Objective: Parasympathetic modulation of the rate dependence of ventricular repolarisation in vivo during steady state conditions was investigated by analysing the effects of removing vagal activity in three groups of anaesthetised cats. Methods: Bilateral vagotomy was performed while different levels of background sympathetic tone were present in the control periods of each group: in group 1 (n = 6), cardiac sympathetic nerves were intact; in group 2 (n = 7), bilateral stellate ganglionectomy was performed; and in group 3 (n = 7), β adrenergic blockade (propranolol, 0.5 mg · kg -1) was performed after stellate ganglionectomy. The duration of a left ventricular endocardial monophasic action potential (APD) was measured during atrial pacing at 7-10 cycle lengths (CL). The APD/CL relation was fitted to a hyperbolic function: APD = CL/[(a x CL) + b]. Two parameters were considered: APD(max) (1/a, ie, APD extrapolated at infinite cycle length, a rate-independent measure of APD) and CL 50 (b x APD(max), ie, the cycle length at which 50% of APD(max) is reached). Results: In control conditions, APD(max) and CL 50 were longer in groups 2 and 3, when cardiac sympathetic effects were reduced or absent. Vagotomy reduced APD(max) and CL 50 similarly in groups 1 and 2 (APD(max), -24% and -18%; CL 50, -36% and -27%) (p <0.05 v control). In group 3, vagotomy did not affect APD(max) and CL 50. Conclusions: No direct parasympathetic influence on the rate dependence of endocardial ventricular repolarisation was observed. The vagal modulation of sympathetic effects may take place either through vago-sympathetic reflexes or via the antagonism of circulating catecholamines distal to the β receptor.
|Number of pages||5|
|Publication status||Published - 1993|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine