The effect of glucose-insulin-potassium on cardiac ultrastructure following acute experimental coronary occlusion.

The effects of glucose-insulin-potassium (GIK) on cardiac ultrastructure following acute experimental coronary occlusion were studied in dogs. Epicardial ST segment elevations at multiple sites on the anterior surface of the left ventricle 15 minutes after ligation of the left anterior descending coronary artery were used to predict infarct development. Biopsies removed from sites of known ST segment elevation were examined with the electron microscope, and the degree of injury was correlated with the ST segment elevation. The animals receiving GIK showed significantly less necrosis than was seen in dogs with occlusion alone at corresponding levels of ST segment elevation. Other evidence suggesting a beneficial effect of GIK was the presence of a fibrillar material in several biopsies from the treated animals, which may indicate the regeneration of myofilaments.

[1]  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.

[2]  P. Libby,et al.  Effect of Glucose‐Insulin‐Potassium Infusion on Myocardial Infarction following Experimental Coronary Artery Occlusion , 1972, Circulation.

[3]  P. Libby,et al.  Effects of Intraaortic Balloon Counterpulsation on the Severity of Myocardial Ischemic Injury following Acute Coronary Occlusion: Counterpulsation and Myocardial Injury , 1972, Circulation.

[4]  J. Dusek,et al.  Early alterations of the cardiac muscle cells in isoproterenol-induced necrosis. , 1972, Archives of pathology.

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

[6]  C. Harnarayan,et al.  Quantitative study of infarcted myocardium in cardiogenic shock. , 1970, British heart journal.

[7]  R. Jennings.  Early phase of myocardial ischemic injury and infarction. , 1969, The American journal of cardiology.

[8]  C. Friedberg.  General Treatment of Acute Myocardial Infarction , 1969 .

[9]  R. Jennings,et al.  Structural and functional abnormalities in mitochondria isolated from ischemic dog myocardium. , 1969, Laboratory investigation; a journal of technical methods and pathology.

[10]  R. Jennings,et al.  Pyruvate metabolism in mitochondria isolated from dog myocardium. , 1969, Laboratory investigation; a journal of technical methods and pathology.

[11]  J. Covell,et al.  A biopsy drill permitting rapid freezing. , 1968, Journal of applied physiology.

[12]  A. Weissler,et al.  Role of anaerobic metabolism in the preservation of functional capacity and structure of anoxic myocardium. , 1968, The Journal of clinical investigation.

[13]  R. Bing,et al.  Stimulation of reparative processes following experimental myocardial infarction. , 1966, Archives of internal medicine.

[14]  A. Bisteni,et al.  OXIDATIVE PHOSPHORYLATION IN CARDIAC INFARCT. EFFECT OF GLUCOSE-KCL-INSULIN SOLUTION. , 1965, The American journal of physiology.

[15]  R. Jennings,et al.  A COMPARATIVE STUDY OF THE FINE STRUCTURE OF NORMAL AND ISCHEMIC DOG MYOCARDIUM WITH SPECIAL REFERENCE TO EARLY CHANGES FOLLOWING TEMPORARY OCCLUSION OF A CORONARY ARTERY. , 1965, The American journal of pathology.

[16]  I. Wool,et al.  INSULIN AND INCORPORATION OF AMINO ACIDS INTO PROTEIN OF MUSCLE. 1. ACCUMULATION AND INCORPORATION STUDIES WITH THE PERFUSED RAT HEART. , 1963, The Biochemical journal.

[17]  J. Caulfield,et al.  Myocardial ischemia and early infarction: an electron microscopic study. , 1959, The American journal of pathology.

[18]  R. O'Neal,et al.  An Electron Microscopic Study of Myocardial Ischemia in the Rat , 1958, Circulation research.