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  • Title: [The effect of hyperoxemia on cerebral blood flow in normal humans].
    Author: Ohta H.
    Journal: No To Shinkei; 1986 Oct; 38(10):949-59. PubMed ID: 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)
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