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Atenolol 전처치 개흉견에서 심근재관류가 좌심실 수축 및 확장기능과 좌심실 크기에 미치는 영향에 관한 연구
오동주,노영무 고려대학교 의과대학 1989 고려대 의대 잡지 Vol.26 No.1
Although early reperfusion limits or even prevents myocardial necrosis, this beneficial effect dose not lead to immediate functional improvement, and the return of contractile function in the myocardium salvaged by reperfusion is delayed for hours or even days (stunning phenomenone or postischemic myocardial dysfunction), and functional expansion in both ischemic and non-ischemic myocardium caused by coronary occlusion does not return immedialely by reperfusion. To investigate the effect of early reperfusion on the left ventricular function and the functional expansion of the left ventricle, left anterior descending coronary artery was occluded by silk snare distal to the first diagonal branch for 30 minutes and was followed by reperfusion for 60 minutes in 9 atenolol pretreated open-chest dogs. Atenolol caused fall in arterial pressure (from 114 to 95 mmHg in systole, 88 to 65 mmHg in diastole, mean), reduced heart rate (from 161/min to 113/min, mean) and cardiac output (from 2.2 L/min, to 1.5L/min, mean) before occlusion, but arterial pressure and heart rate did not change. Both ischemic and non-ischemic areas at end-systole and at end-diastole were increased in 30 seconds after occlusion. After reperfusion rerovery of expansion of ischemic area to pre-occlusion level was achieved in 40 minutes and non-ischemlc area in 20 minutes Decreased cardiac output and percent change in area(% △ A) during occlusion were recovered in 15 minutes and 20 minutes, respectively. The ratio of early peak filling wave to late peak filling wave (E/A velocity) measured by Doppler echocardiography were reversed by occlusion and recovered in 5 minutes after reperfusion. These findings suggest that decreased diastolic function caused by coronary occlusion is recovered earlier than the systolic function, and recovery of systolic function is accompanied by a recovery of non-ischemic area expansion after reperfusion, which may indicate that the change in non-ischemic area during occlusion and after reperfusion is due to the change in systolic function.
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