Komamura K, Kitakaze M, Funaya H, Ueda Y, Node K, Minamino T, Kurihara T, Hori M
The First Department of Medicine, Osaka University School of Medicine, Japan.
J Cardiovasc Pharmacol. 1997 Dec;30(6):775-83. doi: 10.1097/00005344-199712000-00012.
We examined whether ecto-5'-nucleotidase mediates infarct limitation by ischemic preconditioning in the rabbit heart. Ecto-5'-nucleotidase activity in ischemic region after ischemic preconditioning was greater than that in nonischemic regions (23.6 +/- 2.5 vs. 13.6 +/- 1.0 nmol/mg protein/min; p < 0.01). With an inhibitor of 5'-nucleotidase, alpha,beta-methylene adenosine 5'-diphosphate (AMP-CP), ecto-5'-nucleotidase activity in the ischemic region was comparable to that in the nonischemic region. Mean blood pressure was reduced from 73 +/- 2 to 62 +/- 3 mm Hg with intravenous AMP, whereas it did not change with coperfusion of AMP and AMP-CP, suggesting effective inhibition of ecto-5'-nucleotidase. Separately, myocardial infarction was created by 30-min coronary occlusion and 3 h of reperfusion. Infarct size expressed as percentage volume in risk area was reduced by ischemic preconditioning compared with that in the control (7.8 +/- 2.5% vs. 38.1 +/- 4.0%; p < 0.01). However, infarct size in the group given AMP-CP plus ischemic preconditioning was similar to that in the control (36.2 +/- 2.8% vs. 38.1 +/- 4.0%; NS), suggesting that ecto-5'-nucleotidase mediates infarct limitation by ischemic preconditioning in the rabbit.
我们研究了外切5'-核苷酸酶是否通过兔心脏的缺血预处理介导梗死面积的限制。缺血预处理后缺血区域的外切5'-核苷酸酶活性高于非缺血区域（23.6±2.5对13.6±1.0 nmol/mg蛋白/分钟；p<0.01）。使用5'-核苷酸酶抑制剂α,β-亚甲基腺苷5'-二磷酸（AMP-CP）时，缺血区域的外切5'-核苷酸酶活性与非缺血区域相当。静脉注射AMP后平均血压从73±2降至62±3 mmHg，而AMP与AMP-CP联合灌注时平均血压未改变，提示外切5'-核苷酸酶被有效抑制。另外，通过30分钟冠状动脉闭塞和3小时再灌注造成心肌梗死。与对照组相比，缺血预处理使梗死面积（以危险区域的体积百分比表示）减小（7.8±2.5%对38.1±4.0%；p<0.01）。然而，给予AMP-CP加缺血预处理组的梗死面积与对照组相似（36.2±2.8%对38.1±4.0%；无显著性差异），提示外切5'-核苷酸酶通过兔心脏的缺血预处理介导梗死面积的限制。
