摘要
目的:探讨百日咳毒素(PTX)敏感的G蛋白是否介导κ阿片激动剂的心脏效应。方法:应用离体大鼠心脏Langendorf灌流模型观察κ阿片激动剂U50488H的心脏作用并探讨其可能机制。结果:研究结果表明,U50488H可导致心律失常、降低心率、心肌收缩力量和冠脉流量;MR2266和百日咳毒素(PTX)预处理后,可取消U50488H的致心律失常作用,但不能取消其降低心肌收缩力量和冠脉流量的作用。结论:结果提示κ阿片激动剂的致心律失常作用涉及PTX敏感的G蛋白机制。
AIM: To explore whether pertussis toxinsensitive G protein is involved in the cardiac effect of κ opioid agonist. METHODS: In the present study, the Langendorff isolated perfused rat heart was used as a model for study of cardiac effect of κ agonist and its possible mechanisms. RESULTS: It was shown that U50488 H induced arrhythmias, reduced heart rate, myocardial contractile force and coronary flow. Pretreatment with MR2266, a specific κ antagonist, and pertussis toxin, which ribosylates and inactivates the Gilike proteins, abolished the arrhythmogenic effect of U50488 H, but failed to cancel the reduction of contractile force and coronary flow induced by U50488 H. CONCLUSION: The results suggested that the arrhythmogenic effect of κ opioid agonist U50488 H on the isolated rat heart involved pertussis toxinsensitive G proteins.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1997年第6期505-508,共4页
Chinese Pharmacological Bulletin
基金
浙江省自然科学基金