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October 1973

Graded Hypoxia-Oligemia in Rat Brain: I. Biochemical Alterations and Their Implications

Author Affiliations

Lund, Sweden; New York; Lund
From the Brain Research Laboratory, University of Lund, Lund, Sweden (Drs. Salford and Siesjö), and the Department of Neurology, New York Hospital-Cornell Medical Center, New York (Dr. Plum).

Arch Neurol. 1973;29(4):227-233. doi:10.1001/archneur.1973.00490280039005

Brain metabolism was studied in normotensive rats after unilateral carotid artery clamping combined with graded hypoxemia. Clamping plus lowering the arterial oxygen tension (Pao2) to 28 mm Hg for 30 minutes caused a rise in lactate and a moderate change in energy state in the ipsilateral hemisphere. After Pao221 mm Hg for 30 minutes, the ipsilateral hemisphere showed a more pronounced acidosis and energy change, but no decline in glucose substrate. These biochemical changes were interpreted as reflecting profound anoxemia rather than ischemia. Thirty minutes after reoxygenation and release of carotid clamp, both hemispheres of Pao2 28 animals were normal, but the clamped side of Pao2 21 animals still showed an abnormal energy state and lactic acidosis. At least in this model, hypoxemia alone is sufficient to cause irreversible damage to brain tissue.

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