Effects of urapidil on discharges of pain-sensitive neurons in thalamic parafascicular nucleus evoked by coronary artery occlusion in rats
- VernacularTitle:乌拉地尔对大鼠心肌缺血诱发丘脑束旁核痛敏神经元放电的影响
- Author:
Yajuan LEI
;
Zheng GUO
- Publication Type:Journal Article
- Keywords:
Piperazines;
Myocanlial ischemia;
Paraventricular hypothaiamic nuclecus;
Electrophysiology
- From:
Chinese Journal of Anesthesiology
1996;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the changes in discharge rates of pain-sensitive neurons (PSN) in thalamic parafaseicular nucleus ( Pf) following coronary artery occlusion (CAO) and the effects of urapidil, a partial 5-HT agonist. Methods One-hundred male SD rats weighing 260-300 g were operated upon under urethane anesthesia and local infiltration of the skin incision. The animals were tracheotomized and mechanically ventilated. A hole was drilled in the skull until the brain was exposed. A single-barrel glass electrode was inserted, aiming at the PSN, the discharges of which were filtered, amplified and recorded. Chest was opened and heart was exposed. A tie was placed around the anterior descending branch of left coronary artery which can be occluded whenever needed. The study was divided into 3 groups : group I CAO alone; group II CAO + urapidil and group III CAO + urapidil + methysergide ( a potent serotonin antagonist). Urapidil 0.21 mg.kg-1 was given intravenously 15 min after CAO. Methysergide 0.1 mg.kg-1 was given iv 20 min after urapidil. Results Discharges of PSN were recorded in 45 animals out of the 100, and the recordings were complete for investigation in 31 animals. CAO evoked significant increase in the discharge frequency of PSN in 18/31 animals. After intravenous urapidil the increased frequency of nociceptive discharges was inhibited; however intravenous methysergide could partially antagonize the antinociceptive effect of urapidil. Conclusion The results indicate that (1 )the nociceptive response could be induced by CAO in rats; (2) Pf nucleus of thafamus is involved in the myocardial ischemia-induced nociceptive response of central nervous system; (3) serotonin plays a critical role in the modulation of the nociceptive signal of acute myocardial ischemia.
