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高碳酸血症期间的脑内细胞变化:大鼠体内31P核磁共振研究

Cerebral intracellular changes during supercarbia: an in vivo 31P nuclear magnetic resonance study in rats.

作者信息

Litt L, González-Méndez R, Severinghaus J W, Hamilton W K, Shuleshko J, Murphy-Boesch J, James T L

出版信息

J Cereb Blood Flow Metab. 1985 Dec;5(4):537-44. doi: 10.1038/jcbfm.1985.81.

Abstract

31P nuclear magnetic resonance (NMR) spectroscopy was used noninvasively to measure in vivo changes in intracellular pH and intracellular phosphate metabolites in the brains of rats during supercarbia (PaCO2 greater than or equal to 400 mm Hg). Five intubated rats were mechanically ventilated with inspired gas mixtures containing 70% CO2 and 30% O2. Supercarbia in the rat was observed to cause a greater reduction in cerebral intracellular pH (pHi) and increase in PCO2 than observed in other experiments with rats after 15 min of global ischemia. Complete neurologic and metabolic recovery was observed in these animals, despite and average decrease in pHi of 0.63 +/- 0.02 pH unit during supercarbia episodes that raised PaCO2 to 490 +/- 80 mm Hg. No change was observed in cerebral intracellular ATP and only a 25% decrease was detected in phosphocreatine. The concentration of free cerebral intracellular ADP, which can be calculated if one assumes that the creatine kinase reaction is in equilibrium, decreased to approximately one-third of its control value. The calculated threefold decrease in the concentration of free ADP and twofold increase in the cytosolic phosphorylation potential suggest that there is increased intracellular oxygenation during supercarbia. Because a more than fourfold increase in intracellular hydrogen ion concentration was tolerated without apparent clinical injury, we conclude that so long as adequate tissue oxygenation and perfusion are maintained, a severe decrease in intracellular pH need not induce or indicate brain injury.

摘要

采用31P核磁共振(NMR)光谱法对大鼠在高碳酸血症(动脉血二氧化碳分压[PaCO2]大于或等于400 mmHg)期间脑内细胞内pH值和细胞内磷酸盐代谢物的体内变化进行无创测量。五只插管大鼠用含70%二氧化碳和30%氧气的混合气体进行机械通气。观察到大鼠的高碳酸血症导致脑内细胞内pH值(pHi)下降幅度大于其他全脑缺血15分钟后大鼠实验中观察到的情况,且二氧化碳分压升高。尽管在高碳酸血症发作期间(此时PaCO2升高至490±80 mmHg)pHi平均下降0.63±0.02个pH单位,但这些动物仍观察到完全的神经和代谢恢复。脑内细胞内三磷酸腺苷(ATP)未观察到变化,磷酸肌酸仅检测到25%的下降。如果假设肌酸激酶反应处于平衡状态,则可计算出的脑内细胞内游离二磷酸腺苷(ADP)浓度降至其对照值约三分之一。计算得出游离ADP浓度下降三倍,胞质磷酸化电位升高两倍,这表明高碳酸血症期间细胞内氧合增加。由于在没有明显临床损伤的情况下耐受了细胞内氢离子浓度超过四倍的增加,我们得出结论,只要维持足够的组织氧合和灌注,细胞内pH值的严重下降不一定会诱发或表明脑损伤。

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