Objective The purpose of this study was to determine if parafascicular nucleus of thalamus is involved in the nociceptive stimulation evoked by coronary artery occlusion-induced acute myocardial ischemia and to investigate the effect of fentanyl on this nociceptive stimulation. Methods Male SD rats weighing 260-300 g were operated upon under general anesthesia with intraperitoneal urethane (1.2 g ? kg -1 ) and local infiltration of the skin incision. The discharges of pain-sensitive neurons (PSN) were recorded for 20 seconds every 5 min using single-barrel glass electrode before and after the coronary artery occlusion ( CAO) . The study was divided into 3 groups: group Ⅰ CAO alone ( n = 9); group Ⅱ CAO + fentanyl ( n = 6) : fentanyl 0.01 mg ?kg-1 was administered iv 15 min after CAO; group Ⅲ CAO + fentanyl + naloxone ( n = 6) : naloxone 0.04 mg? kg-1 was administered iv 15 min after intravenous fentanyl administration. Results The discharge frequency was significantly increased following CAO and peaked within 5-10 min after CAO and maintained for 60 min. The increased frequency of nociceptive discharge was significantly inhibited within 10 min after fentanyl and intravenous naloxone could completely antagonize the inhibitory effect of fentanyl. Conclusion Visceral pain can be evoked by acute myocardial ischemia induced by coronary artery occlusion. Thalamic parafascicular nucleus is involved in the perception of nociception in CNS. Opioid receptors play a critical role in the modulation of the nociception.