Effects of urotensin Ⅱ on isolated rat hearts under normal perfusion and ischemia-reperfusion
- Author:
- No author available
- Journal Title:
- ACTA PHYSIOLOGICA SINICA
- Issue:
- 4
- DOI:
- 10.3321/j.issn:0371-0874.2003.04.013
- Key Word:
- 病理学;尾加压素Ⅱ;心脏离体灌流;缺血 - 再灌注;大鼠
Abstract： 在正常Langendorff灌流与缺血 - 再灌注(停灌20 min - 复灌20 min)离体大鼠心脏模型, 观察尾加压素Ⅱ (urotensin Ⅱ, UⅡ)对冠脉流量、心功能和心肌代谢的影响以及心肌UⅡ受体的功能, 以探讨UⅡ的心脏效应.对正常心脏给予0.1、 1和10 nmol/L UⅡ各5 min, 然后换洗5 min, 对停灌缺血 - 再灌注心脏在再灌注期给予1或10 nmol/L UⅡ.监测心率、左室内压和左室内压升降的最大变化率等心功能指标, 计算冠脉流量, 测定冠脉流出液中总蛋白和肌红蛋白含量以及乳酸脱氢酶(LDH)活性. 灌流结束后, 测定心肌丙二醛(MDA)含量和质膜UⅡ结合位点(放射性配基结合法).结果如下: (1)正常心脏灌流UⅡ后, 冠脉流量和心功能呈浓度依赖下降, 换洗后没有完全恢复.心肌蛋白、肌红蛋白和LDH漏出随UⅡ浓度的增加而增加, 换洗后迅速减少.UⅡ组心肌MDA含量与对照组差异无显著性.(2)缺血 - 再灌注后, 冠脉流量显著减少, 心功能显著抑制, 再灌注期心肌蛋白、肌红蛋白和LDH明显漏出; 给予UⅡ后, 上述变化增强, 且高浓度组更强, 与对照组差异有显著性(P<0.01), 再灌注后心肌MDA含量亦显著高于对照(P<0.01). (3) 缺血 - 再灌注心肌质膜UⅡ受体的Bmax显著高于正常对照心肌(14.65±1.78 vs 20.53±1.98 fmol/mg pr, P<0.01), Kd值变化无统计学意义.上述结果表明, 在正常灌流的离体大鼠心脏, UⅡ使冠脉流量减少、心功能抑制, 并可造成心肌损伤; 在缺血 - 再灌注心脏, UⅡ受体上调, UⅡ加重冠脉流量减少、心功能抑制以及心肌损伤.
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