CEREBROVASCULAR RELAXATION RESPONSES TO ENDOTHELIUM-DEPENDENT AND ENDOTHELIUM-INDEPENDENT VASODILATORS AFTER NORMOTHERMIC AND HYPOTHERMIC CARDIOPULMONARY BYPASS IN THE RABBIT

Background: Cardiopulmonary bypass causes activation of leukocytes and increased concentrations of proinflammatory mediators, which may resu lt in endothelial dysfunction. Because hypothermia attenuates many inf lammatory processes, the authors hypothesized that hypothermic cardiop ulmonary bypass would be associated with better endothelial function t han normothermic cardiopulmonary bypass.Methods: Isoflurane-anesthetiz ed New Zealand White rabbits mere randomized to undergo 90 min of eith er normothermic (37 degrees C, n = 9) or hypothermic (27 degrees C, n = 9) cardiopulmonary bypass with terminal rewarming. A third group ser ved as anesthetized normothermic non-cardiopulmonary bypass surgical c ontrols (n = 8), Basilar artery and descending thoracic aorta were iso lated from each animal. In vivo vessel relaxation responses to increas ing concentrations of acetylcholine (which induces endothelial release of nitric oxide) and nitroprusside (which provides exogenous nitric o xide) were measured in phenylephrine-precontracted vessel rings, Resul ts: There were no differences in vessel relaxation responses between n ormothermic and hypothermic cardiopulmonary bypass groups in basilar a rtery or aorta. In contrast, basilar arteries from non-cardiopulmonary bypass controls had increased relaxation responses to both acetylchol ine (P = 0.004) and nitroprusside (P = 0.031) compared with the pooled cardiopulmonary bypass animal data. Conclusions: The authors observed no differences in endothelial or vascular smooth muscle function betw een normothermic and hypothermic cardiopulmonary bypass groups. Compar ed with non-cardiopulmonary bypass controls, cardiopulmonary bypass ap peared to decrease basilar artery smooth muscle relaxation in response to endogenous and exogenous nitric oxide.