Abstract

Previous studies on the effect of changes in blood osmolality on the cerebral vasculature have been made by observing the pial or cortical vessels, or by indirect methods of estimating flow. In these studies the hyperosmotic solutions were injected intravenously or intraperitoneally; the results obtained were at variance though a dilator effect followed by delayed constriction seemed to be the most frequent response reported [5, 8]. Interpretations of the mechanisms of the hyperosmotic response were also at variance; most workers considered the hyperosmolar response as secondary to cerebrospinal fluid or arterial blood pressure changes. Intravenous infusions of hyperosmolar solutions have been used in the treatment of increased cerebrospinal pressure [3], and induced hyperosmolality has been reported to reduce the histological damage resulting from a period of cerebral ischemia [2]. Until recently, the osmolality of the immediate environment surrounding vascular smooth muscle has not been considered as a variable likely to regulate the “tone” of blood vessels. Mellander [6], and Johansson [4] have postulated, respectively, that hyperosmolality may play a role in exercise hyperemia of skeletal muscle and in the electrical and mechanical events of vascular smooth muscle in vitro. We have been studying the effects of hyperosmolar solutions [1] by means of a direct method to measure cerebral venous blood flow in the dog [7]. The confluence of the cerebral sinuses was cannulated and, with the lateral sinuses occluded, the cerebral venous outflow was passed through an electromagnetic flowmeter. Brain perfusion pressure was taken as the mean between common carotid and wedged vertebral artery pressures. Cerebral venous outflow osmolality and hematocrit were measured during induced changes of blood osmolality produced by rapid intracarotid injection of hyperosmolar solutions in volumes not producing marked changes in mean arterial pressure or systemic blood osmolality.

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