June 1973
Volume 12, Issue 6
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Articles  |   June 1973
The Effect of Arterial PCOCO2 On Inner-Retinal Oxygen Consumption Rate in Monkeys
Author Affiliations
  • MARCOS TSACOPOULOS
    Departments of Ophthalmology, Neurology, and Pediatrics, University of Miami School of Medicine, and the Neurology Service, Veterans Administration Hospital, Miami, Fla.; Clinique Universitaire d'Ophthalmologie, Hò‚pital Cantonal, Geneva, Switzerland
  • REX BAKER
    Departments of Ophthalmology, Neurology, and Pediatrics, University of Miami School of Medicine, and the Neurology Service, Veterans Administration Hospital, Miami, Fla.
  • NOBLE J. DAVID
    Departments of Ophthalmology, Neurology, and Pediatrics, University of Miami School of Medicine, and the Neurology Service, Veterans Administration Hospital, Miami, Fla.
  • JOSE STRAUSS
    Departments of Ophthalmology, Neurology, and Pediatrics, University of Miami School of Medicine, and the Neurology Service, Veterans Administration Hospital, Miami, Fla.
Investigative Ophthalmology & Visual Science June 1973, Vol.12, 456-460. doi:
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      MARCOS TSACOPOULOS, REX BAKER, NOBLE J. DAVID, JOSE STRAUSS; The Effect of Arterial PCOCO2 On Inner-Retinal Oxygen Consumption Rate in Monkeys. Invest. Ophthalmol. Vis. Sci. 1973;12(6):456-460.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Inner-retinal oxygen consumption rate (VOO2) varies with Pacoco2 in monkeys. When Pacoco2 increases, inner-retinal (VOO2 increases, until Pacoco2 reaches approximately 70 mm. Hg. Above this level VOO2 is depressed but never returns to the VOO2 of normocapnia. The most likely explanation for this phenomenon is that the intracellular increase in HCO3- accelerates the citric acid cycle turnover. In hypocapnia, inner-retinal VOO2 is lower than under normocapnia. The most likely explanation for this phenomenon is the accompanying reduction in intracellular POO2

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