The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · May 1990
Clinical Trial Controlled Clinical TrialAprotinin protects platelets against the initial effect of cardiopulmonary bypass.
Remarkable improvement in hemostasis after cardiopulmonary bypass has been achieved by treatment with the proteinase inhibitor aprotinin, but the mechanism is still unclear. The present study is designed to elucidate the importance of platelet adhesive (glycoprotein Ib) or aggregatory (glycoprotein IIbIIIa) receptors on this hemostatic function in cardiopulmonary bypass and its improvement by aprotinin treatment. To determine whether the first pass of blood through the circuit or a continuous proteolytic attack is the main cause of platelet damage, we gave two different dose regimens of aprotinin treatment to patients undergoing coronary artery bypass grafting. ⋯ Although the fibrinolytic activity was effectively inhibited in both aprotinin groups, fibrinolytic activity became apparent only at the end phase of bypass in the placebo group. However, improved hemostasis was observed intraoperatively from the start of bypass and resulted in a 40% lower blood loss intraoperatively and postoperatively and consequently a 40% lower total blood requirement in the aprotinin-treated patients than in the untreated patients. Our results therefore demonstrate that the improved hemostasis during and after bypass in patients treated with aprotinin has specifically to be attributed to a preserved adhesive capacity of platelets that was affected in the first pass of blood through the cardiopulmonary bypass circuit.
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J. Thorac. Cardiovasc. Surg. · May 1990
Effects of temperature on myocardial calcium homeostasis and mitochondrial function during ischemia and reperfusion.
An isolated rabbit heart preparation was used to characterize the effects of hypothermia on the deterioration in mitochondrial respiratory function and on the calcium overload that occurs during ischemia and reperfusion. Hearts were perfused aerobically with an asanguineous solution for 120 minutes or made totally ischemic for 90 minutes at 37 degrees, 34 degrees, 28 degrees, 22 degrees C, respectively, and reperfused for 30 minutes at 37 degrees C. Mitochondrial function was assessed by measuring calcium content, yield, oxygen consumption, and adenosine triphosphate-producing capacities. ⋯ These data suggest that a decrease in temperature from 37 degrees to 22 degrees C during ischemia did not significantly prevent depletion of adenosine triphosphate at the end of ischemia but reduced tissue and mitochondrial calcium overload, maintaining mitochondrial function. Thus in our experiments the protective effect of hypothermia might be related to a direct reduction of tissue and mitochondrial calcium accumulation rather than to a slowing in rates of energy utilization. This possibility is supported by the finding that in freshly excised, nonperfused rabbit hearts, hypothermia significantly reduced the initial rate of mitochondrial calcium transport.
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J. Thorac. Cardiovasc. Surg. · May 1990
Latissimus dorsi dynamic cardiomyoplasty of the right ventricle. Potential for use as a partial myocardial substitute.
Full-thickness right ventricular latissimus dorsi dynamic cardiomyoplasty with the Medtronic Cardiomyostimulator (Medtronic, Inc., Minneapolis, Minn.) was performed in a chronic canine model. In one group (n = 2) the latissimus dorsi was electrically preconditioned before cardiomyoplasty. In a second group (n = 3) cardiomyoplasty was performed and the muscle was progressively stimulated, with conditioning accomplished while the latissimus dorsi was functioning on the ventricle. ⋯ Latissimus dorsi dynamic cardiomyoplasty can function as a partial myocardial replacement in a chronic canine model, apparently without preconditioning of the muscle. The degree of cardiac assist obtained with cardiomyoplasty appears to be influenced by the voltage and frequency of the stimulus applied to the muscle. Although it is unclear whether these results can be extrapolated to the left ventricle, this technique may find application in the treatment of ventricular aneurysm or ventricular tumor.
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J. Thorac. Cardiovasc. Surg. · May 1990
Intermittent hypothermic asanguineous cerebral perfusion (cerebroplegia) protects the brain during prolonged circulatory arrest. A phosphorus 31 nuclear magnetic resonance study.
A system has been developed for the nuclear magnetic resonance spectroscopic evaluation of cerebral high-energy phosphate levels during hypothermic total circulatory arrest and reperfusion by means of cardiopulmonary bypass in large animals. The use of intermittent hypothermic asanguineous cerebral perfusion, termed cerebroplegia, for the preservation of cerebral high-energy phosphates during a 2-hour period of hypothermic total circulatory arrest and reperfusion has been evaluated. Cardiopulmonary bypass was used to achieve deep hypothermia (12 degrees to 15 degrees C) during 2 hours of circulatory arrest and reperfusion. ⋯ Electroencephalographic activity returned after 36 minutes of reperfusion in group 2, but it did not return until 117 minutes in group 1 (p less than 0.05). In summary, cerebral high-energy phosphates and pH were maintained and the electroencephalographic signal returned more rapidly during circulatory arrest with the institution of cerebroplegia. These studies suggest that cerebroplegia is protective of the brain during circulatory arrest.
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J. Thorac. Cardiovasc. Surg. · Apr 1990
Hemodynamic response to pumpless extracorporeal membrane oxygenation.
Respiratory support by means of arteriovenous extracorporeal membrane oxygenation driven by systemic arterial pressure, in contrast to pump-driven venoarterial extracorporeal membrane oxygenation, is attractive because of its simplicity and lack of trauma to formed blood elements. Although arteriovenous extracorporeal membrane oxygenation has been shown to improve arterial blood gases, useful levels of arteriovenous extracorporeal membrane oxygenation shunt flow may exert detrimental effects on systemic and pulmonary hemodynamics. Therefore the hemodynamic consequences of arteriovenous extracorporeal membrane oxygenation were studied in 11 dogs that were anesthetized, heparinized, and their lungs mechanically ventilated (FIO2 = 0.21) before and after induction of oleic acid pulmonary edema. ⋯ Dopamine infusion (5 micrograms/kg/min) proved to be more effective than volume expansion (15 ml/kg) in maintaining cardiac output, arterial blood pressure, and arterial blood gases. We conclude that pumpless arteriovenous extracorporeal membrane oxygenation, at flow rates adequate for respiratory support, can adversely alter systemic hemodynamics. However, these effects can be beneficially modulated by a moderate dose of inotropic medication.