论文信息 - Distribution of myocardial injury and its relation to epicardial ST-segment changes after coronary artery occlusion in the dog.

Distribution of myocardial injury and its relation to epicardial ST-segment changes after coronary artery occlusion in the dog.

From 1969 to 1970 I was a fortunate Fogarty research fellow in Professor Eugene Braunwalds Department at UCSD on the Pacific brim in sunny San Diego. While John Glenn stepped down on the moon we discussed MJRU-projects. My particular undertaking was to develop methods to assess infarct size in order to examine the effect of interventions designed to prevent development of myocardial injury following an acute coronary occlusion. Together with Professor Burton Sobel, a large number of candidates for marker of myocardial injury was tested in order to determine the evolving infarct size. Of all enzymes and cellular constituents tested, creatinekinase (CK) was best in show [1]. Myocardial depletion …

[1] J. Covell,et al. Factors Influencing Infarct Size Following Experimental Coronary Artery Occlusions , 1971, Circulation.

[2] B. Sobel,et al. Depressed Myocardial Creatine Phosphokinase Activity Following Experimental Myocardial Infarction in Rabbit , 1970, Circulation research.

[3] P. Libby,et al. Coronary artery reperfusion. I. Early effects on local myocardial function and the extent of myocardial necrosis. , 1972, The Journal of clinical investigation.

[4] J. Kjekshus,et al. Effect of inhibition of lipolysis on infarct size after experimental coronary artery occlusion. , 1973, The Journal of clinical investigation.