INVESTIGATION OF MECHANISM AT REPERFUSION INJURY AFTER ACUTE MYOCARDIAL INFARCTION

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Reperfusion injury should be important complication and poor prognosis of acute myocardial infarction. In the coronary circulation, depletion and excessiveness of NO have been considered to play crucial roles in coronary and cardiac diseases. The aim of this study was to develop a catheter-type NO sensor for the coronary sinus and evaluate its applicability in vivo, and whether this catheter-type NO sensor would be useful in the investigation of reperfusion injury. An NO sensor(Innovative Instruments) mounted in 4-Fr catheter with soft tip for protection of vascular wall was placed in the coronary sinus through a 7-Fr JR catheter from the right jugular vein of anesthetized dogs. Coronary flow velocity was measured by a Doppler flowire(Volcano) in the left anterior descending artery, simultaneously. Acetylcholine (ACh,0.4 and 1.0μg/kg) and N^G-methyl-L-arginine(L-NAME,10μg/kg/min for 20min) were infused into the left coronary artery to stimulate and inhibit NO production, respectively. ACh increased the plasma NO concentration in the coronary sinus in a dose-dependent manner(6.8±2.1nM and 8.2±2.5nM, respectively, p=0.05). L-NAME decreased basal NO concentration(3.1±0.8nM) and suppressed the NO synthesis in response to ACh intracoronary injection(1.9±0.6nM, p=0.03 and 2.8±0.8nM, p=0.05 before L-NAME, respectively). The time for base-to-peak change in NO concentration was longer than that in coronary flow velocity after ACh injection(118±48 sec and 52±21,p=0.04). In conclusion, the newly developed catheter-type NO sensor can assess the real-time changes of NO concentration in the coronary sinus. This NO sensor will contribute to understanding the roles of NO in regulations of coronary blood flow and cardiac function in health and disease, diagnosing coronary endothelial dysfunction and lead to the investigation of reperfusion injury.