953-34 Pulmonary Vascular Endothelium is Capable of Producing Nitric Oxide After Cardiopulmonary Bypass and Circulatory Arrest

• Published in: Journal of the American College of Cardiology 1995-02, Vol.25 (2), p.200A-201A
• Main Authors: Kirshbom, Paul M., Tsui, Steven S.L., DiBernardo, Louis R., Meliones, Jon N., Schwinn, Debra A., Ungerleider, Ross M., William Gaynor, J.
• Format: Article
• Language: English
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/0735-1097(95)92291-C

Cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) can lead to clinically significant pulmonary dysfunction and increased pulmonary vascular resistance (PVR). Endothelial production of nitric oxide (NO), a vasodilator, is an important mediator of pulmonary vascular tone. Endothelial injury during CPB and DHCA with loss of NO production may result in elevated PVR postoperatively. To assess the importance of NO production before and after CPB and DHCA, twelve 4–6 week old piglets were instrumented with pulmonary artery (PA) and left atrial Millar micromanometers and a PA ultrasonic flow probe. NO synthase was blocked with a 5mg/kg bolus of Nw-Nitro-L-Arginine Methyl Ester (L-NAME) into the main PA either before (Control, n=6) or after CPB and DHCA (DHCA, n=6). The DHCA animals were placed on CPB, cooled to 18°C, arrested for 60 minutes, rewarmed to 37°C, and weaned from CPB. The L-NAME bolus was given 15minutes after weaning from CPB in this group. PVR and input impedance Ilin) were measured immediately before and 10 minutes after L-NAME in both groups. The results are expressed as means±SEM.MinutesPVR (dyne sec cm-5)Zin(dyne sec cm-5)Post-L-NAMEControlPost-DHCAControlPost-DHCA0526±531993±399†1006±522543±436†101456±136*3578±668*2100±69*4323±687*†p<0.006 vs Control by unpaired two-tailed t-test.*p<0.01 vs Time 0 by paired twotailed t-test 1) PVR and Zinare significantly increased by CPB and DHCA. 2) Blockade of NO synthase increases PVR and Zinto a similar degree preand post-DHCA, demonstrating that the pulmonary endothelium produces NO after CPB and DHCA. 3) Since the endothelium continues to produce NO following CPB and DHCA, other mechanisms, such as increased endothelial production of vasoconstrictors or interstitial edema, may be important mediators of post-CPB pulmonary dysfunction.