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目的:探讨茶色素(tea pigment,TP)对离体蟾蜍心肌收缩力的保护作用机制。方法:将蟾蜍随机分为对照组和实验组,对照组又分为正常任氏液组、阴性组、阳性组和药品组,正常任氏液组为蟾蜍离体心脏标本只灌流正常任氏液,阴性组为蟾蜍离体心脏标本在灌流正常任氏液后改灌流低钙任氏液,阳性组为蟾蜍离体心脏标本在灌流正常任氏液后改灌流高钙任氏液,药品组为蟾蜍离体心脏标本在灌流正常任氏液后分别改灌流TP,维拉帕米,阿托品和异丙肾上腺素溶液,观察药物本身作用;实验组分为维拉帕米组、阿托品组和异丙肾上腺素组,每一药品组又分为低钙组和高钙组,低钙组或高钙组又分为TP前或后加药2组,每组8只。采用斯氏法制备离体蛙心灌流标本,在灌流200 mg·L-1TP前或后分别灌流7.27 mg·L-1维拉帕米、10 mg·L-1阿托品或10 mg·L-1异丙肾上腺素,应用BL-420F生物机能实验系统记录离体蟾蜍心肌收缩曲线,并对心肌收缩力进行统计学分析。结果:TP可使心肌收缩力在低钙时增强(P<0.05),高钙时抑制(P<0.05)的心肌保护作用,可部分被维拉帕米阻断(P<0.01),被异丙肾上腺素兴奋(P<0.01),对阿托品既有协同又有拮抗作用(P<0.05)。结论:TP对离体蟾蜍心肌收缩力的保护作用可能与钙离子通道,M受体及β受体有关。
Objective: To investigate the protective mechanism of tea pigment (TP) on isolated contractile force of Bufo bufo gargarizans. Methods: Toad was randomly divided into control group and experimental group. The control group was divided into normal Renshi group, negative group, positive group and drug group. The normal Renshi group was only perfusion normal Renshi liquid , The negative group of toad isolated heart specimens after perfusion of normal ringer’s solution to change irrigation perfusion low calcium rinse solution, the positive group toad isolated heart specimens in perfusion of normal ringer’s solution after perfusion of high calcium rinse solution, the drug group Toad isolated heart specimens were perfusion of TP, verapamil, atropine and isoproterenol solution after perfusion of normal Renal fluid to observe the effect of the drug itself; the experimental components were verapamil, atropine group and isopropyl Epinephrine group, each drug group is divided into low calcium group and high calcium group, low calcium group or high calcium group is divided into TP before or after the dosing group 2, 8 in each group. The isolated frog heart perfusion specimens were prepared by the method of Aspergillus fumigatus, and were pretreated with verapamil (7.27 mg · L -1), atropine 10 mg · L -1 or 10 mg · L -1 Isoproterenol was used to record the contraction curve of isolated Bufo bufo gargarizans with BL-420F bio-functional system. The myocardial contractility was analyzed statistically. Results: TP could enhance myocardial contractility at low calcium (P <0.05), inhibit myocardial protection at high calcium (P <0.05) and partially block verapamil (P <0.01) Propranolol was significantly (P <0.01) synergistic and antagonistic to atropine (P <0.05). Conclusion: The protective effect of TP on contractile force of isolated toad may be related to calcium channel, M receptor and β receptor.