Mechanism of cardiovascular changes produced in cats by activation of the central nervous system with picrotoxin.

The mechanism of cardiovascular changes produced by activation of the central nervous system with picrotoxin (2 mg/kg, iv) was studied in chloralose-anesthetized cats. Effects occurred in two phases. During the early phase, there were decreases in arterial blood pressure and heart rate, and in a few cats, bradyarrhythmias. These changes were transient and superceded by an increase in arterial blood pressure and, in most cases, ventricular tachyarrhythmias. The early phase changes were mediated primarily by the cardiac vagus nerve whereas the later phase changes were mediated primarily by sympathetic nerves and the adrenal medulla. The ventricular tachyarrbythmias were unaffected by pretreatment with atropine, bilateral vagotomy, or beta adrenergic blocking agents. On the other hand, bilateral extirpation of the stellate ganglia and adrenal glands prevented the ventricular arrhythmias from occurring. In addition, administration of drugs that blocked alpha adrenergic receptors effectively counteracted picrotoxin-induced ventricular arrhythmias. These results indicate that the centrally induced ventricular arrhythmias were mediated by cardiac sympathetic nerves and/or release of catecholamines from the adrenal medulla. More importantly, these results indicate that one cannot equate beta adrenergic blockade with elimination of sympathetic influence on the heart. Finally, sympathetically induced arrhythmias resistant to beta adrenergic blockade appear to respond to drugs that block cardiac adrenergic alpha receptors.