Dose-related attenuation of cardiac sympathetic nerve activity and intracardiac conduction with thoracic epidural clonidine in alpha-chloralose-anesthetized cats.

Epidural clonidine produces hypotension, bradycardia and sympatholysis. We studied the dose-effects of thoracic epidural and intravenous clonidine (1 to 8 microg/kg) on cardiac sympathetic nerve activity (CSNA), hemodynamics and intracardiac conduction in cats anesthetized with alpha-chloralose. Mean arterial pressure was decreased with epidural clonidine doses above 2 microg/kg, and to a greater extent with 4 microg/kg than 8 microg/kg. Sinus heart rate, Wenckebach atrial rate and CSNA were significantly decreased and corrected sinus node recovery time and Atrium-His interval were significantly prolonged with doses above 2 microg/kg. Vagotomy induced no significant change in these parameters. Thoracic epidural clonidine doses above 2 microg/kg caused a similar extent of sympatholysis. Less of CSNA decrease and hemodynamic changes by intravenous clonidine suggested that sympatholysis caused by epidural clonidine was primarily mediated by spinal mechanism, although hemodynamic changes were influenced by clonidine systemically redistributed from epidural space. Vagal facilitation played no role in suppression of the sinoatrial and AV nodal functions.