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在一氧化二氮或氮气诱导的低氧性缺氧中脑血流量与动脉血氧饱和度的线性关系。

The linear relation of cerebral blood flow to arterial oxygen saturation in hypoxic hypoxia induced with nitrous oxide or nitrogen.

作者信息

Stoyka W W, Frankel D Z, Kay J C

出版信息

Can Anaesth Soc J. 1978 Nov;25(6):474-8. doi: 10.1007/BF03007409.

Abstract

This study has demonstrated a linear relationship between cerebral blood flow and arterial oxygen saturation (Sao2) in the cerebral blood flow response in the hypoxic range of Pao2 values, which we believe is documented for the first time. The cerebral blood flow increased 1.02 per cent for each percentage decrease in Sao2 in hypoxia induced with nitrogen. Hypoxia induced with nitrous oxide increased cerebral blood flow at the rate of 2.09 per cent for each one per cent decrease in Sao2 which was dramatically more than the increase associated with hypoxia induced with nitrogen. Increased survival rates at lower Sao2 levels suggested that nitrous oxide also exerts a protective effect on dog myocardium. The mechanism by which hypoxia increases cerebral blood flow is unclear but the prevalent theory is one of neurogenic control which causes cerebral blood flow to increase as the intracellular hydrogen ion ([H+]I) increases in the progressive lactacidosis of hypoxia. The demonstration of a linear relationship between cerebral blood flow and Sao2 will provide the statistician, the researcher and the clinician with a useful tool for the neurophysiological assessment of cerebral blood flow.

摘要

本研究已证实在动脉血氧分压(Pao2)值的低氧范围内,脑血流量与动脉血氧饱和度(Sao2)在脑血流反应中呈线性关系,我们认为这是首次有文献记载。在用氮气诱导的低氧状态下,Sao2每降低1个百分点,脑血流量增加1.02%。在用一氧化二氮诱导的低氧状态下,Sao2每降低1个百分点,脑血流量以2.09%的速率增加,这显著高于与氮气诱导的低氧相关的增加幅度。较低Sao2水平下存活率的提高表明一氧化二氮对犬心肌也有保护作用。低氧增加脑血流量的机制尚不清楚,但普遍的理论是神经源性控制机制,即在低氧进行性乳酸性酸中毒过程中,随着细胞内氢离子([H+]I)增加,导致脑血流量增加。脑血流量与Sao2之间线性关系的证明将为统计学家、研究人员和临床医生提供一个用于脑血流神经生理学评估的有用工具。

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