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Article
August 1967

The Physiologic Response to Therapy in Experimental Cerebral Ischemia

Author Affiliations

Seattle
From the Department of Surgery and Neurosurgery, Veterans Administration Hospital, and University of Washington School of Medicine, Seattle. Dr. Brawley's present address is Department of Surgery, Division of Neurosurgery, University of Florida College of Medicine, Gainesville, Fla. Dr. Strandness is on the Career Development Award Program 1-K3-HE-9583, National Institute of Health.

Arch Neurol. 1967;17(2):180-187. doi:10.1001/archneur.1967.00470260070008
Abstract

The BENEFICIAL effect of therapy in the acute stage of cerebral infarction is difficult to demonstrate conclusively either experimentally or clinically. In addition to general supportive measures, six general methods of protecting against ischemia have been advocated: (1) increasing central arterial pressure by the use of vasopressors,1,2 (2) decreasing viscosity of the blood by the use of low molecular weight dextran and anticoagulants,3-5 (3) reduction in peripheral resistance in the cerebrovascular bed by the use of 5% carbon dioxide inhalation,6,7 (4) hyperoxygenation of the blood using a hyperbaric chamber,8 (5) reduction of cerebral metabolism by the use of hypothermia and anesthetic agents,9,10 and (6) the use of agents to protect against the postnecrotic edema.5 The first three methods should produce an increase in blood flow through the brain, and this present study was designed to test the effects of these three approaches on blood

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