EFFECT OF PROGRESSIVE SYMPATHECTOMY ON HYPERTENSION PRODUCED BY INCREASED INTRACRANIAL PRESSURE

Abstract

The effect of progressive sympathectomy upon the rise in blood pressure induced by increased intracranial pressure was studied in dogs under pcntobarbital anesthesia. Bilateral lower thoracic sympathectomy (T10 [long dash]L1) including splanch-nicectomy did not prevent the development of hypertension from increased intracranial pressure. Complete cardiac de-nervation (Stellate [long dash]T 6, and vagus fibers) did not interfere with the full development of the pressor response. The increase in blood pressure from cerebral compression was prevented by bilateral upper (Stellate [long dash]T 5) and lower (T 10 [long dash]L 1) thoracic sympathectomy. It was also abolished by total sympathectomy. Evidence indicates that the lower thoracic sympathetic impulses facilitate the development of the hypertensive reaction through the medium of adrenal secretion which acts upon the heart. A rise in blood pressure from cerebral compression can be obtained in a dog with sympathetic cardiac derivation, only if medulli-adrenal secretion is present. Extensive sympathectomy which leaves intact only the upper thoracic sympathetic ganglia (Stellate [long dash]T 4) on one side, does not prevent the development of a rise in blood pressure under the exptl. conditions. The hypertensive reaction is evidently dependent upon the activity of the cardiac rather than upon the pulmonary sympathetics. Sympathetic cardiac innervation, neural or humoral, is necessary for the development in anesthetized dogs of the rise in blood pressure produced by increased intracranial pressure.