Because cytokines are known to exert negative inotropic effects [16], the reduced levels of IL-6 and IL-8 (seen in the presence of SNP) could benefit myocardial function. Cardiac production of IL-8 has been shown during recanalization with percutaneous transluminal coronary angioplasty in acute myocardial infarction, along with a significant cardiac production of IL-6 during reperfusion of the infarcted hearts [9]. Interestingly, such cardiac inflammatory responses were not observed following percutaneous transluminal coronary angioplasty without acute myocardial infarction [9]. Cardiac protection during surgical ischemia, afforded by the use of cardioplegic solution, may be the cause for the absence of production of IL-6 during cardiac reperfusion in the present study.

Neumann and colleagues [9] found no retention of activated PMN immediately and 5 minutes after balloon inflation. Also in the present study, we found no change in the expression of the adhesion molecule CD11b on PMN and monocytes during reperfusion. Activated blood platelets express the adhesion molecule CD41 (GpIIb/IIIa) on the membrane surface. This molecule (among others) allows platelets to coaggregate with the larger leukocytes, especially monocytes and PMN. Reduced cardiac retention of CD41-positive monocytes and PMN in the present study indicates less interaction between the coronary vascular endothelium and platelet/leukocyte aggregates with the administration of SNP. There are no comparable results in the literature.

The effect on quantitative platelet count (washout in the presence of SNP) may correlate with the reduced retention of platelet/leukocyte aggregates. Because the amount of platelets forming aggregates with single leukocytes is always greater than one [17], the corresponding effect on leukocyte count will be far less. In our study it was below the level of detection. The sudden intracoronary sequestration of blood platelets after the application of protamine (35 minutes of reperfusion), seen in both groups, is in accordance with the proinflammatory effects reported for this drug [18].

Clinical effects, timing of intervention, involved mechanism
Postoperative medical treatment of the patients was not standardized and recovery of myocardial function was not an end point of the present study. A direct relation between the amount of proinflammatory cytokines, such as IL-6, and postoperative myocardial recovery has been reported [19]. However, there is no study that has demonstrated a functional benefit after an intervention that helped to reduce the inflammatory response. This may be because, as in our case, the vast majority of patients investigated had a preoperative left ventricular function that was not compromised. These patients tend to have an uneventful postoperative course and it may not be possible to achieve any clinical improvement. Possibly studies may have to focus more on multimorbid patients with compromised cardiac function to demonstrate a functional improvement after an intervention that reduces the inflammatory response. Also, the optimal timing of intervention with a donor of NO is unclear in the literature. Inhibition of the production of endogenous NO was found to be greatest starting with postischemic reperfusion [12]. On the other hand, it was reported that recovery of the reperfused heart was greatest when NO was supplemented even before cardioplegia and that the application during reperfusion may even be detrimental [20]. In our own experience from animal studies [4], best results were obtained with the short-term postischemic application of a NO donor. In a study performed on children undergoing cardiac operation for congenital malformations, the application of sodium nitroprusside (average dose, 1.6 µg · kg^-1 · min^-1) during cooling and rewarming on CPB had an inhibiting effect on systemic complement activation [13]. The complement system is located centrally in the inflammatory cascade. Inhibition of complement activation may well be the reason for the reduced cytokine levels with the application of SNP in this study. All in all, a tempting but unproved mechanism of action could be that NO released from SNP is serving as an antioxidant and radical scavenger in the situation of acute postischemic reperfusion of the heart [4].

In conclusion, an antiinflammatory action is described for SNP in patients undergoing routine coronary artery bypass grafting. Further studies on patients with preoperatively compromised left ventricular function have to show whether a functional improvement can also be achieved.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
The work was supported by the Deutsche Forschungsgemeinschaft (MA 1731/3-1).

