Mendelman Avivit, Zarchin Nili, Meilin Sigal, Guggenheimer-Furman Esther, Thom S R, Mayevsky Avraham
Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel.
Neurol Res. 2002 Dec;24(8):765-72. doi: 10.1179/016164102101200861.
This study examined the effect of 2000 ppm CO on the brain of an awake rat. Measurements of regional perfusion as well as metabolic, ionic and electrical activities were used to examine whether mechanisms responsible for changes in brain perfusion were separable from those attributable to compromises in neuronal metabolism. Exposure to 2000 ppm CO resulted in elevation of cerebral blood flow. The stability of mitochondrial NADH redox level during CO exposure indicated that tissue hypoxia did not develop. The elevation in blood flow was inhibited by L-nitroarginine methyl ester, indicating that nitric oxide was responsible for the CO-induced elevation in blood flow. Exposure to 2000 ppm CO also triggered a significant decrease in pH and rise in extracellular potassium ion, possibly due to ion-pump inhibition. The amplitude of the electrocorticogram wave activity decreased, indicative of a compromise to physiological activity. These changes were not observed in rats anesthetized with pentobarbital during CO exposure, although anesthesia had no effect on the CO-induced elevation in blood flow and there was still no change in mitochondrial NADH redox level. We concluded that CO acts by separate mechanisms to alter cerebral vasoactivity and neuronal metabolic responses and that both processes are independent of hypoxic stress.
本研究检测了2000 ppm一氧化碳对清醒大鼠大脑的影响。通过测量局部灌注以及代谢、离子和电活动，来检验负责脑灌注变化的机制是否与那些归因于神经元代谢受损的机制相分离。暴露于2000 ppm一氧化碳会导致脑血流量升高。一氧化碳暴露期间线粒体NADH氧化还原水平的稳定性表明未发生组织缺氧。L-硝基精氨酸甲酯抑制了血流量的升高，表明一氧化氮是一氧化碳诱导血流量升高的原因。暴露于2000 ppm一氧化碳还引发了pH值的显著降低和细胞外钾离子的升高，这可能是由于离子泵抑制所致。脑电图波活动的幅度降低，表明生理活动受到损害。在一氧化碳暴露期间用戊巴比妥麻醉的大鼠中未观察到这些变化，尽管麻醉对一氧化碳诱导的血流量升高没有影响，并且线粒体NADH氧化还原水平仍然没有变化。我们得出结论，一氧化碳通过不同机制作用于改变脑血管活性和神经元代谢反应，并且这两个过程均独立于缺氧应激。
