Schaer G L, Karas S P, Santoian E C, Gold C, Visner M S, Virmani R
Division of Cardiology, Georgetown University Medical Center, Washington, D.C.
J Am Coll Cardiol. 1990 May;15(6):1385-93. doi: 10.1016/s0735-1097(10)80029-4.
Because myocardial reperfusion injury may be caused by various blood constituents, a transient period of blood-free reperfusion was evaluated in closed chest dogs subjected to a 90 min angioplasty balloon occlusion of the left anterior descending coronary artery. In the treated group (n = 13), the balloon remained inflated for an additional 15 min while the infarct vessel was perfused with an acellular oxygenated perfluorochemical emulsion (Fluosol). The balloon was then deflated, permitting blood reperfusion. In the control group (n = 13), the balloon was deflated after 90 min of coronary occlusion. One week after infarction, the area at risk was defined in vivo by monastral blue dye staining, and the area of myocardial necrosis was assessed using triphenyltetrazolium chloride staining with histologic confirmation. Major determinants of infarct size, including rate-pressure product, area at risk and severity of myocardial ischemia (assessed by the extent of ST segment elevation during coronary occlusion), were not significantly different in the two groups. Treated dogs demonstrated a 47% reduction in infarct size expressed as a percent of the area at risk compared with control dogs (27.0 +/- 4.4% versus 50.8 +/- 4.4%, p less than 0.01). Treated dogs also demonstrated a superior global left ventricular ejection fraction (57.5 +/- 2.5% versus 51.0 +/- 2.2%, p less than 0.05) and anterolateral (regional) ejection fraction (32.6 +/- 3.6% versus 19.8 +/- 3.9%, p less than 0.05) compared with values in control dogs assessed by contrast ventriculography after 1 week of reperfusion. It is concluded that a transient period of blood-free reperfusion with an oxygenated perfluorochemical reduces reperfusion injury in a canine model of myocardial infarction.
由于心肌再灌注损伤可能由多种血液成分引起，因此在左前降支冠状动脉接受90分钟血管成形术球囊闭塞的开胸犬中评估了无血再灌注的短暂时期。在治疗组（n = 13）中，球囊再充盈15分钟，同时用无细胞氧合全氟化学乳剂（氟碳化合物）灌注梗死血管。然后球囊放气，允许血液再灌注。在对照组（n = 13）中，冠状动脉闭塞90分钟后球囊放气。梗死后一周，通过亚甲蓝染料染色在体内确定危险区域，并使用氯化三苯基四氮唑染色评估心肌坏死区域，并进行组织学确认。两组梗死面积的主要决定因素，包括心率血压乘积、危险区域和心肌缺血严重程度（通过冠状动脉闭塞期间ST段抬高程度评估），差异无统计学意义。与对照犬相比，治疗犬梗死面积减少了47%（以危险区域的百分比表示）（27.0±4.4%对50.8±4.4%，p<0.01）。与再灌注1周后通过对比心室造影评估的对照犬的值相比，治疗犬还表现出更好的整体左心室射血分数（57.5±2.5%对51.0±2.2%，p<0.05）和前外侧（区域）射血分数（32.6±3.6%对19.8±3.9%，p<0.05）。结论是，在犬心肌梗死模型中，用氧合全氟化学物质进行短暂的无血再灌注可减少再灌注损伤。
