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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. MATERIALS AND METHODForty-four patients were studied. The subjects in whom hypotension was drug-induced were separated into the following four groups so that the influence of age and hypertension on the susceptibility of the brain to cerebral ischemia could be determined: Group 1, seven normotensive subjects under 50 years of age; Group 2, ten normotensive subjects over 60 years of age; Group 3, eight patients with essential hypertension; and Group 4, seven patients with malignant hypertension. In seven subjects, the mean arterial pressure was reduced significantly below normal but not to the extent of inducing signs of cerebral ischemia. Five patients with spontaneous postural hypotension were also studied.Control studies were obtained after the subject had been tilted (head up) 30 to 40 degrees for a period of at least 30 minutes. The subjects in the drug-induced hypotension group were then given a 1 per cent solution of hexamethonium 2 intravenously at a rate of 1 mg. of the ion per minute and carefully observed for signs of cerebral ischemia. In the subjects with spontaneous postural hypotension, control studies were done in the horizontal position, and the subjects were then tilted 30 degrees head up, and the experimental flow was done when they developed signs of cerebral ischemia.The manifestations of cerebral circulatory insufficiency were Father stereotyped and easily recognized. Sighing, yawning, staring, and confusion, i.e., the inability to follow simple commands, were the first indications of cerebral ischemia. When any of these signs appeared, the hexamethonium injection was promptly discontinued, and the second, or experimental flow was begun. A fairly steady state was maintained during the first few minutes making postural adjustments unnecessary. If during the experimental flow, the patient became either unresponsive or too al...

Carbonic anhydrase inhibitors have been used in clinical medicine as diuretics,1-3 as anticonvulsants,4,5 to reduce intraocular tension,6,7 to lower intracranial pressure,8,9 and in the treatment of respiratory insufficiency.10,11 In the course of investigation of the effects of acetazolamide in hepatic encephalopathy, Posner and Plum 12 observed without comment a considerable increase in rate of cerebral blood flow after intravenous administration of 1 to 2 gm. of acetazolamide. Such a cerebral circulatory change had previously been considered to account for the brief elevation of cerebrospinal fluid pressure after intravenous acetazolamide.9,13In view of these findings, we felt that the usefulness of carbonic anhydrase inhibitors might be extended to the management of patients with intermittent cerebral vascular insufficiency. In this preliminary report, observations of the quantitative cerebral hemodynamic effects of intravenous acetazolamide are presented. In several subjects, the effects of inhalation of 5% CO2 were also noted for comparative purposes. MethodThe subjects of this investigation were 10 pa¬ tients hospitalized for clinical study of cerebral vascular disease believed to be the cause of cir¬ culatory insufficiency of internal carotid or vertebral-basilar artery systems. In all cases, the disorder was manifested by recurrent, transitory neurological dysfunction, considered on clinical grounds to involve the cerebral areas primarily supplied by the arterial systems noted, and assumed to be due to intermittent ischemia of these areas.Cerebral hemodynamic studies were performed before and 30 to 60 minutes after the intravenous administration of 1 gm. of acetazolamide (2 gm. in one instance) over a 10-minute period. In 8 of these patients, the effects of inhalation of S'%

The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.

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The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.