Peripheral and central actions of sodium azide on circulatory and respiratory homeostasis in anesthesized cats
Kaplita, P.V.; Borison, H.L.; Mccarthy, L.E.; Smith, R.P.
Journal of Pharmacology and Experimental Therapeutics 231(1): 189-196
1984
ISSN/ISBN: 0022-3565 PMID: 6436470 Document Number: 233975
In pentobarbital-anesthesized cats, bolus i.v. injections of sodium azide produced dose-dependent transient hypotension accompanied by a modest tachycardia and a brief hyperpnea. Intracerebroventricular injections of azide elicited graded effects similar to the i.v. doses, but the responses were slower in onset and could be delayed by occluding the cranial blood supply. This is interpreted to mean that intracerebroventricular azide acts systematically after escaping from the SCF into the bloodstream. The hypotensive response to i.v. azide was not affected by cholinergic or adrenergic blockage or buffer nerve section. The tachycardia was blocked by sympathetic neural blockade or buffer nerve section indicating that it is a baroreflex response to the vasodepressor effect. Respiratory effects of bolus i.v. azide occurred independently of the hypotensive response and were abolished by peripheral chemodenervation. Infusion of azide facilitated CO2-tidal volume responsiveness in the steady-state, an effect that was essentially eliminated by carotid sinus neurotomy. The azide did not affect the tidal volume-respiratory frequency relationship mediated by the pulmonary stretch receptors. The respiratory stimulant effect of azide in subtoxic doses is attributable to an excitatory action on the arterial chemoreceptors. Toxic doses of azide resulted in centrally mediated hypertension, tachycardia, cardiac arrhythmia, respiratory depression, seizures and death.