CORONARY-ARTERY ENDOTHELIAL DYSFUNCTION AFTER GLOBAL-ISCHEMIA, BLOOD CARDIOPLEGIA, AND REPERFUSION

This study tests the hypothesis that blood cardioplegia (BCP) attenuat es endothelial dysfunction related to nitric oxide after global normot hermic ischemia, cardioplegic arrest, and reperfusion in anesthetized open-chest dogs plated on cardiopulmonary bypass. The dogs were divide d into five groups to identify the time when endothelial injury occurr ed: group 1 = control without ischemia; group 2 = 45 minutes of normot hermic ischemia only; group 3 = 45 minutes of normothermic ischemia pl us unmodified reperfusion; group 4 = 45 minutes of ischemia plus inter mittent BCP without reperfusion; and group 5 = ischemia plus BCP and r eperfusion. In vitro coronary vascular relaxation responses to the nit ric oxide stimulator acetylcholine (endothelium-dependent, receptor-de pendent), the calcium ionophore A23187 (endothelium-dependent, recepto r-independent), and acidified NaNO2 (endothelium-independent) were mea sured at the end of the protocol. Maximum in vitro coronary vascular r esponses to acetylcholine were similar among groups 1, 2, and 4, indic ating an absence of endothelial injury. In contrast, significantly imp aired relaxations to acetylcholine were demonstrated in the two reperf used groups (groups 3 and 5). Relaxation responses to A23187 and NaNO2 were not altered markedly in any group. Electron microscopy showed in tact endothelium in groups 1, 2, and 4. However, moderately severe end othelium damage was seen in groups 3 and 5. We conclude that morpholog ic and functional endothelial damage occurs after blood reperfusion wi th or without BCP, and 1-hour hypothermic BCP arrest after normothermi c ischemia is not associated with extension of endothelial damage.