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Ann Thorac Surg 1994;57:999-1006
© 1994 The Society of Thoracic Surgeons

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Articles

Thromboxane A₂ receptor-specific antagonism in hypothermic cardiopulmonary bypass

Surgery Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA

Accepted for publication August 30, 1993.

^_* Address reprint requests to Dr clark, Cardiovascular and Pulmonary Research Center, Allegheny-Singer Research Institute, 320 E North Ave, Pittsburgh, PA 15212.

Using a thromboxane A₂ receptor-specific antagonist, SQ 30,741, this study was undertaken to define the role of thromboxane A₂ in postischemic myocardial reperfusion injury and in the heparin-protamine reaction. Eighteen heparinized (300 units/kg) sheep were placed on cardiopulmonary bypass (CPB) after complete instrumentation, cooled to 28°C, and had their aortas crossclamped for 1 hour. They were then rewarmed to 36°C and weaned from CPB without inotropic support. Control sheep (n = 6) received a saline infusion throughout the procedure. Bolus animals (n = 6) received 5 mg/kg of SQ 30,741 at 5 minutes after discontinuation of CPB and before protamine sulfate administration. Infusion animals (n = 6) received an SQ 30,741 bolus of 5 mg/kg followed by a continuons infusion of 5 mg · kg^–1 hr^–1 of SQ 30,741 initiated before CPB. All animals received 5 mg/kg of protamine sulfate over a 15-second period 15 minutes after being weaned from CPB. Control animals exhibited significantly decreased global myocardial function after the 1-hour ischemic interval. Further significant functional decline and increase in pulmonary pressure occurred after protamine sulfate administration. Bolus animals experienced a similar postischemic injury, but had no further decrease in function following protamine infusion. Infusion animals had significantly improved global myocardial function after bypass compared with both other groups and were also protected from the deleterious effects of protamine sulfate administration. We conclude that (1) thromboxane A₂ receptor-specific blockade prevents the marked increase in pulmonary vascular resistance index resulting from protamine sulfate administration and (2) a major component of the ischemic-reperfusion injury associated with CPB is mediated by thromboxane a₂ receptors. Blockade of these receptors markedly preserved ventricular function in a severe injury model.

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