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目的:观察低渗膨胀对豚鼠胃窦环行肌细胞钙激活钾电流和延迟整流型钾电流的影响。方法:采用传统全细胞膜片箱技术,对以胶原酶急性分离的单细胞进行低渗灌流,观察钾电流的变化。结果:低渗 灌流液(200 Osmmol/kg)可增加钙激活钾电流和延迟整流型钾电流,钙激活钾电流的增加可被四乙基胺4mmol·L~(-1)和Charybdotoxin 200nmol·L~(-1)完全抑制;延迟整流型钾电流的增加可被四乙基胺4mmol·L~(-1)部分抑制,可被4-氨基吡啶10mmol·L~(-1)完全抑制。两种钾电流的增加幅度无显著性差异(P>0.05)。钙激活钾电流在施加低渗灌流(17.0±4.8)s后增加;延迟整流型钾电流在(30.7±13.7)s后增加,两者的潜伏期存在显著性差异(P<0.05)。结论:低渗膨胀可增加钙激活钾电流和延迟整流型钾电流,这种增加效应可能与细胞容积调节有关。
Objective: To observe the effect of hypotonic dilation on calcium-activated potassium current and delayed rectifier potassium current in antral myocytes of guinea-pig. Methods: The traditional whole-cell patch-box technique was used to perfuse single cells acutely isolated from collagenase to observe the change of potassium current. Results: Low osmolar perfusion fluid (200 Osmmol / kg) increased calcium-activated potassium current and delayed rectifier potassium current, and the increase of calcium-activated potassium current could be inhibited by tetraethylamine 4 mmol·L -1 and Charybdotoxin 200 nmol·L ~ (-1). The increase of delayed rectifier potassium current was partially inhibited by 4 mmol·L -1 tetraethylammonium, which could be completely inhibited by 10 mmol·L -1 4-aminopyridine. There was no significant difference between the two potassium currents (P> 0.05). Calcium-activated potassium currents increased after low-infiltration perfusion (17.0 ± 4.8) s, while delayed rectifier potassium currents increased after (30.7 ± 13.7) s. There was a significant difference between the two groups in latency (P <0.05). Conclusion: Hypotonic swelling can increase calcium-activated potassium currents and delayed rectifier potassium currents, which may be related to the regulation of cell volume.