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The Journal of Thoracic and Cardiovascular Surgery, Vol 92, 99-104, Copyright © 1986 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Prevention of ischemia-induced myocardial platelet deposition by exogenous prostacyclin

T Aherne, DC Price, ES Yee, WR Hsieh and PA Ebert

The antithrombotic effects of prostacyclin infusion on myocardial platelet deposition were studied in a canine model during and after global ischemia. Eleven isolated heart preparations were subjected to 1 hour of cardioplegic arrest under moderate hypothermia (27 degrees to 28 degrees C), including a control group (n = 7) and a prostacyclin- treated group (n = 4). The hearts of four other dogs were continuously perfused for 180 minutes. Platelet deposition was measured at 15 minute intervals throughout the 3 hour study. Serial full-thickness myocardial biopsy specimens were analyzed for activity of 111In-labeled platelets with 99mTc-labeled erythrocyte correction for tissue blood content. The pattern of platelet distribution was determined by scintiscans of each heart, taken with a gamma camera at the end of the 60 minute reperfusion period. Substantial myocardial platelet deposition was found in the control hearts after ischemia but not in the prostacyclin- treated group (p less than 0.05). Furthermore, prostacyclin infusion had a significant disaggregatory effect on intracoronary platelet deposits when the precardioplegic and postcardioplegic biopsy specimens were analyzed (p less than 0.05). Three hours of continuous perfusion did not increase tissue 111In-labeled platelet activity. Ex vivo images showed platelet deposition to be a diffuse patchy process with significantly more 111In activity in the endocardium than in the epicardium after global ischemia (p less than 0.05). These data show the potent antithrombotic properties of prostacyclin in preventing and disaggregating ischemia-induced intracoronary platelet deposition during and after cardioplegic arrest.

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