论文部分内容阅读
目的 探讨 β1肾上腺素受体对心肌钙通道的调节及其在心肌重塑中的作用。方法 建立Wistar大鼠心肌梗死后心肌重塑模型 ,用免疫组化法观测心肌I型、III型胶原和纤维连接蛋白 (FN)表达的变化 ;RT -PCR和原位杂交方法检测Ica -T通道、Ica -L通道、β1受体mRNA表达的变化 ,原子吸收光谱法测定心肌总Ca2 +浓度。结果 倍他乐克组心肌Ⅰ型、Ⅲ型胶原及纤维连接蛋白的表达均比梗死组显著减少 (P <0 0 5或P <0 0 1) ,胚胎型Ica -L通道mRNA表达被抑制 ,Ica -T通道mRNA表达无明显改变 ,β1受体mRNA的表达比梗死组减少 4 1 18% ,心肌总Ca2 +浓度比梗死组显著降低 (P <0 0 5 )。结论 心肌梗死后胚胎型Ica -T通道和Ica -L通道的mRNA表达增强可能在于增加Ca2 +内流 ,触发心肌重塑 ;β1受体可能是通过胚胎型Ica -L通道参与心肌重塑过程
Objective To investigate the regulation of β1 adrenergic receptor on cardiac calcium channel and its role in myocardial remodeling. Methods The myocardial remodeling model of myocardial infarction was established in Wistar rats. The expression of type I collagen, fibronectin and fibronectin (FN) in myocardium was detected by immunohistochemical method. Ica-T channel was detected by RT-PCR and in situ hybridization , Ica-L channel, the expression of β1 receptor mRNA, and the concentration of total Ca2 + in myocardium by atomic absorption spectrometry. Results The expression of type Ⅰ, type Ⅲ collagen and fibronectin in the betaine group was significantly lower than that in the infarcted group (P <0.05 or P <0.01), and the mRNA expression of the embryonic Ica-L channel was inhibited. The mRNA expression of Ica-T channel did not change significantly. The expression of β1 receptor mRNA was decreased by 41.18% in infarction group and the total myocardial Ca2 + concentration was significantly lower than that in infarction group (P <0.05). Conclusion The increased mRNA expression of embryonic Ica-T channel and Ica-L channel after myocardial infarction may be due to increased Ca2 + influx, triggering myocardial remodeling; β1 receptor may participate in myocardial remodeling through embryonic Ica-L channel