Lignocaine exerts a specific endoanaesthetic effect on left ventricular mechanoreceptors during coronary occlusion, independent of its negative inotropic effects.
Animal data suggest lignocaine modulates ischemic mechanoreceptor activity; leaves open relevance to human acute coronary care.
We recorded the afferent activity of 11 left ventricular mechanoreceptors in filaments of the vagus nerve in 10 chloralose-anaesthetised cats. The fibres showed low irregular spontaneous activity of 2.9 (0.2 to 8.4) spikes X s-1. During temporary occlusion of the left anterior descending or left main coronary artery they were activated to 19.1 (4.8 to 47.0) spikes X s-1. Intravenous infusion of 0.175 and 0.35 mg X kg-1 X min-1 lignocaine lowered heart rate and blood pressure. The spontaneous nerve fibre activity remained unchanged by the local anaesthetic, whereas the maximum activity evoked by coronary artery occlusion was reduced to 14.7 (2.6 to 34.1) and 10.9 (2.4 to 27.6) spikes X s-1. An additional infusion of 5 and 10 micrograms X kg-1 X min-1 dopamine during continued application of 0.35 mg X kg-1 X min lignocaine raised heart rate and blood pressure to control values but had only minimal effects on the response of the fibres to coronary occlusion. It is concluded that lignocaine exerts a specific endoanaesthetic effect on the left ventricular mechanoreceptors, which is not mediated by its negative inotropic side effect.
No takes yet. Share an insight, caveat, or question.
Vogt et al. (1983) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: