中文摘要：

目的 观察外源性精胺对大鼠胸主动脉环张力的影响并初步探讨其可能机制。方法 采用离体血管环灌流方法，分别观察不同浓度外源性精胺对正常孵育以及无Ca^2＋、去内皮、去甲肾上腺素（NA）或60mmol／L KCl预处理、存在维拉帕米、加入咖啡因等条件下血管张力的影响。结果 内皮完整含Ca^2＋液中，精胺（50μmol／L～5mmol／L）对NA和高钾预处理的血管环，既无舒张作用，也不进一步引起收缩；内皮完整含Ca^2＋液中，外源性精胺在一定浓度范围内（50～200μmol／L）呈浓度依赖性使血管收缩；在无Ca^2＋ Krebs液中，精胺（200μmol／L）无缩血管作用；含Ca^2＋去内皮条件下，精胺（200μmol／L）对正常血管有收缩作用，但明显弱于内皮完整者；含Ca^2＋ Krebs液预先加入维拉帕米，精胺（200μmol／L）对正常血管无作用；加入咖啡因引起血管短暂而快速收缩后，加入200μmol／L精胺缩血管效应降低；内皮完整含钙液加入200μmol／L精胺后，再加入30mmol／L咖啡因后，不进一步引起血管收缩。结论 外源性精胺在一定的浓度范围内呈浓度依赖性收缩血管平滑肌，其作用机制可能主要是与L广型钙通道开放来促进血管平滑肌外钙内流，并进一步诱导内钙释放有关。

英文摘要：

Objective To investigate the effects of exogenous spennine （Sp） on the tension of rat＇s thoracic aortic artery ring and its possible mechanisms. Methods The contracting responses of vascular smooth muscles to the normal and Ca^2＋ -free bath solutions with exogenous spennine had been observed by means of thoracic aortic artery rings. By the same way, the influences of exogenous spennine on the vascular smooth muscles by adding noradrenalin （NA）, KCl （60mmol/L）,verapamil （Vp）,and caffeine were observed.The effects of exogenous spennine on endothelium-denuded rings were also studied. Results Spennine（50μmol/L - 5μmol/L） induced neither relaxing nor repressively contracting of the aortic rings pretreated by NA or KCl; exogenous Sp evoked contraction of the rings in a dose-dependent manner in certain concentration （50 - 200μmol/L） ;The cantracting effect of Sp （2（10μmol/L） was abolished in Ca^2＋ -free bath solution;in Ca^2＋ -contained bath solution,the contraction caused by Sp on endothelium-denuded rings was lower than rings with endothelium;Sp had no effect on the rings pretreated with Vp in Ca^2＋ bath solution.After transient contraction of rings pretreated by caffeine, the effect of Sp （200μmol/L） degraded; the addition of Sp （200μmol/L） into Ca^2＋ -contained bath solution, rings could not contract further by caffeine （30mmol/L）. Condusion Vascular smooth muscles could contract triggered by spennine in a dose-dependent manner.The mechanisms may related to the opening of L-type Ca^2＋ channel,the promoting of Ca^2＋ influx and further release of calcium from sarcoplasmic reticulum （SR）.