Real-time measurement of nitric oxide in coronary circulation during ischemia reperfusion and analysis of pathophysiological effects

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Isolated rat hearts perfused in Langendorff mode were used in this experiment. NO concentration in the coronary perfusate ejected from the pulmonary artery was measured using an NO microelectrode (100 mum ; 1 pA corresponds to about 1.5 nM NO).1. Effect of superoxide scavenger during ischemia reperfusionProduction of superoxide radical (・O_2) is considered to increase during ischemia reperfusion. In order to investigate the effect of superoxide on NO concentration in the coronary circulation during ischemia reperfusion, superoxide dismutase (SOD) or synthesized superoxide scavenger was perfused. We were unable to observe any noticeable effects, i.e., NO scavenged by ・O_2 due to seemingly unstable scavenging activities of both scavengers. Perfusion method is currently being modified to maintain the scavenging activities of those scavengers.2. Effdct of angiotensin converting enzyme inhibitor during hypoperfusionNO concentration in the coronary perfusate decreased with decreasing perfusion pressure (100 cmH<@D22@>D2O to 50 cmH<@D22@>D2O,49(]SY.+-。[)4% vs 100 cmH<@D22@>D2O,p<0.05). Perfusion of angiotensin converting enzyme (ACE) inhibitor, imidaprilat (50 nM), increased both perfusion rate (57(]SY.+-。[)3% vs 100 cmH<@D22@>D2O,p<0.05) and NO concentration (44(]SY.+-。[)9 pA,75(]SY.+-。[)6% vs 100 cmH<@D22@>D2O,p<0.05). These results indicate that NO concentration in the coronary perfusate increased with increasing perfusion rate by increased NO.It is supposed that deactivation of bradykinin (agonist of NO synthase ) by ACE was inhibited by ACE inhibitor, resulting in the increase in NO concentration.