噻庚啶的抗心律失常作用和对心肌代谢的影响  

Antiarrhythmic effect of cyproheptadine and its role on myocardial metabolism

作　　者：韩红[1] 何洁[1] 郭泽云[1] 

机构地区：[1]昆明医学院病理生理教研室

出　　处：《中国药理学通报》1994年第1期64-67,共4页Chinese Pharmacological Bulletin

摘　　要：在结扎大鼠左冠状动脉主支５ｍｉｎ．再灌注１５ｍｉｎ造成的再灌心律失常模型中．噻庚啶（Ｃｙｐ．４ｍｇ·ｋｇ－１，ｉｖ）明显降低再灌心律失常发生率，消除再灌引起的心室纤颤和室性心动过速．显著减少室性早搏个数．明显减慢心率．显著降低Ⅱ导ＥＣＧ的Ｐ波和Ｔ波电压．防止缺血所致ＳＴ段抬高。在离体灌流大鼠心脏心肌缺血再灌损伤模型中．Ｃｙｐ显著降低再灌心肌Ｃａ２＋聚积，有效防止Ｋ＋丢失．显著提高能量负荷（ＥＣ）．轻度提高腺苷三磷酸（ＡＴＰ）水平．显著降低腺苷一磷酸（ＡＭＰ）及次黄嘌呤核苷（ＩＮＯ）含量。表明：Ｃｙｐ有显著抗缺血再灌心律失常作用。并有拮抗钙．减轻Ｋ＋丢失和改善缺血再灌注心肌能量代谢作用。In the model of reperfusion arrhythmias generated by ligation of left coronaryartery for 5 min followed by 15 min recirculation,eyproheptadine(Cyp,11.4×10- 6 mol ·kg-1,iv) significantly reduced the incidence of reperfusion arrhytthmias (RAr), abolished ventricular fibrillation (VF) and tachycardia (VT),markedly decreased the number of totalpremature ventricular complexes (PVC),slowed down heart rate, lowered the amplitude of P and T waves in ECG(Ⅱlead) and prevented the rise of ST segment caused by ischemia. In the isolated rat heart subjected to 30 min global ischemia and 20 min reperfusion, Cyp (20×10-6mol·L-1) obviously alleviated Ca2+ accumulation and K+ loss in reperfused myocardium, elevated energy charge (EC) markedly and adenosine triphosphate (ATP) level slightly, and reduced adenosine monophosphate (AMP) and inosine (INO) content very much. The results indicated that Cyp possessed antagonizing action on arrhythmias induced by ischemia and repexfusion. Besides, it can antagonize Ca2+, modify K+and improve energy metabolism in reperfusedmyocardium.

关 键 词：噻庚啶 心肌缺血 再灌注损伤 

分 类 号：R965.1[医药卫生—药理学]