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Posthypoxic jugular venous hyperoxia

From the Section on Experimental Neuropathology, Laboratory of Perinatal Physiology, National Institute of Neurological Diseases and Stroke, National Institutes of Health, United States Public Health Service, Department of Health, Education, and Welfare, Bethesda, Maryland.

SUMMARYThe phenomenon of jugular venous hyperoxia following episodes of hypoxic injury has been evaluated. In monkeys respiring 3.5% oxygen in nitrogen for intervals as long as thirty minutes, it was found that the duration of postinsult cerebral venous hyperoxygenation related to the duration of hypoxic exposure as long as the blood pressure was maintained above a mean of 80 mm. Hg. When episodes of hypotension below 80 mm. Hg occurred, the duration of the venous hyperoxic phase was extended in a nonpredictable manner. Recovery of brain electrical activity followed a similar pattern and occurred in approximately one-half of the time required for the normalization of the venous hyperoxia. The hypoxic episodes produced a CSF acidosis which also was more severe in animals whose episodes of hypoxia were complicated by hypotension.

Posthypoxic cerebral venous hyperoxia is indicative of a derangement in the regulatory relationship between cerebral metabolism and cerebral blood flow which normally results in a constant cerebral arteriovenous difference for oxygen. Hypoxia alters this relationship, producing a decrease in the oxygen arteriovenous differential probably due to a diminished cerebral utilization of oxygen or an increased cerebral blood flow or both. A quantitative evaluation of the duration and degree of the cerebral venous hyperoxia phase, particularly with 100% oxygen inhalation, provides a measure of the degree of abnormality in the relation between brain metabolism and cerebral perfusion.

Dr. Myers' address is Laboratory of Perinatal Physiology, NINDS, NIH, Bethesda, Maryland 20014.

Presented at the annual meeting of the American Academy of Neurology, April 25, 1969, Washington, D.C.

Dr. Shapiro is currently in the Department of Neurological Surgery, University of Washington School of Medicine, Seattle, Washington 98105.

Submitted for publication Nov. 21, 1969; accepted Dec. 15, 1969.

The authors wish to acknowledge the valuable technical assistance of Mr. Esteban Monell Torrens and Mrs. Carmen Freixas. We are also indebted to Dr. Martin Reivich and Dr. Arthur Ward for their review and helpful criticism of the manuscript.

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				M. D. Ginsberg and R. E. Myers Experimental Carbon Monoxide Encephalopathy in the Primate: I. Physiologic and Metabolic Aspects Arch Neurol, March 1, 1974; 30(3): 202 - 208. [Abstract] [PDF]