| The purpose of this study is to investigate if the nucleus parafascicular (Pf) in thalami is involved in nociception of acute myocardial ischemia evoked by occlusion of the anterior descending branch of the left coronary artery, furthermore, to determine the effects of tramadol on this nociceptive process. Methods Male SD rats weighing 260g-300g were operated under urethane anesthesia and local anesthesia. 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 + tramadol (12mg/kg), the drug was intravenously administrated at 15 minutes after CAO; group III: CAO + tramadol + naloxone (0.04mg/kg), naloxone was administrated at 15 minutes after intravenous tramadol. Results The results demonstrated that 9 out of 33 neurons studied did not show changes in the discharge frequency following the CAO while the frequency of cell discharge of the other 24 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 tramadol administrated intravenously, the increased frequency of nociceptive discharges was completely inhibited within 10 minutes; however, the effect of naloxone on the antinociceptive effect of tramadol was not detected. 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) tramadol could inhibit the increase in the discharge rate of the PSN in Pf of thalami evoked by the CAO.
|
PDF Full Text Request