一氧化碳对缺血脑组织神经细胞胞内Ca2+浓度的影响

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,12 h后制成MCAO模型。栓塞后24 h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<0.05);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<0.05)。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>0.05)。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。

Effect of endogenous carbon monoxide on intracellular calcium concentration in focal ischemic cerebral tissue in rats

AIM: To study effect of endogenous carbon monoxide on intracellular calcium concentration and explore the mechanism in brain protection of endogenous CO in focal cerebral ischemia in rats. METHODS: SD rats were divided into three groups randomly, which including hemin, ZnPP group and saline group as control. Respectively saline, hemin, ZnPP were injected intra-peritoneally twelve hours before middle cerebral artery was occluded. Twenty four hours after MCAO model was set up, the concentration of carbon monoxide in blood and intracellular calcium in neural cells was examined. RESULTS: Contrast to saline group, the concentration of CO in blood rose up while intracellular calcium in occluded side decreased in hemin group; the concentration of CO in blood went down while intracellular calcium in occluded side rose up in ZnPP group, there was significant difference among them (P<0.05). Hemin and ZnPP had no effect on intracellular calcium in non-occluded sides (P>0.05). CONCLUSIONS: It may be one of mechanisms on brain protection in ischemic cerebral tissue that carbon monoxide affected intracellular calcium concentration of neural cells by regulating Ca~(2 )-K~ channel on cell membrane as a messenger gaseous molecular and neurotransmitter.