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A Review

Edwin G. Fischer, MD

Arch Neurol. 1973;29(6):361-366.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The possibility that a vascular phenomenon might contribute to the brain's inability to survive ischemia for more than several minutes was initially suggested by observations such as those of Ames and Gurian¹ and Neely and Youmans.² The former noted that isolated rabbit retina and optic nerve recovered nearly normal electrical activity following a 20-minute deprivation of oxygen and glucose at 37 C. The latter group demonstrated recovery of dogs from periods of up to 25 minutes of total cerebral ischemia, when produced by intrathecal infusion of saline to a pressure of 400 mm Hg resulting in exsanguination of the brain.

This report summarizes the pertinent work done by the group based mostly at the Massachusetts General Hospital, demonstrating and characterizing an impairment of cerebrovascular perfusion, which begins within the first five to ten minutes of total cerebral circulatory arrest. In addition, it discusses the mechanisms that have thus . . . [Full Text PDF of this Article]

Author Affiliations
Boston

From the departments of neurosurgery, Children's Hospital Medical Center and Massachusetts General Hospital; and the departments of surgery (Neurosurgery), Peter Bent Brigham Hospital and Harvard Medical School, Boston.

Footnotes
Read before the symposium held at New York Hospital—Cornell Medical Center: The Threshold and Mechanisms of Anoxic-Ischemic Brain Injury, New York, June 10,1973.

Reprint requests to Department of Neurosurgery, Children's Hospital Medical Center, Boston 02115 (Dr. Fischer).

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