【摘要】 目的通过对缺血预适应动物模型与单纯心肌缺血动物模型之间的对照研究,探讨预适应对心肌细胞膜水通道蛋白Aquaporin-1表达的影响及与心肌水肿的关系。方法以Real-time PCR及Western blotting了解在心肌组织AQP1基因转录及蛋白表达的动态变化趋势;采用Evan blue定量测定法了解心肌组织中微血管通透性的变化及用心肌水含量测定法了解缺血心肌的水肿程度。结果与缺血对照组相似,缺血预适应后心肌AQP1基因及其蛋白的表达呈现先减后增的趋势,但增加的程度较对照组为高。预适应后组织血管通透性增高明显受到抑制,但仅伴随着缺血后早期阶段心肌水肿的减轻。与微血管通透性的持续降低形成对比的同时,心肌水肿状态在之后一段时期内保持较高水平与AQP1蛋白表达增高在时间关系上相对应。结论预适应早期心肌水肿的减轻与血管通透性的抑制有关,而AQP1蛋白表达的增加可能是心肌水肿状态维持的因素。更多还原

【Abstract】 Objective by compared with ischemic control animals,to investigate AQP1 expression status after ischemic preconditioning and its relationship with myocardial interstitial edema.Methods To detect AQP1 transcription and the protein expression in infarct-border tissue by real-time PCR and western blotting.To exam permeability of micro-vessel in ischemic myocardium by dectation the content of Evan’s blue in myocardium and myocardial edema was investigated by detection of myocardial water content.Results Being Similar to ischemic control group,transcription and expression of AQP1 elevated but in higher level after transient depression.Increased permeability of micro-vessel in ischemic myocardium was inhibited markedly in ischemic preconditioning group,however,compared with alleviated interstitial edema only in early period.Conclusion alleviative interstitial edema in early period after ischemia is relevant to suppressed permeability of micro-vessels induced by ischemic preconditioning.Elevated expression of AQP1 may function as one of factor that maintain myocardial interstitial edema status.更多还原