{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:16:21Z","timestamp":1777792581897,"version":"3.51.4"},"reference-count":35,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[1995,9,1]],"date-time":"1995-09-01T00:00:00Z","timestamp":809913600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[1995,9]]},"abstract":"<jats:p>\n                    Acute hyperammonemia causes cerebral edema, elevated intracranial pressure and loss of cerebral blood flow (CBF) responsivity to CO\n                    <jats:sub>2<\/jats:sub>\n                    . Inhibition of glutamine synthetase prevents these abnormalities. If the loss of CO\n                    <jats:sub>2<\/jats:sub>\n                    responsivity is secondary to the mechanical effects of edema, one would anticipate loss of responsivity to other physiological stimuli, such as hypoxia and changes in mean arterial blood pressure (MABP). To test this possibility, pentobarbital-anesthetized rats were subjected to either hypoxic hypoxia (P\n                    <jats:sub>a<\/jats:sub>\n                    o\n                    <jats:sub>2<\/jats:sub>\n                    \u2248 30 mm Hg), hemorrhagic hypotension (MABP \u224870 and 50 mm Hg), or phenylephrine-induced hypertension (MABP \u2248 125 and 145 mm Hg). CBF was measured with radiolabeled microspheres. Experimental groups received intravenous ammonium acetate (\u224850 \u03bcmol min\n                    <jats:sup>\u22121<\/jats:sup>\n                    kg\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) for 6 h to increase plasma ammonia to 500\u2013600 \u03bcM. Control groups received sodium acetate plus HCl to prevent metabolic alkalosis. The increase in CBF during 10 min of hypoxia after 6 h of ammonium acetate infusion (84 \u00b1 19 to 259 \u00b1 52 ml min\n                    <jats:sup>\u22121<\/jats:sup>\n                    100 g\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) was similar to that after sodium acetate infusion (105 \u00b1 20 to 265 \u00b1 76 ml min\n                    <jats:sup>\u22121<\/jats:sup>\n                    100 g\n                    <jats:sup>\u22121<\/jats:sup>\n                    ). Cortical glutamine concentration was elevated equivalently in hyperammonemic rats subjected to normoxia only or to 10 min of hypoxia. With severe hypotension, CBF was unchanged in both the ammonium (80 \u00b1 20 to 76 \u00b1 24 ml min\n                    <jats:sup>\u22121<\/jats:sup>\n                    100 g\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) and the sodium (80 \u00b1 14 to 73 \u00b1 16 ml min\n                    <jats:sup>\u22121<\/jats:sup>\n                    100 g\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) acetate groups. With moderate hypertension, CBF was unchanged. With the most severe hypertension, significant increases in CBF occurred in both groups, but there was no difference between groups. We conclude that hypoxic and autoregulatory responses are intact during acute hyperammonemia. The previously observed loss of CO\n                    <jats:sub>2<\/jats:sub>\n                    responsivity is not the result of a generalized vasoparalysis to all physiological stimuli.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.1995.104","type":"journal-article","created":{"date-parts":[[2011,4,8]],"date-time":"2011-04-08T13:21:16Z","timestamp":1302268876000},"page":"835-844","source":"Crossref","is-referenced-by-count":14,"title":["Preservation of Cerebral Blood Flow Responses to Hypoxia and Arterial Pressure Alterations in Hyperammonemic Rats"],"prefix":"10.1177","volume":"15","author":[{"given":"Takahiko","family":"Hirata","sequence":"first","affiliation":[{"name":"Department of AnesthesiologylCritical Care Medicine and Pediatrics, The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Raymond C.","family":"Koehler","sequence":"additional","affiliation":[{"name":"Department of AnesthesiologylCritical Care Medicine and Pediatrics, The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Saul W.","family":"Brusilow","sequence":"additional","affiliation":[{"name":"Department of AnesthesiologylCritical Care Medicine and Pediatrics, The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard J.","family":"Traystman","sequence":"additional","affiliation":[{"name":"Department of AnesthesiologylCritical Care Medicine and Pediatrics, The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[1995,9,1]]},"reference":[{"key":"bibr1-jcbfm.1995.104","first-page":"H500","volume":"248","author":"Barzilay Z","year":"1985","journal-title":"Am J 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