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Research Article Free access | 10.1172/JCI107889

Coronary Reperfusion in Primates SERIAL ELECTROCARDIOGRAPHIC AND HISTOLOGIC ASSESSMENT

Gregory T. Smith, John R. Soeter, Harold H. Haston, and J. Judson McNamara

Department of Surgery, University of Hawaii School of Medicine, Honolulu, Hawaii 96808

Queen's Medical Center, Honolulu, Hawaii 96808

Find articles by Smith, G. in: PubMed | Google Scholar

Department of Surgery, University of Hawaii School of Medicine, Honolulu, Hawaii 96808

Queen's Medical Center, Honolulu, Hawaii 96808

Find articles by Soeter, J. in: PubMed | Google Scholar

Department of Surgery, University of Hawaii School of Medicine, Honolulu, Hawaii 96808

Queen's Medical Center, Honolulu, Hawaii 96808

Find articles by Haston, H. in: PubMed | Google Scholar

Department of Surgery, University of Hawaii School of Medicine, Honolulu, Hawaii 96808

Queen's Medical Center, Honolulu, Hawaii 96808

Find articles by McNamara, J. in: PubMed | Google Scholar

Published December 1, 1974 - More info

Published in Volume 54, Issue 6 on December 1, 1974
J Clin Invest. 1974;54(6):1420–1427. https://doi.org/10.1172/JCI107889.
© 1974 The American Society for Clinical Investigation
Published December 1, 1974 - Version history
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Abstract

After acute coronary occlusion in primates, the time period during which reperfusion results in significant salvage of reversibly injured myocardium was investigated. In 23 monkeys, the left anterior descending coronary artery was occluded from 1 to 6 h; and in 5 others, occlusion was maintained for the 1-wk study. Unipolar epicardial electrocardiograms were monitored from mapping points on the anterior and lateral left venticle. S-T segment elevation (S-T↑) and R + S wave amplitude (RS) were measured before occlusion and at regular intervals during occlusion and reperfusion. Summated S-T↑ (ΣS-T↑) and summated RS (ΣRS), computed for mapping points demonstrating greater than 2 mV S-T↑, were used as serial measures of electrical injury. ΣS-T↑ peaked within 2-h postocclusion and then gradually declined throughout the period of occlusion suggesting the progress of infarction within the area of injury. After reperfusion ΣS-T↑ rapidly declined to near cnotrol values indicating the extent of reversible injury. During the period of occlusion, the magnitude of voltage loss in ΣS-T↑ as a percent of maximum ΣS-T↑ was proportional to the duration of occlusion, though the rate of loss decreased with increasing time of occlusion. Reperfusion after 6 h of occlusion resulted in reversal of only a small remaining component of the maximum current of injury. The voltage decrease in ΣRS (from control values) was proportional to the duration of occlusion, though the decrease was accelerated during the first 2-h postocclusion. Whereas reperfusion interrupted the decline in ΣRS, a consistent increase in ΣRS postreperfusion was observed only after occlusion of 1 h. With respect to reperfusion groups, significance in ΣS-T↑ voltage loss as a percent of maximum ΣS-T↑ was demonstrated between 2-h and 4-h, 4- and 6-h, and 6-h and chronically ligated animals. Significance in ΣRS voltage loss as a percent of control ΣRS was demonstrated between 2- and 4-h, and 4- and 6-h reperfusion groups. Hearts were excised at 7 days for histological assessment of infarct size. Planimetric determination of left ventricular areas and areas of necrosis using slides made from 10 serial cross sections were used in estimating the percent of left ventricle infarcted. A significant reduction in infarct size was demonstrated between reperfused animals at 2 h and the 4- and 6-h reperfusion groups. A trend was noted suggesting increasing infarct size up to 6 h after experimental occlusion.

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