Propofol suppresses activation of the nociception specific neuron in the parafascicular nucleus of the thalamus evoked by coronary artery occlusion in rats

Abstract

The neural response to acute myocardial ischaemia was reported as increases in neuronal activity of spinal projecting neurons and the neurons in the parafascicular nucleus (Pf) of the thalamus. The aim of this study was to investigate electrophysiologically the response of the nociception specific neuron (NSN) in the Pf to coronary artery occlusion (CAO) and a potential antinociceptive effect of propofol on the response in rats. The left anterior descending branch of the coronary artery was instrumented with a snare occluder in anaesthetized Sprague-Dawley rats. The unit discharges of the NSN were recorded using a single-barrel glass microelectrode and analysed to examine the response to CAO. Once the effect of CAO on the discharge was detected, the antinociceptive effect of propofol was examined. The NSN (30/46) showed a significant increase in the discharge rate following CAO. The increased discharge was suppressed immediately after intravenous injection of propofol at doses of 0.2 and 2 mgkg(-1). The inhibitory effect reached the maximum at 7 min (59.78 +/- 11.17% of suppression, P < 0.05) and 5 min (95.21 +/- 4.79% of suppression, P < 0.05) following administration of 0.2 and 2 mgkg(-1) of propofol, respectively. The effect of propofol was dose dependent and reversible. The maximum dose of propofol used in this study did not produce an anaesthetic effect and did not affect the spontaneous activity of the NSN. The findings of this study suggest that propofol plays a role in modulation of the nociception associated with acute myocardial ischaemia, displaying an antinociceptive effect on cardiac visceral pain evoked by acute myocardial ischaemia.