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

1. Ferrari R., Alfieri O., Curello S., et al. Occurrence of oxidative stress during reperfusion of the human heart. Circulation 1990;81:201-211.[Abstract/Free Full Text]
2. Hearse D.J., Bolli R. Reperfusion induced injury: manifestations, mechanisms, and clinical relevance. Cardiovasc Res 1992;26:101-108.[Abstract/Free Full Text]
3. Kukreja R.C., Hess M.L. The oxygen free radical system: from equations through membrane-protein interactions to cardiovascular injury and protection. Cardiovasc Res 1992;26:641-655.[Abstract/Free Full Text]
4. Massoudy P., Becker B.F., Gerlach E. Nitric oxide accounts for postischemic cardioprotection resulting from angiotensin-converting enzyme inhibition: indirect evidence for a radical scavenger effect in isolated guinea pig heart. J Cardiovasc Pharmacol 1995;25:440-447.[Medline]
5. Kupatt C., Zahler S., Seligmann C., et al. Nitric oxide mitigates leukocyte adhesion and vascular leak after myocardial ischemia. J Mol Cell Cardiol 1996;28:643-654.[Medline]
6. Lefer D.J., Nakanishi K., Johnston W.E., Vinten Johansen J. Antineutrophil and myocardial protecting actions of a novel nitric oxide donor after acute myocardial ischemia and reperfusion of dogs [see comments]. Circulation 1993;88:2337-2350.[Abstract/Free Full Text]
7. Cameron D. Initiation of white cell activation during cardiopulmonary bypass: cytokines and receptors. J Cardiovasc Pharmacol 1996;27(suppl 1):S1-S5.
8. Rinder C., Fitch J. Amplification of the inflammatory response: adhesion molecules associated with platelet/white cell responses. J Cardiovasc Pharmacol 1996;27(suppl 1):S6-S12.
9. Neumann F.J., Ott I., Gawaz M., et al. Cardiac release of cytokines and inflammatory responses in acute myocardial infarction. Circulation 1995;92:748-755.[Abstract/Free Full Text]
10. Wan S., DeSmet J.M., Barvais L., et al. Myocardium is a major source of proinflammatory cytokines in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996;112:806-811.[Abstract/Free Full Text]
11. Zahler S.M.P., Becker B.F., Hartl H., Hähnel C.J., Meisner H. Acute cardiac inflammatory response during cardiopulmonary bypass. Cardiovasc Res 1998 (in press).
12. Sato H., Zhao Z.Q., Jordan J.E., et al. Basal nitric oxide expresses endogenous cardioprotection during reperfusion by inhibition of neutrophil-mediated damage after surgical revascularization. J Thorac Cardiovasc Surg 1997;113:399-409.[Abstract/Free Full Text]
13. Seghaye M.C., Duchateau J., Grabitz R.G., et al. Effect of sodium nitroprusside on complement activation induced by cardiopulmonary bypass: a clinical and experimental study. J Thorac Cardiovasc Surg 1996;111:882-892.[Abstract/Free Full Text]
14. Tassani P., Richter J., Barankay A., et al. Does high-dose methylprednisolone attenuate the systemic inflammatory response during CABG procedures?. J Cardiothorac and Vasc Anaesth 1998 (in press).
15. Wan S., Marchant A., DeSmet J.M., et al. Human cytokine responses to cardiac transplantation and coronary artery bypass grafting. J Thorac Cardiovasc Surg 1996;111:469-477.[Abstract/Free Full Text]
16. Finkel M.S., Oddis C.V., Jacob T.D., et al. Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 1992;257:387-389.[Abstract/Free Full Text]
17. Rinder H.M., Bonan J.L., Rinder C.S., Ault K.A., Smith B.R. Dynamics of leukocyte-platelet adhesion in whole blood. Blood 1991;78:1730-1737.[Abstract/Free Full Text]
18. Habazettl H., Martinek V., Vollmar B., Conzen P. Enhancement of the leukocyte-endothelial cell interaction in collecting venules of skeletal muscle by protamine. J Thorac Cardiovasc Surg 1997;113:784-791.[Abstract/Free Full Text]
19. Hennein H.A., Ebba H., Rodriguez J.L., et al. Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization. J Thorac Cardiovasc Surg 1994;108:626-635.[Abstract/Free Full Text]
20. Engelman D.T., Watanabe M., Maulik N., et al. Critical timing of nitric oxide supplementation in cardioplegic arrest and reperfusion. Circulation 1996;94(suppl 2):407-411.[Abstract/Free Full Text]

This article has been cited by other articles:

