Cyclooxygenase Inhibition Potentiates the Pulmonary Vascular Responses to Ethanol in Dogs

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Abstract
The effects of ethanol on pulmonary hemodynamics and the role of arachidonic acid metabolites in mediating these responses were studied in the isolated, blood-perfused canine lung lobe. Ethanol added directly to the venous reservoir at a concentration of 0.01 or 0.1 % did not alter the pulmonary vascular resistance, however, 1.0% ethanol increased (p < 0.05) the pulmonary resistance. Indometacin, a cyclooxygenase inhibitor, significantly increased baseline pulmonary vascular resistance and markedly potentiated the pulmonary vascular responses to the three concentrations of ethanol. Addition of nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, followed by indometacin, did not diminish the indometacin-induced increases in basal tone or enhancement of the responses to ethanol indicating that leukotrienes are not involved in mediating the responses to ethanol. These results suggest that in isolated, blood-perfused dog lung lobe, a high concentration of ethanol increases the pulmonary vascular resistance and that cyclooxygenase inhibition markedly potentiated the responses to ethanol by reducing the production of vasodilator prostaglandin, most probably prostacyclin.