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SUMMARY We studied 25 anesthetized and thoracotamized dogs before and during 5 hours of acute regional myocardial ischemia. Krypton-81m ( 8Xm Kr) was infused constantly into the aortic sinuses. The myocardial equilibrium of this tracer was used to image and assess the distribution of regional myocardial perfusion using a gamma camera and digital computer. The epicardial ECG was recorded, S-T segment elevation and the loss of R and appearance of Q waves were measured, and the plasma activity of creatine kinase (CK) was determined in aortic and coronary venous blood throughout these experiments. Ten dogs underwent left anterior descending coronary artery (LAD) narrowing for 5 hours and received no drugs. Five dogs received nifedipine 13 fig/kg, and another five received 1.0 /ig/kg intravenously 30 minutes after LAD narrowing. Those dogs receiving nifedipine, 13 fig/kg, showed a 30% fall in aortic pressure, a 12% rise in heart rate, and an extension of regional ischemia. The ECG showed an extension of infarct size, and CK release into the coronary vein appeared earlier than in the controls. Dogs receiving nifedipine, 1 /ig/kg, showed a 12% fall in blood pressure, no rise in heart rate, an improvement in regional perfusion, and ECG signs that suggested limitation of infarct size. There also was delayed release of coronary venous CK. The effects of nifedipine on the natural history of regional myocardial perfusion, the electrocardiogram, and enzyme release from the heart were dose related and cannot be generalized. These observations warrant further clinical investigation to improve the use of this agent in man. Circ Res 44: 16-23, 1979 THE extent of ischemic myocardial damage during acute myocardial infarction is one of the important determinants of morbidity and mortality. Recent studies have encouraged a search for interventions that can affect the balance between energy supply and demand during acute infarction of the heart (Maroko et al., 1971; Braunwald andMaroko, 1974). Nifedipine (4-(2'-nitrophenyl)-2,6-dimethyl-l,4-dihydropyridine-3,5-dicarboxylic acid dimethyl ester) has been shown to retard the transmembrane influx of calcium into ischemic myocardial cells, increase coronary blood flow, delay ischemic contracture, and preserve myocardial creatine kinase activity (Henry, 1975;Fleckenstein, 1975;Vater, 1975;Schmier et al., 1975). These combined pharmacological properties suggest that a favorable effect on acutely ischemic myocardium may be possible.The purpose of this study was to observe the changes of regional myocardial perfusion, the epicardial ECG, and the appearance of creatine kinase activity in coronary venous blood in dogs during the 5 hours following occlusion of the left anterior descending coronary artery (LAD). The dose-related effects of nifedipine on these parameters were measured, and the use of this drug to protect the ischemic myocardium is discussed. MethodsTwenty-five mongrel dogs weighing 30-55 kg were anesthetized with intravenous sodium thiopental (Pentothal, 12 mg/kg). Respiration ...

A reduction in post-operative blood loss in primary elective CABG surgery with intra-operative Aprotinin treatment could be confirmed. A low-dose ASA treatment combined with a high-dose aprotinin administration during surgery not only neutralized a potentially higher risk of bleeding, but did in fact reduce the post-operative blood loss. The protective effect of ASA on peri-operative MI has been evident through a reduction of MI rate in ASA treated patients.

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