Cerebral hemodynamics during cerebral ischemia induced by acute hypotension.

The extreme dependence of the brain upon its circulation for substrates essential for the maintenance of its metabolic activity is well recognized. A cessation of the cerebral circulation for only a few minutes, as occurs in cardiac arrest, results in irreversible brain damage. The brain, for the most part, is an aerobic organ and its large oxygen demands probably account for its unusual susceptibility to circulatory disturbances. The oxygen consumed by the normal adult brain (3.5 cc. per 100 Gm. per min.) is extracted from approximately 800 cc. of blood passing through it each minute. The minimum blood flow requirements of the brain, i.e., the rate at which signs of cerebral ischemia become manifest, have not been accurately determined. Previous efforts to estimate the critical rate have been made both in animals (1) and in man (2) but the procedures utilized for the determination of cerebral blood flow were not sufficiently quantitative to warrant definite conclusions. In order to study this problem, cerebral hemodynamic and metabolic changes were determined before and during acute reductions in arterial pressure induced by drug administration and/or postural adjustments.

[1]  A. Bessman,et al.  Cerebral hemodynamics in cerebral arteriosclerosis. , 1953, Journal of gerontology.

[2]  J. Fazekas,et al.  Apparatus for continuous blood-pressure observation. , 1953, The New England journal of medicine.

[3]  A. Bessman,et al.  Effect of acute hypotension on cerebral hemodynamics and metabolism of elderly patients. , 1952, A.M.A. archives of internal medicine.

[4]  S. Kety,et al.  The effects of an acute reduction in blood pressure by means of differential spinal sympathetic block on the cerebral circulation of hypertensive patients. , 1950, The Journal of clinical investigation.

[5]  J. Moyer,et al.  The effects of dihydroergocornine on the cerebral circulation of patients with essential hypertension. , 1950, The Journal of clinical investigation.

[6]  S. Kety,et al.  THE EFFECT OF BILATERAL STELLATE GANGLION BLOCK ON THE CEREBRAL CIRCULATION IN NORMOTENSIVE AND HYPERTENSIVE PATIENTS. , 1949, The Journal of clinical investigation.

[7]  S. Kety,et al.  THE NITROUS OXIDE METHOD FOR THE QUANTITATIVE DETERMINATION OF CEREBRAL BLOOD FLOW IN MAN: THEORY, PROCEDURE AND NORMAL VALUES. , 1948, The Journal of clinical investigation.

[8]  S. Kety,et al.  The blood flow, vascular resistance, and oxygen consumption of the brain in essential hypertension. , 1948, The Journal of clinical investigation.

[9]  S. Kety,et al.  Cerebral blood flow and metabolism in schizophrenia; the effects of barbiturate semi-narcosis, insulin coma and electroshock. , 1948, The American journal of psychiatry.

[10]  M. Fog CEREBRAL CIRCULATION: THE REACTION OF THE PIAL ARTERIES TO A FALL IN BLOOD PRESSURE , 1937 .

[11]  F. Gibbs,et al.  RELATIONSHIP OF UNCONSCIOUSNESS TO CEREBRAL BLOOD FLOW AND TO ANOXEMIA , 1935 .

[12]  C. F. Adams Quantitative Clinical Chemistry , 1932 .

[13]  P. Scheinberg,et al.  THE CEREBRAL BLOOD FLOW IN MALE SUBJECTS AS MEASURED BY THE NITROUS OXIDE TECHNIQUE. NORMAL VALUES FOR BLOOD FLOW, OXYGEN UTILIZATION, GLUCOSE UTILIZATION, AND PERIPHERAL RESISTANCE, WITH OBSERVATIONS ON THE EFFECT OF TILTING AND ANXIETY. , 1949, The Journal of clinical investigation.