{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T03:09:23Z","timestamp":1780110563775,"version":"3.54.0"},"reference-count":25,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":11445,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1984,5]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Permeability of the blood brain barrier in relation to the development of hepatic encephalopathy was investigated in two animal models of acute hepatic failure, in one of which there was the potential for recovery (D-galactosamine-induced hepatitis). In both this and the hepatic devascularization model, there was an approximate 3-fold increase in the passive permeability of the blood brain barrier to inulin and sucrose. Transport of amino acids was also significantly affected, with approximate 30% increases in the brain uptake of phenylalanine, tyrosine and arginine and a 65% increase in uptake of leucine. These changes are attributed to the action of circulating toxic substances, some of which increase blood brain barrier permeability in normal animals.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.1840040302","type":"journal-article","created":{"date-parts":[[2008,8,22]],"date-time":"2008-08-22T13:28:13Z","timestamp":1219411693000},"page":"359-363","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":76,"title":["Experimental Studies of Blood Brain Barrier Permeability in Acute Hepatic Failure"],"prefix":"10.1097","volume":"4","author":[{"given":"Ahmed E. 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