噻庚啶对离体大鼠心脏心肌缺血再灌注损伤的保护作用  

Protective Effect of Cyproheptadine on MyocardialIschemia and Reperfusion Injury in Isolated Rat Heart

作　　者：韩红[1] 叶冀明 许贤芳[1] 郭亚东[1] 孙继英[1] 

机构地区：[1]昆明医学院病理生理教研室,昆明医学院分析生化室

出　　处：《昆明医学院学报》1994年第1期48-51,共4页Journal of Kunming Medical College

摘　　要：采用Ｌａｎｇｅｎｄｏｒｆｆ离体心脏灌流模型，观察噻庚啶对全心缺血再灌损伤的保护作用，并探讨其可能机理。结果显示。噻庚啶（ｃｙｐｒｏｈｅｐｔａｄｉｎｅ，ＣＹＰ）明显抑制缺血后静息张力的升高，并延迟其升高起始时间，减轻心肌线粒体肿胀，减少收缩带形成，提高再灌心肌三磷酸腺苷（ＡＴＰ）水平和能量负荷（ＥＣ），降低—磷酸腺苷（ＡＭＰ）及次黄嘌呤核苷（ＩＮＯ）含量，防止心肌钙聚积和钾丢失，结果提示ＣＹＰ对心肌缺血再灌损伤具有保护作用，其机理可能与拮抗钙离于和改善能量代谢有关。Experiments were performed on isolated perfused rat heart (Langendorffe heart preparation) subjected to 30 min global ischemia and 20 min reperfusion. After ischemia and reperfusion,myocardial injury occured.Cyproheptadine ( CYP,20 μmol· L-1)significantly suppressed the rise of resting tension induced by ischemia and reperfusion,and delayed the time of inception for its rise,markedly alleviated mitochondria swelling and reduced the formation of contraction band in reperfused myocardium. in addition,wuth CYP treatment,Ca2+content much lowered and Potassium level increased in reperfused myocardium,Adenosine triphosphate (ATP) content and energy charge(EC)elivated very much,but adenosine monophosphate(AMP) and inosine (INO) concentrations decreased obviously.The results above indicated that CYP possessed protective effects on myocardial injury caused by ischemia and reperfusion,and also suggested the underlying protective mechanisms were probably associated with Calcium antagonism of CYP and its improvement on energy metabonism.

关 键 词：心肌缺血 再灌注损伤 噻庚啶 钙 

分 类 号：R972.9[医药卫生—药品]