| Objective The purpose of this study was to investigate the changes in the discharge rates of pain-sensitive neurons of thalamic parafascicular nucleus following coronary artery occlusion and the interventive effects of urapidil, a partial agonist of 5-HT receptor. Methods Male SD rats weighing 260g-300g were operated under urethane anaesthesia and local anaesthesia. The recordings of the discharges of the pain-sensitive neurons (PSN) were made using single-barrel glass electrode for 20 seconds every 5 minutes before and after the coronary artery occlusion (CAO). The recorded cells were divided into 3 groups as following: group I: CAO alone; group II: CAO + Urapidil (0.21mg/kg), the drug was intravenously administrated at 15 minutes after CAO; group III: CAO + urapidil + methysergide, methysergide (0.1mg/kg) was administrated (i.v.) at 20 minutes after intravenous urapidil. Results Thirteen out of 31 neurons studied did not show changes in the discharge frequency following the CAO while the frequency of cell discharge of the other 18 neurons was markedly increased immediately following the CAO. Only the cells responding to somatic nociceptive stimulation were further examined and maintained during the 60 minutes after the CAO. After urapidil administrated intravenously, the increased frequency of nociceptive discharges was inhibited; however, methysergide (i.v.)could partially antagonize the antinociceptive effect of urapidil. Conclusions These results indicated that (1) Pf of thalami is involved in nociception of acute myocardial ischemia evoked by occlusion of the branch of coronary artery;(2) serotoninergic receptors play a critical role in the modulation of nociceptive signal of acute myocardial ischemia and urapidil could play the role of antinociception in the case. |
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