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Journal of Pharmacology And Experimental Therapeutics, Vol. 164, Issue 2, 333-341, 1968
Copyright © 1968 by American Society for Pharmacology and Experimental Therapeutics


VASODILATATION OF BRAINSTEM ORIGIN SUPPRESSED BY NEUROMUSCULAR BLOCKADE IN THE CAT

P. M.S. MIRANDA 1, B. GóMEZ 1, and H. L. BORISON 1

1 Departarnento de Ciencias Fisiológicas, Facuitad de Medicina, Universidad del Valle, Cali, Colombia

Stereotaxic technique was employed for simultaneous placement of stimulating electrodes in the pressor and depressor areas of the medulla oblongata in cats that were either anesthetized with pentobarbital or decerebrated midcolhicularly under ether anesthesia. Arterial blood pressure, heart rate and respiration were recorded electrographically through appropriate transducers. Bilateral vagotomy or administration of atropine plus treatment with propranolol eliminated all cardiac responses but did not alter remarkably the blood pressure responses elicited both from pressor and depressor points. Thus, neither muscarinic chohinergic processes nor beta adrenergic effector mechanisms, whether cardiac or vascular, contributed significantly to the centrally evoked responses in the blood pressure. By contrast, application of alpha adrenergic blockade with phcntolamine or phenoxy-benzamine erased the pressor response but partially spared the depressor effect. The ``residual'' depressor response was not further influenced by complete autonomic blockade with hexamethonium or by injection of the antihistamine promethazine (Phenergan), but the effect was invariably abolished by use of the skeletal neuromuscular blocking drugs d-tubocurarine, gahlamine or succinyichohine. Evoked vasodepression was generally accompanied by a sustained inspiratory effort; however, the residual depressor component continued to be elicited after thoracotomy and phrenicotomy in the presence of artificial ventilation. Similar results were obtained in flow-controlled autoperfused hindhimb preparations, some of which were subjected to abdominal sympathectomy. We conclude that a specific somatic vasodilator response is elicitable from the bulbar depressor center and that it is effected independently of autonomic activity, changes in cardiac output and ventilatory mechanical events.

Submitted on April 15, 1968
Accepted on September 7, 1968







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Copyright © 1968 by the American Society for Pharmacology and Experimental Therapeutics.