Summary: A new experimental model was employed to investigate alterations of cerebral metabolic activity in rats subjected to extensive subarachnoid hemorrhage (SAH). The hemorrhages were produced in anesthetized animals by inserting 0.37 ml fresh autologous arterial blood into the subarachnoid space. Rats that underwent sham operations received subarachnoid injections of mock CSF to study the effects of sudden raised intra cranial pressure (lCP). Forty-eight hours after subarach noid injection, the unanesthetized rats were given intra venous injections of [14Cl2-deoxyglucose. Experiments were terminated 45 min later by decapitation, and the brains were removed and frozen. Regional brain meta bolic activity was studied employing quantitative autora diography. In comparison with control animals, cerebral (Ferguson et aI., 1972; Granowska et aI., 1980; Grubb et aI., 1977; Hashi et aI., 1972;Ishii, 1979;James, 1968; Kamiya et aI., 1983; Knuckey et aI., 1985; Meyer et aI., 1983; Mickey et aI., 1984; Montgomery et aI., 1981; Petruk et aI., 1972; Sol omon et aI., 1985; Umansky et aI., 1983; Voldby et Received July 25, 1986; accepted October 7, 1986. Address correspondence and reprint requests to Dr. R. A. Sol omon at The Neurological Institute of New York, 710 West 168th Street, New York, NY 10032, U.S.A.Abbreviations used: EM, electron microscopic; ICP, intra cranial pressure; SAH, subarachnoid hemorrhage. 193metabolic activity was diffusely decreased following SAH. Statistically significant decreases in metabolic ac tivity of <34% were observed in 17 of 30 brain regions studied. The largest percentage reductions were in re gions displaying the highest basal metabolic rates. Sub arachnoid injections of mock CSF also produced depres sion of cerebral metabolic activity, but quantitatively these changes were not as pronounced as in the hemor rhage group. These studies demonstrate regional changes in brain function following SAH. The data relate these changes to both the presence of blood in the subarach noid space and sudden raised ICP. In an effort to define the underlying pathophysi ology of the circulatory and metabolic defects en countered following SAH, a new rat model of this clinical condition has been created (Solomon et aI., 1985). Initial studies of this model have demon-