				G. M. Marcus and J. E. Olgin Preventing Atrial Fibrillation After Cardiac Surgery: A New Method Using an Old Tool Circulation, July 29, 2008; 118(5): 467 - 468. [Full Text] [PDF]

				R. Cavolli, K. Kaya, A. Aslan, O. Emiroglu, S. Erturk, O. Korkmaz, M. Oguz, R. Tasoz, and U. Ozyurda Does Sodium Nitroprusside Decrease the Incidence of Atrial Fibrillation After Myocardial Revascularization?: A Pilot Study Circulation, July 29, 2008; 118(5): 476 - 481. [Abstract] [Full Text] [PDF]

				A. Boning, J. Scheewe, T. Ivers, C. Friedrich, J. Stieh, S. Freitag, and J. T. Cremer Phosphorylcholine or heparin coating for pediatric extracorporeal circulation causes similar biologic effects in neonates and infants J. Thorac. Cardiovasc. Surg., May 1, 2004; 127(5): 1458 - 1465. [Abstract] [Full Text] [PDF]

				D. L. Ngaage Off-pump coronary artery bypass grafting: the myth, the logic and the science Eur. J. Cardiothorac. Surg., October 1, 2003; 24(4): 557 - 570. [Abstract] [Full Text] [PDF]

				O. Cakir, A. Oruc, S. Eren, H. Buyukbayram, L. Erdinc, and N. Eren Does sodium nitroprusside reduce lung injury under cardiopulmonary bypass? Eur. J. Cardiothorac. Surg., June 1, 2003; 23(6): 1040 - 1045. [Abstract] [Full Text] [PDF]

				P. Tassani, A. Barankay, F. Haas, S. U. Paek, M. Heilmaier, J. Hess, R. Lange, and J. A. Richter Cardiac surgery with deep hypothermic circulatory arrest produces less systemic inflammatory response than low-flow cardiopulmonary bypass in newborns J. Thorac. Cardiovasc. Surg., April 1, 2002; 123(4): 648 - 654. [Abstract] [Full Text] [PDF]

				D. Paparella, T.M. Yau, and E. Young Cardiopulmonary bypass induced inflammation: pathophysiology and treatment. An update Eur. J. Cardiothorac. Surg., February 1, 2002; 21(2): 232 - 244. [Abstract] [Full Text] [PDF]

				P. Massoudy, S. Zahler, B. F. Becker, S. L. Braun, A. Barankay, and H. Meisner Evidence for Inflammatory Responses of the Lungs During Coronary Artery Bypass Grafting With Cardiopulmonary Bypass Chest, January 1, 2001; 119(1): 31 - 36. [Abstract] [Full Text] [PDF]

				P. Massoudy, S. Zahler, P. Tassani, B. F. Becker, J. A. Richter, M. Pfauder, R. Lange, and H. Meisner Reduction of pro-inflammatory cytokine levels and cellular adhesion in CABG procedures with separated pulmonary and systemic extracorporeal circulation without an oxygenator Eur. J. Cardiothorac. Surg., June 1, 2000; 17(6): 729 - 736. [Abstract] [Full Text] [PDF]

				P. Massoudy, S. Zahler, T. Freyholdt, R. Henze, A. Barankay, B. F. Becker, S. L. Braun, and H. Meisner SODIUM NITROPRUSSIDE IN PATIENTS WITH COMPROMISED LEFT VENTRICULAR FUNCTION UNDERGOING CORONARY BYPASS: REDUCTION OF CARDIAC PROINFLAMMATORY SUBSTANCES J. Thorac. Cardiovasc. Surg., March 1, 2000; 119(3): 566 - 574. [Abstract] [Full Text] [PDF]

				R. A. Guyton, V. H. Thourani, J. D. Puskas, J. S. Shanewise, M. A. Steele, C. L. Palmer-Steele, and J. Vinten-Johansen Perfusion-assisted direct coronary artery bypass: selective graft perfusion in off-pump cases Ann. Thorac. Surg., January 1, 2000; 69(1): 171 - 175. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) 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): Hans Meisner Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Massoudy, P. Articles by Meisner, H. Search for Related Content PubMed PubMed Citation Articles by Massoudy, P. Articles by Meisner, H.