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作 者:金发光[1] 钱桂生[1] 毛宝龄[1] 郭生健 赵自强[1] 黄桂君[1]
出 处:《中国病理生理杂志》1995年第3期281-285,共5页Chinese Journal of Pathophysiology
摘 要:本文旨在探讨急性代酸时CSFpCO_2在CSF酸碱调节中的作用及其机制。4组急性代酸犬模型均由静脉内输入0.2NHCl产生,血浆[HCO_3-]lh内下降到12±2mmol/L,实验持续6h。Ⅰ组控制PaCO_2常,6h时CSF[HCO_3-]下降了1.1mmol/L;Ⅱ组自然呼吸,CSFpCO_2伴随PaCO_2下降,6h时CSF[HCO_3-]下降了6.5mmol/L;Ⅲ组机械通气,PaCO_2和CSFpCO2均迅速下降,6h时CSF[HCO_3-]下降了8.2mmol/L;Ⅳ组控制PaCO_2正常,脑室注入乙酰唑胺,6h时CSF[HCO_3-]下降了11.4mmol/L。结果说明急性代酸时.CSF[HCO_3-]取决于CSFpCO_2。CSFHCO_3-主要来源于CNSCO_2的水化作用,与CA活性显著相关。The role of pCO_2 in cerebrospinal fluid(CSF)acid-base regulation inacute metabolic acidosis was studied. Acute metabolic acidosis was induced by the intra-venous infusion of 0.2N HCl in four groups of anesthetized dogs(n=5)fOr six hourswhen PaCO_2 was changed at different rates. Plasma[HCO_3-]was lowered to 12 ± 2mmol/Lwithin one hour and maintained at that level thereafter in all groups.(1) In groupIPaCO_2 were kept normal while metabolic acidosis was induced.The CSF[HCO_3-]fell by only 1. 1mmol/L after sixhours and was not significantly different from control.(2)Group Ⅱdogs breathed spontaneously while metabolic acidosis was induced. There wasa gradual drop in PaCO_2 accompanied by a similar drop in CSF pCO_2 CSF[HCO_3-]fell significanly by 6.5mmol/L at 6 hours and was parallel with the fall in CSF pCO_2.(3)In order to show interdependence of the rate of fall in CSF[HCO_3-]with rate of fall inCSF pCO_2 five dogs were hyperventilated mechanically and PaCO_2 reduced rapidly andmaintained there for six hours .CSF pCO_2 followed PaCO_2 CSF bicarbonate fell rapidlyand droped 8.2mmol/L.In group Ⅱ and group Ⅲ the fall in CSF[HCO_3-]paralleledthe drop in pCO_2-.(4)Group Ⅳ PaCO_2 were kept normal while metabolic acidosis wasinduced, but ventricles of brain was injected actazolamide. The CSF[HCO_3-]droped1.4mmol/L after six hours. It suggested that the CSF[HCO_3-]is dependent upon CSFpCO_2,and the formation of HCO_3 in CSF is closely related to pCO-2 and the activityof carbonic anhydrase.CSF HCO-3- come from effects of CO_2 hydroxylation.
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