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

隔离的大鼠心脏在Langendorff模式中完全使用了在这个实验中。从脉冲式电池中发射的冠状完全放电的NO集中，用NO微电极测量（100毫米; 1 pA对应约1.5 nM NO）。超氧化物清除剂在ischemia reperfusion生产的超氧化物激进物（·O_2）中的作用被认为在ischemia reperfusion期间增加。按顺序调查超氧化物对NO浓度的影响在循环中发生化学重组、超氧化物歧化酶（SOD）或合成的超氧化物清除剂被充分利用。我们不可能看到任何明显的影响，我是。没有被O_2清除，似乎对两个清除者来说是不稳定的清除活动。灌注方法目前被修改为维护那些清道夫的清道夫活动。在去除渗透压力下，在冠状渗透压力下降解超融合NO浓度（100 cmH<@D22 @> D2 O至50 cmH<@D22 @> D2 O，49（]SY.+-）。[）4%vs 100 cmH<@D22 @>D2O，p<0. 05。血管紧张素转化酶的灌注（ACE）抑制剂，异黄酮（50 nM），增加两种灌注率（57（）SY.+-。[）3%vs 100 cmH<@D22 @>D2O，p<0. 05） and NO concentration （44（）SY.+-。[）第75章（]SY.+-。[）6%vs 100 cmH<@D22 @>D2O，p<0. 05。这些结果表明，在冠状渗透率增加的情况下，不集中导致渗透率增加的情况;它被ACE抑制者抑制的情况下，结果表明在不集中引起布雷迪金素的破坏（不合成的抑制剂）。

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.