SHRの心阻血時における心筋代謝と再灌流障害(I 発生病理)(A 基礎的研究)

概要

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By using fluorometry for pyridine nucleotides (NAD) and measuring the levels of residual ATP in the myocardium, the effects of various cardioplegias and myocardial temperatures were investigated on SHR hypertrophied heart and WKR non-hypertrophied heart. Myocardial injury under ischemia was also studied in terms of both tissue injury under anoxia and reperfusion. (1) On Wistar-Kyoto rat (WKR) heart, the safe allowance time of coronary occlusion was approximately 45 minutes at 36℃, and it was possible to elongate the time to 210 minutes under myocardial protection. (2) On spontaneously hypertensive rat (SHR) heart, the safe allowance time of coronary occlusion was approximately 70-80% of WKR heart, and it was possible to elongate the time to the extent as same as the WKR heart by the intravenous injection of 10 mg/kg of CoQ_<10> 30 minutes before coronary occlusion. (3) During the coronary reperfusion of ischemic dog heart 60 minutes after the coronary occlusion at 36℃, post-ischemic hyperoxidation was observed on fluorometry. (4) With 60 minutes of reperfusion 120 minutes after the coronary occlusion at 36℃, an increase of thiobarbituric acid reactive substance (TBARS) was seen and it was thought due to a lipid peroxide production. The increase of TBARS in the myocardium was suppressed with either 10 mg/kg of CoQ_<10> or 5 mg/kg of betamethasone by the intra venous injection 30 minutes before coronary occlusion.
近畿大学の論文
1981-09-25