|
|
||||||||
J Thorac Cardiovasc Surg 1996;111:882-892
© 1996 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Received for publication Nov. 21, 1994 Accepted for publication June 14, 1995. Address for reprints: Marie-Christine Seghaye, MD, Department of Pediatric Cardiology, RWTH Aachen, Pauwelsstrasse 30, D-52057, Aachen, Germany.
Abstract
Complement activation and leukocyte stimulation were prospectively studied during and after cardiopulmonary bypass in 16 children receiving sodium nitroprussidea nitrovasodilator releasing nitric oxidefor vasodilation during the cooling and rewarming periods of extracorporeal circulation. Results were compared with those in 29 patients who were not treated with sodium nitroprusside during the operation. Patients treated with sodium nitroprusside had significantly less C3 conversion during cardiopulmonary bypass as measured by the ratio C3d/C3 (p< 0.05) and significantly less C5a liberation immediately after cardiopulmonary bypass (p< 0.005) than patients not treated with sodium nitroprusside. C4 was not overtly consumed in our series. Leukocyte count during the rewarming period of cardiopulmonary bypass, but not leukocyte elastase release during cardiopulmonary bypass, was significantly reduced in patients treated with sodium nitroprusside (p< 0.05). In vitro experiments were conducted to analyze the effect of sodium nitroprusside on complement hemolytic activity initiated by the classic and the alternate pathways and on zymosan-induced C3 conversion by the activation of the alternate pathway. The in vitro experiments clearly demonstrate inhibition of complement hemolytic activity by sodium nitroprusside in the sera tested. The 50% inhibitory concentration of sodium nitroprusside on the available complement hemolytic activity was less through the alternate pathway than through the classic one (4.2 ± 0.8 mmol/L and 14.0 ± 2.88 mmol/L, respectively). The decrease of complement hemolytic activity measured was dose-dependent and was enhanced by the sodium nitroprusside preincubation of the sera tested. This effect was related to the duration of preincubation. Sodium nitroprusside photodegradation (enhancing nitric oxide release) increased the anticomplementary effect of the drug, reducing the 50% inhibitory concentration on complement hemolytic activity to 0.24 to 0.02 mmol/L for the alternate pathway and 2.74 to 0.3 mmol/L for the classic pathway. The zymosan-induced C3 conversion was inhibited by sodium nitroprusside. Nitroglycerin and isosorbide dinitrate (other nitric oxide donors) had in vitro effects on complement hemolytic activity similar to those of nonphotodegraded sodium nitroprusside at similar concentrations (1 mmol/L). Our results suggest that sodium nitroprusside, both in vitro and in vivo, has an inhibiting effect on complement activation initiated by both classic and alternate pathways and that this effect is mediated by nitric oxide release from sodium nitroprusside. This is the first report on the anticomplementary effect of sodium nitroprusside by nitric oxide release. (J THORAC CARDIOVASC SURG 1996;111:882-92)
This article has been cited by other articles:
![]() |
K. Kaya, M. Oguz, A. R. Akar, S. Durdu, A. Aslan, S. Erturk, R. Tasoz, and U. Ozyurda The effect of sodium nitroprusside infusion on renal function during reperfusion period in patients undergoing coronary artery bypass grafting: a prospective randomized clinical trial Eur. J. Cardiothorac. Surg., February 1, 2007; 31(2): 290 - 297. [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. Menasche and L. H. Edmunds Jr. Extracorporeal Circulation: The Inflammatory Response Card. Surg. Adult, January 1, 2003; 2(2003): 349 - 360. [Full Text] |
||||
![]() |
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] |
||||
![]() |
M. Sigler, J. F. Vazquez-Jimenez, R. G. Grabitz, H. H. Hovels-Gurich, B. J. Messmer, G. von Bernuth, and M.-C. Seghaye Time course of cranial ultrasound abnormalities after arterial switch operation in neonates Ann. Thorac. Surg., March 1, 2001; 71(3): 877 - 880. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. M. Matata and M. Galinanes Cardiopulmonary bypass exacerbates oxidative stress but does not increase proinflammatory cytokine release in patients with diabetes compared with patients without diabetesRegulatory effects of exogenous nitric oxide J. Thorac. Cardiovasc. Surg., July 1, 2000; 120(1): 1 - 11. [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] |
||||
![]() |
G. Asimakopoulos Mechanisms of the systemic inflammatory response Perfusion, July 1, 1999; 14(4): 269 - 277. [PDF] |
||||
![]() |
P. Massoudy, S. Zahler, A. Barankay, B. F. Becker, J. A. Richter, and H. Meisner Sodium nitroprusside during coronary artery bypass grafting: evidence for an antiinflammatory action Ann. Thorac. Surg., April 1, 1999; 67(4): 1059 - 1064. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |