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为了研究呼吸性酸碱失衡时内髓集合管 (IMCD)细胞病理生理学改变 ,分别以 3%CO2 和 10 %CO2 模拟慢性呼碱和慢性呼酸家兔肾脏IMCD细胞培养模型 ,对照组用 5 %CO2 。荧光探针法测定IMCD细胞H+ /K+ 交换功能 ,原位杂交和RT PCR检测IMCD细胞cH K ATP酶mRNA表达。结果显示 ,呼酸组H+ /K+ 交换显著高于对照组 (P <0 0 5 ) ,呼酸组cH K ATP酶mRNA原位杂交积分光密度和RT PCR积分光密度比值均非常显著地高于对照组 (P <0 0 1) ;而这三项指标 ,对照组与呼碱组之间差异均无显著性意义 (P >0 0 5 )。提示慢性呼酸显著增加IMCD细胞H+ /K+ 交换和cH K ATP酶mRNA表达 ,慢性呼碱有抑制和下调趋势 ,但差异无显著性意义 ,其原因尚待进一步研究
In order to study the pathophysiology changes of IMCD in respiratory acid-base imbalance model, IMCD cell culture model was simulated by 3% CO 2 and 10% CO 2, respectively. The control group was treated with 5% CO2. The H + / K + exchange function of IMCD cells was detected by fluorescent probe method. The mRNA expression of cH K ATPase in IMCD cells was detected by in situ hybridization and RT PCR. The results showed that the exchange rate of H + / K + was significantly higher than that of the control group (P <0 05), and the ratios of cH K ATPase mRNA in situ hybridization and RT PCR integrated optical density were significantly higher Control group (P <0.01). However, there was no significant difference between the three groups (P> 0.05). The results suggest that chronic acidosis can significantly increase the exchange of H + / K + mRNA and mRNA of cHK ATPase in IMCD cells, and there is a trend of inhibition and down-regulation of chronic alkalosis, but the difference is not significant, the reason remains to be further studied