Hsu W H, Rong Y F, Hembrough F B
Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine, Iowa State University, Ames 50011.
J Vet Pharmacol Ther. 1989 Sep;12(3):283-8. doi: 10.1111/j.1365-2885.1989.tb00672.x.
The effects of jingsongling (JSL) and xylazine on heart rate (HR) and mean arterial pressure (MAP) were studied in five conscious male dogs. An i.v. injection of xylazine (1 mg/kg) caused a bradycardia, an initial hypertension, and a subsequent hypotension. An i.v. injection of JSL (1 mg/kg) caused a bradycardia and a 20-min hypertension without a subsequent hypotension. Atropine sulfate (45 micrograms/kg, i.v.) increased HR for 30 min without changing MAP, and antagonized JSL-induced bradycardia for at least 60 min. There was a subsequent rebound bradycardia. Atropine sulfate potentiated JSL-induced hypertension in both magnitude and duration. Yohimbine (0.1 mg/kg, i.v.), an alpha 2-adrenoceptor antagonist, increased HR and MAP for 110 and 70 min, respectively. Yohimbine not only failed to potentiate but even reversed the pressor effect of JSL in a dose-dependent manner. Yohimbine also caused a dose-dependent reversal of JSL-induced bradycardia. Tolazoline (5 mg/kg, i.v.), a nonselective alpha-adrenoceptor antagonist, increased MAP for 20 min without changing HR. Tolazoline also reversed JSL-induced hypertension and bradycardia. Prazosin (1 mg/kg), an alpha 1-adrenoceptor antagonist, decreased MAP and increased HR for at least 110 min. Prazosin reversed JSL-induced hypertension but failed to affect JSL-induced bradycardia. These results indicated that: (1) JSL-induced bradycardia and hypertension are mediated by alpha 2-adrenoceptors; (2) yohimbine and tolazoline may be useful in antagonizing these untoward reactions associated with JSL administration, whereas prazosin and atropine were not found to be beneficial in this regard.
在5只清醒雄性犬中研究了颈松灵(JSL)和赛拉嗪对心率(HR)和平均动脉压(MAP)的影响。静脉注射赛拉嗪(1毫克/千克)引起心动过缓、初始高血压和随后的低血压。静脉注射JSL(1毫克/千克)引起心动过缓和20分钟的高血压,随后无低血压。硫酸阿托品(45微克/千克,静脉注射)使心率增加30分钟而不改变MAP,并拮抗JSL诱导的心动过缓至少60分钟。随后出现反弹性心动过缓。硫酸阿托品在幅度和持续时间上均增强了JSL诱导的高血压。育亨宾(0.1毫克/千克,静脉注射),一种α2肾上腺素能受体拮抗剂,分别使心率和MAP增加110分钟和70分钟。育亨宾不仅未能增强反而以剂量依赖的方式逆转了JSL的升压作用。育亨宾还引起JSL诱导的心动过缓的剂量依赖性逆转。妥拉唑啉(5毫克/千克,静脉注射),一种非选择性α肾上腺素能受体拮抗剂,使MAP增加20分钟而不改变HR。妥拉唑啉也逆转了JSL诱导的高血压和心动过缓。哌唑嗪(1毫克/千克),一种α1肾上腺素能受体拮抗剂,使MAP降低并使HR增加至少110分钟。哌唑嗪逆转了JSL诱导的高血压,但未能影响JSL诱导的心动过缓。这些结果表明:(1)JSL诱导的心动过缓和高血压由α2肾上腺素能受体介导;(2)育亨宾和妥拉唑啉可能有助于拮抗与JSL给药相关的这些不良反应,而哌唑嗪和阿托品在这方面未发现有益作用。