Konorev E A, Polumiskov V Iu, Avilova O A, Golikova A P
Biull Eksp Biol Med. 1990 Sep;110(9):252-4.
The effects of synthetic antioxidant emoxypine on infarct size and plasma creatine kinase (CK) activity was studied on open-chest anesthetized dogs with 180-min myocardial ischemia followed by reperfusion. Emoxypine (10 and 40 mg/kg) was injected intravenously, beginning since 120th min of coronary artery occlusion. Emoxypine (10 mg/kg) resulted in infarct size limitation and reduction in plasma CK activity. An increase in dose of emoxypine to 40 mg/kg largely attenuated its protective effect on infarct size. CK activity during post-ischemic reperfusion was even higher in emoxypine (40 mg/kg) group compared with control. Augmented CK leakage from irreversibly injured myocardium to plasma under these experimental conditions may be owing to preservation of microvascular integrity and improving of drainage of infarcted tissue exerted by emoxypine.
在开胸麻醉犬身上研究了合成抗氧化剂依莫昔平对梗死面积和血浆肌酸激酶（CK）活性的影响，这些犬经历180分钟心肌缺血后再灌注。从冠状动脉闭塞第120分钟开始静脉注射依莫昔平（10毫克/千克和40毫克/千克）。依莫昔平（10毫克/千克）可限制梗死面积并降低血浆CK活性。将依莫昔平剂量增加到40毫克/千克很大程度上减弱了其对梗死面积的保护作用。与对照组相比，依莫昔平（40毫克/千克）组缺血后再灌注期间的CK活性甚至更高。在这些实验条件下，不可逆损伤心肌向血浆中CK漏出增加可能是由于依莫昔平保持了微血管完整性并改善了梗死组织的引流。
