Accession Number : ADA307505
Title : Factors Affecting CNS Oxygen Toxicity in Humans.
Descriptive Note : Final rept.,
Corporate Author : DUKE UNIV MEDICAL CENTER DURHAM NC F G HALL LAB FOR ENVIRONMENTAL RESEARCH
Personal Author(s) : Natoli, Michael J. ; Vann, Richard D.
PDF Url : ADA307505
Report Date : 19 JAN 1996
Pagination or Media Count : 282
Abstract : This project investigated the effects of elevated oxygen partial pressure, inspired CO2, immersion, and work on ventilatory response to CO2, brain cortical oxygenation, and the occurrence of symptoms of CNS oxygen toxicity in humans. Relative changes in cerebral oxygenation from a baseline were measured by near-infrared (NIR) spectroscopy. Ventilatory response was measured during CO2 rebreathing in a computer-controlled, closed-circuit breathing apparatus. The results of this study suggest that inspired CO2 is a potent instigator of CNS oxygen toxicity, more potent than oxygen alone or in combination with immersion and work. Most (31) symptoms were reported while the inspired CO2 was 7.0% - 7.5% and P102 was 2.80 ATA. Hyperoxia, P102 = 1.75 or 2.80 ATA, leads to increased cerebrovascular oxygenation despite vasoconstriction. Inspired CO2 reversed vasoconstriction and increasing cerebral oxygenation further. Subjects with symptoms consistent with oxygen toxicity did not show a CO2--induced vasoconstrictive reversal despite increased cerebral oxygenation. Ventilatory response to CO2 did not correlate well with symptom incidence but the subject who convulsed had the lowest ventilatory response to CO2 at 0.21 ATA P102. Facial immersion led to increased cerebrovascular blood volume and cytochrome a,a3 oxidation at both 0.21 and 2.80 ATA P102 and with both positive and negative static lung loads.
Descriptors : *INFRARED SPECTROSCOPY, *TOXICITY, *OXYGEN, *NEAR INFRARED RADIATION, *CENTRAL NERVOUS SYSTEM, SPECTROSCOPY, HUMANS, STATIC LOADS, SIGNS AND SYMPTOMS, HIGH PRESSURE, LUNG, IMMERSION, BLOOD VOLUME, CEREBRUM, VASOCONSTRICTING, FACE(ANATOMY), PARTIAL PRESSURE, CEREBROVASCULAR SYSTEM, HYPEROXIA.
Subject Categories : Anatomy and Physiology
Distribution Statement : APPROVED FOR PUBLIC RELEASE