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[高氧血症对正常人脑血流量的影响]

[The effect of hyperoxemia on cerebral blood flow in normal humans].

作者信息

Ohta H

出版信息

No To Shinkei. 1986 Oct;38(10):949-59.

PMID:3098265
Abstract

The aim of this study was to evaluate the effect of various degrees of hyperoxemia on cerebral blood flow (CBF), including the hyperbaric oxygenation (HBO) environment. Study subjects were 28 healthy volunteers (17 males and 9 females) from 26 to 60 (average: 42 +/- 11) years old. CBF measurements were done by 19 mCi 133Xe intravenous injection method using rCBF analyzer BI-1400 (Valmet). Two-compartmental analysis was used for the calculation of Fast, Slow Flow and initial slope index (ISI). The three CBF study series included: Rest (before HBO 1 ATA.air)-1 ATA.O2-2 ATA.O2 series in 8 cases; Rest-1 ATA.O2 50% N2 50%-1.5 ATA.O2 series in 10 cases; and Rest-2.5 ATA.O2-after HBO (1 ATA.air) series in 8 cases. CBF measurements commenced 5 to 10 minutes after fixing a mask for oxygen inhalation. Arterial blood gas analyses using IL-813 (IL) and blood pressure measurements were done immediately after CBF measurements. CBF changes evaluated by ISI, estimating resting flow as 100% (PaO2: 93 +/- 8 mmHg), were 91% at 1 ATA.O2 50% (PaO2: 201 +/- 50 mmHg), 79% at 1 ATA.O2 (PaO2: 432 +/- 44 mmHg), 77% at 1.5 ATA.O2 (PaO2: 693 +/-79 mmHg) and 71% at 2 ATA.O2 (PaO2: 838 +/- 95 mmHg). CBF gradually decreased to the level shown for 2 ATA.O2, but CBF showed a tendency to increase somewhat at 2.5 ATA.O2 (81%, PaO2: 1103 +/- 111 mmHg). CBF decreases were statistically significant at 1 ATA.O2, 1.5 ATA.O2, 2 ATA.O2 and also 2.5 ATA.O2 compared with Rest (P less than 0.05). Arterial blood gas analyses clearly showed the stepwise increase in PaO2 to the level of 2.5 ATA.O2 (P less than 0.01). Changes in PaCO2 and blood pressure were slight and not significant statistically in each series. Since the data showed no significant change in the PaCO2 level in each series, it was concluded that the CBF decrease was due to vasoconstriction caused by the elevated PaO2. The mechanism of cerebral vasoconstriction caused by hyperoxemia is not yet clearly understood, but the direct vasoconstrictive effect of oxygen, neurogenic control and the metabolic effect of an elevated cerebral tissue oxygen level may contribute to the CBF decrease. CBF decrease during elevated PaO2 may be a protective physiological response to maintain normal brain metabolism and function against the excessive oxygen supply. Disturbance of this regulatory mechanism may result in oxygen poisoning of the central nervous system.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

本研究的目的是评估不同程度的高氧血症对脑血流量(CBF)的影响,包括高压氧环境。研究对象为28名健康志愿者(17名男性和9名女性),年龄在26至60岁之间(平均:42±11岁)。使用rCBF分析仪BI - 1400(瓦尔梅特)通过19毫居里133Xe静脉注射法进行CBF测量。采用两室分析法计算快速、慢速血流和初始斜率指数(ISI)。三个CBF研究系列包括:8例的静息状态(高压氧1个绝对大气压空气之前) - 1个绝对大气压氧气 - 2个绝对大气压氧气系列;10例的静息状态 - 1个绝对大气压氧气50%氮气50% - 1.5个绝对大气压氧气系列;以及8例的静息状态 - 2.5个绝对大气压氧气 - 高压氧(1个绝对大气压空气)之后系列。在固定吸氧面罩5至10分钟后开始进行CBF测量。在CBF测量后立即使用IL - 813(IL)进行动脉血气分析并测量血压。以静息血流为100%(动脉血氧分压:93±8 mmHg),通过ISI评估的CBF变化在1个绝对大气压氧气50%(动脉血氧分压:201±50 mmHg)时为91%,在1个绝对大气压氧气(动脉血氧分压:432±44 mmHg)时为79%,在1.5个绝对大气压氧气(动脉血氧分压:693±79 mmHg)时为77%,在2个绝对大气压氧气(动脉血氧分压:838±95 mmHg)时为71%。CBF逐渐下降至2个绝对大气压氧气时所示水平,但在2.5个绝对大气压氧气时CBF有某种程度的上升趋势(81%,动脉血氧分压:1103±111 mmHg)。与静息状态相比,在1个绝对大气压氧气、1.5个绝对大气压氧气、2个绝对大气压氧气以及2.5个绝对大气压氧气时CBF下降具有统计学意义(P小于0.05)。动脉血气分析清楚地显示动脉血氧分压逐步升高至2.5个绝对大气压氧气的水平(P小于0.01)。在每个系列中,动脉血二氧化碳分压和血压的变化轻微且无统计学意义。由于数据显示每个系列中动脉血二氧化碳分压水平无显著变化,得出CBF下降是由动脉血氧分压升高引起的血管收缩所致的结论。高氧血症引起脑血管收缩的机制尚未完全清楚,但氧气的直接血管收缩作用、神经源性控制以及脑组织氧水平升高的代谢作用可能导致CBF下降。动脉血氧分压升高期间CBF下降可能是一种保护性生理反应,以维持正常的脑代谢和功能免受过多的氧气供应。这种调节机制的紊乱可能导致中枢神经系统氧中毒。(摘要截断于400字)

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