Cardiorespiratory effects of cocaine and procaine at the ventral brainstem

The caudal ventrolateral medulla (CVLM) is an area of the brainstem, in the vicinity of the hypoglossal nerve roots, where cholinergic and adrenergic neurons participate in respiratory and vasomotor control. Cardiorespiratory depression has been produced by topical application of cocaine to the CVLM. In the present studies, the effects of topical pretreatments of the CVLM with alpha-adrenergic blockers (prazosin 4.8 mM) and beta-adrenergic blockers (propranolol 11.3 mM) on the cardiorespiratory responses to topically administered cocaine (37 mM) were investigated in urethane anesthetized cats. Both prazosin and propranolol failed to produce ventilatory responses and to counteract cocaine-induced apneustic breathing. However, the cocaine-induced decrement in mean arterial blood pressure (MABP) following pretreatment of the CVLM with propranolol was found to be 11 +/- 5%, compared to the 18 +/- 5% decrement produced by cocaine alone. These differences were not statistically significant. Procaine (37 mM) in equimolar doses to cocaine, produced a small statistically significant decrement in MABP (P < 0.05) without ventilatory effects. Topical administration of procaine (73.3 mM), at approximately twice the equimolar dosage of cocaine, produced apneustic breathing that was indistinguishable from that produced by cocaine. The neurotoxic properties of cocaine that produce apneustic breathing appear to be similar to that produced by the anesthetic agent procaine, and the alpha- and beta-adrenoceptor blockers prazosin and propranolol do not appear to antagonize the vasomotor depression induced by cocaine at the CVLM.