Adrenergic Mechanisms in the Effects of Histamine in the Pulmonary Circulation of the Cat

¹ School of Medicine, University of New South Wales, Prince Henry Hospital, Little Bay, N.S.W., Australia

Histamine constricts airways and pulmonary blood vessels in isolated lungs, but is said to dilate pulmonary blood vessels in intact animals. The present experiments test the hypothesis that histamine only constricts pulmonary blood vessels, and that dilatation depends on epinephrine released by histamine from the adrenal glands. In cats anesthetized with pentobarbital, the difference in pressure between the pulmonary artery (PA) and left atrium (LA) was related to pulmonary blood flow measured by dye dilution before, and at intervals of 0.5 to 2 minutes after PA injection of histamine. In intact or vagotomized cats histamine increased PA-LA pressure difference and pulmonary blood flow, but calculated pulmonary vascular resistance (PVR) decreased significantly at 1 minute; control values were restored in 4 minutes. In adrenalectomized cats, histamine (10 to 40 µg) increased PA-LA pressure and PVR, but did not change pulmonary blood flow. After beta-receptor blockade with propranolol, histamine (10 to 20 µg) had the same effect as in adrenalectomized cats. After adrenalectomy or propranolol, the histamine-induced increase in PVR was prolonged. When histamine had increased PVR in adrenalectomized cats, epinephrine (5 µg iv) reduced PA-LA pressure and PVR. Histamine infusion (5 µg/kg/min iv) decreased PVR in intact cats, increased PVR in adrenalectomized cats, and when epinephrine (5 µ/kg/min) was also infused, decreased PVR in adrenalectomized cats. The results support the proposed hypothesis. Release of histamine locally in the lungs may encourage distribution of both blood and gas flows away from damaged and toward normal respiratory tissue.

Submitted on August 29, 1969
Accepted on January 13, 1970