论文部分内容阅读
目的 :研究一氧化碳对局灶性缺血脑组织神经细胞胞内Ca2 + 浓度的影响 ,试图从离子水平阐明CO对脑组织保护作用的机制。方法 :将SD大鼠随机分为 3组 (n =6 ) ,使用HO诱导剂、HO抑制剂腹腔注射为实验组 ,等量生理盐水腹腔注射为对照组 ,12h后制成MCAO模型。栓塞后 2 4h检测血浆CO浓度、神经细胞胞内Ca2 + 浓度。结果 :HO诱导剂组CO浓度明显高于生理盐水组 ,而胞内Ca2 + 浓度低于生理盐水组 (P <0 0 5 ) ;HO抑制剂组CO浓度明显低于生理盐水组 ,胞内Ca2 + 浓度高于生理盐水组 (P <0 0 5 )。HO诱导剂、HO抑制剂对非栓塞侧神经细胞胞内Ca2 + 浓度没有影响 (P >0 0 5 )。结论 :CO通过作用于细胞膜上的Ca2 + -K+ 通道 ,引起缺血脑组织神经细胞胞内Ca2 + 浓度的变化可能是CO脑保护作用的机制之一
Objective: To investigate the effect of carbon monoxide on intracellular Ca2 + concentration in focal ischemic neuronal cells in order to elucidate the protective mechanism of CO on brain tissue at ion level. Methods: The SD rats were randomly divided into 3 groups (n = 6). The HO inducer and HO inhibitor were injected intraperitoneally into the experimental group. The rats in the same volume of normal saline were injected intraperitoneally into the control group. After 12 hours, MCAO model was established. 24 h after embolization plasma CO concentration, intracellular Ca2 + concentration in nerve cells. Results: The CO concentration in HO inducer group was significantly higher than that in saline group, while the intracellular Ca2 + concentration was lower than that in saline group (P <0.05). The CO concentration in HO inhibitor group was significantly lower than that in saline group and intracellular Ca2 + + Concentration higher than the saline group (P <0 05). HO inducer and HO inhibitor had no effect on intracellular Ca2 + concentration in non-embolic neurons (P> 0.05). CONCLUSION: Changes of intracellular Ca2 + concentrations induced by CO in Ca2 + -K + channels in ischemic brain tissue may be one of the protective mechanisms of CO brain