Matsuura A, Ishihara T, Nakamura K, Himori N, Nakamura K
J Cardiovasc Pharmacol. 1986 Jan-Feb;8(1):90-8. doi: 10.1097/00005344-198601000-00015.
We examined the effects of tiapamil, a Ca2+ antagonist, on infarct size, lymphatic enzyme release, and arrhythmias in reperfused, ischemic canine hearts. Three-hour reperfusion of the left anterior descending coronary artery, which had been ligated for 3 h, significantly increased cardiac lymphatic release of lactate dehydrogenase (LDH), cathepsin D and creatine phosphokinase (CPK), and the incidence of ventricular premature contractions (VPCs), the increases being markedly higher than those in ligation period. Tiapamil, at the i.v. dose of 3 mg/kg/h for 6 h during the ligation and reperfusion periods markedly reduced these increases in lymphatic levels of LDH and cathepsin D and in VPCs, and significantly decreased infarct size. Tiapamil treatment only during the ligation period had similar preserving effects, but tiapamil treatment only during reperfusion did not. These results suggest that blockade of the Ca2+ channel must be achieved during the early phase of an ischemic episode in order to prevent myocardial deterioration during reperfusion.
我们研究了钙拮抗剂硫氮䓬酮对再灌注的缺血犬心脏梗死面积、淋巴酶释放及心律失常的影响。对结扎3小时的左冠状动脉前降支进行3小时再灌注，显著增加了心肌淋巴中乳酸脱氢酶（LDH）、组织蛋白酶D和肌酸磷酸激酶（CPK）的释放，以及室性早搏（VPC）的发生率，这些增加显著高于结扎期。在结扎和再灌注期间，以3mg/kg/h的静脉注射剂量给予硫氮䓬酮6小时，可显著降低LDH和组织蛋白酶D的淋巴水平升高以及VPC，并显著减小梗死面积。仅在结扎期进行硫氮䓬酮治疗具有类似的保护作用，但仅在再灌注期进行硫氮䓬酮治疗则没有。这些结果表明，必须在缺血发作的早期阶段阻断钙通道，以防止再灌注期间心肌恶化。
