CARDIORESPIRATORY EFFECTS OF COCAINE AND PROCAINE AT THE VENTRAL BRAIN-STEM

The caudal ventrolateral medulla (CVLM) is an area of the brainstem, i n the vicinity of the hypoglossal nerve roots, where cholinergic and a drenergic neurons participate in respiratory and vasomotor control. Ca rdiorespiratory depression has been produced by topical application of cocaine to the CVLM. In the present studies, the effects of topical p retreatments of the CVLM with a-adrenergic blockers (prazosin 4.8 mM) and beta-adrenergic blockers (propranolol 11.3 mM) on the cardiorespir atory responses to topically administered cocaine (37 mM) were investi gated in urethane anesthetized cats. Both prazosin and propranolol fai led to produce ventilatory responses and to counteract cocaine-induced apneustic breathing. However, the cocaine-induced decrement in mean a rterial blood pressure (MABP) following pretreatment of the CVLM with propranolol was found to be 11 +/- 5%, compared to the 18 +/- 5% decre ment produced by cocaine alone. These differences were not statistical ly significant Procaine (37 mM) in equimolar doses to cocaine, produce d a small, statistically significant decrement in MABP (P<0.05) withou t ventilatory effects. Topical administration of procaine (73.3 mM), a t approximately twice the equimolar dosage of cocaine, produced apneus tic breathing that was indistinguishable from that produced by cocaine . The neurotoxic properties of cocaine that produce apneustic breathin g appear to be similar to that produced by the anesthetic agent procai ne, and the alpha- and beta-adrenoceptor blockers prazosin and propran olol do not appear to antagonize the vasomotor depression induced by c ocaine at the CVLM. (C) 1996 Intox Press, Inc.