Journal of Applied Physiology, Vol 77, Issue 4 1584-1590, Copyright © 1994 by American Physiological Society

ARTICLES

Prolonged pulmonary vascular hyperreactivity in conscious dogs after cardiopulmonary bypass

D. P. Nyhan, J. M. Redmond, A. M. Gillinov, K. Nishiwaki and P. A. Murray
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287-4961.

Although cardiopulmonary bypass (CPB) is required in all surgical procedures involving open-heart surgery, the extent to which CPB alters pulmonary vascular regulation has not been systematically investigated. Our objectives were to investigate the acute, subacute, and chronic effects of CPB on the left pulmonary vascular pressure-flow (LP-Q) relationship in conscious dogs. Continuous LP-Q plots were generated in chronically instrumented conscious dogs 2-4 days pre-CPB and again 4 h and 1, 2, 7, and 14 days after 2.5 h of closed-chest hypothermic CPB. In addition, pulmonary vascular reactivity was assessed by examining the dose-response relationship to the thromboxane analogue U-46619 pre- and post-CPB. CPB resulted in an acute (4 h post-CPB) shift in the baseline LP-Q relationship, indicating an increase in pulmonary vascular resistance (P < 0.01). The baseline LP-Q relationship returned to pre-CPB values by 1 day post-CPB. Despite this return of the baseline LP-Q relationship to pre-CPB values, the pulmonary vasoconstrictor response to U-46619 was markedly potentiated 2 days post-CPB compared with the pre-CPB response (P < 0.01). This enhanced pulmonary vasoconstrictor response to U-46619 was still apparent 7 days post-CPB (P < 0.01) but was not evident 14 days post-CPB. These results indicate that CPB results in a pronounced, but transient, increase in pulmonary vascular resistance. Moreover, CPB causes a protracted increase in pulmonary vascular reactivity even when the baseline LP-Q relationship has returned to pre-CPB values.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				C. S. Thompson-Torgerson, H. C. Champion, L. Santhanam, Z. L. Harris, and A. A. Shoukas Cyclohexanone contamination from extracorporeal circuits impairs cardiovascular function Am J Physiol Heart Circ Physiol, June 1, 2009; 296(6): H1926 - H1932. [Abstract] [Full Text] [PDF]

				I. Schulze-Neick, D. J. Penny, M. L. Rigby, C. Morgan, A. Kelleher, P. Collins, J. Li, A. Bush, E. A. Shinebourne, and A. N. Redington L-Arginine and Substance P Reverse the Pulmonary Endothelial Dysfunction Caused by Congenital Heart Surgery Circulation, August 17, 1999; 100(7): 749 - 755. [Abstract] [Full Text] [PDF]

				S. Seki, N. A. Flavahan, N. G. Smedira, and P. A. Murray Superoxide anion scavengers restore NO-mediated pulmonary vasodilation after lung transplantation Am J Physiol Heart Circ Physiol, January 1, 1999; 276(1): H42 - H46. [Abstract] [Full Text] [PDF]

				A. Serraf, M. Robotin, N. Bonnet, H. Detruit, B. Baudet, M. G. Mazmanian, P. Herve, and C. Planche ALTERATION OF THE NEONATAL PULMONARY PHYSIOLOGY AFTER TOTAL CARDIOPULMONARY BYPASS J. Thorac. Cardiovasc. Surg., December 1, 1997; 114(6): 1061 - 1069. [Abstract] [Full Text]

				P. Zanaboni, P. A. Murray, B. A. Simon, K. Zehr, K. Fleischer, E. Tseng, and D. P. Nyhan Selective endothelial dysfunction in conscious dogs after cardiopulmonary bypass J Appl Physiol, June 1, 1997; 82(6): 1776 - 1784. [Abstract] [Full Text] [PDF]

				V. M. Reddy, K. D. Hendricks-Munoz, H. A. Rajasinghe, E. Petrossian, F. L. Hanley, and J. R. Fineman Post–Cardiopulmonary Bypass Pulmonary Hypertension in Lambs With Increased Pulmonary Blood Flow: A Role for Endothelin 1 Circulation, February 18, 1997; 95(4): 1054 - 1061. [Abstract] [Full Text]