MECHANISM OF THE DECLINE IN VAGAL CARDIAC ACCELERATION IN DOGS IN NEUROLEPTANESTHESIA

Abstract

Muscarinic receptor blockade in beta-adrenoceptor blocked dogs in neuroleptanaesthesia reveals a vagally-mediated cardiac acceleration ('inherent VCA'); the heart rate reaches a maximum level within 10 min, then declines spontaneously. Experiments were designed to settle whether the decline in the VCA is due to a decrease in peripheral responsiveness and/or a decrease in central vagal tone. The decline in VCA was assessed in one group of dogs (n = 12) over a period of 170 min, after which ganglionic nicotinic blockade (Exp 1) or vagotomy (Exp 2) was carried out. The maximum 'inherent VCA', defined as the difference between maximum heart rate after muscarinic blockade and the rate after nicotinic blockade or vagotomy, was 68 +/- 10 and 64 +/- 11 bpm, respectively. The VCA declined to 75, 50 and 25% of the maximum levels after 23 +/- 7, 42 +/- 8 and 127 +/- 18 min (Exp 1) or 21 +/- 4, 51 +/- 12 and 113 +/- 20 min (Exp 2). The maximum heart rate in response to electrical vagal stimulation (maximum 'stimulation VCA') was established according to two scenarios in two groups of dogs matched for maximum 'inherent VCA' (n = 7). In the 0-min (Exp 3) and 170-min scenario (Exp 4) vagotomy was carried out 10 and 180 min after the muscarinic blockade. Expressed as percentage of the maximum 'inherent VCA', the maximum 'stimulation VCA' was 116 +/- 7 and 41 +/- 8%, respectively. This implies that the peripheral neuroeffector responsiveness declined by 75% over the given time period. The rate of the spontaneous decline of 'inherent VCA' over the same period was 77% (Exp 4), being not significantly different from the rate of decline of the maximum 'stimulation VCA;. This result excludes a decrease in central vagal tone and indicates that the spontaneous decline in VCA is due to a decrease in response of the peripheral neuroeffector system only