{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,20]],"date-time":"2026-04-20T17:00:50Z","timestamp":1776704450488,"version":"3.51.2"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":10166,"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":[[1987,11]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Brain edema is a major complication of fulminant hepatic failure and is responsible for death in a large percentage of patients. We previously demonstrated the progressive accumulation of water in grey matter areas of the brain in the rabbit with galactosamine-induced fulminant hepatic failure. We now report the electron microscopic morphology of the brain in the same model of acute hepatic failure following the intravenous injection of horseradish peroxidase, an intravascular tracer which forms an electron-dense reaction product. Rabbits with both mild and severe encephalopathy had normal blood pressures and blood gases at the time of study. Fixation of brain tissue was obtained by whole-body perfusion. Marked swelling of the cytoplasm, perineuronal and perivascular processes of astrocytes were noted in cortical gray, but not white, matter areas; the other cellular components of the brain had normal morphology. Capillary endothelial cells were normal, and there was no evidence of horseradish peroxidase in endothelial cell vesicles, basement membranes or the brain parenchyma, suggesting that the blood-brain barrier was impermeable to large molecules. Histologic evidence of brain edema is seen in this model, with swelling of astrocytes as the primary manifestation of the accumulation of water. Damage to astrocytes or inhibition of their function may contribute to the pathogenesis of hepatic encephalopathy in this model.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.1840070616","type":"journal-article","created":{"date-parts":[[2007,3,3]],"date-time":"2007-03-03T21:13:23Z","timestamp":1172956403000},"page":"1272-1277","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":129,"title":["Electron microscopic evaluation of brain edema in rabbits with galactosamine-induced fulminant hepatic failure: Ultrastructure and integrity of the blood-brain barrier"],"prefix":"10.1097","volume":"7","author":[{"given":"Peter G.","family":"Traber","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mauro","family":"Dal Canto","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel R.","family":"Ganger","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andres T.","family":"Blei","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"10.1002\/hep.1840070616-BIB1","first-page":"415","volume-title":"Hepatology","author":"Jones","year":"1981","unstructured":". Fulminant hepatic failure. In: , eds. Hepatology. Philadelphia, Pennsylvania: W. B. Saunders, 1981: 415\u2013445."},{"key":"10.1002\/hep.1840070616-BIB2","first-page":"615","volume":"64","author":"Gazzard","year":"1975","journal-title":"Q J Med"},{"key":"10.1002\/hep.1840070616-BIB3","doi-asserted-by":"crossref","first-page":"1347","DOI":"10.1016\/0016-5085(86)90186-1","volume":"91","author":"Traber","year":"1986","journal-title":"Gastroenterology"},{"key":"10.1002\/hep.1840070616-BIB4","first-page":"55","volume-title":"Advances in neurology, Vol. 28. Brain edema","author":"Westergaard","year":"1980","unstructured":"Ultrastructural permeability properties of cerebral microvasculature under normal and experimental conditions after application of tracers. In: , eds. Advances in neurology, Vol. 28. Brain edema. New York: Raven Press, 1980: 55\u201374."},{"key":"10.1002\/hep.1840070616-BIB5","doi-asserted-by":"crossref","first-page":"664","DOI":"10.1016\/0016-5085(78)90241-X","volume":"74","author":"Blitzer","year":"1978","journal-title":"Gastroenterology"},{"key":"10.1002\/hep.1840070616-BIB6","doi-asserted-by":"crossref","first-page":"540","DOI":"10.1016\/S0016-5085(84)80025-6","volume":"86","author":"Schafer","year":"1984","journal-title":"Gastroenterology"},{"key":"10.1002\/hep.1840070616-BIB7","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1007\/978-1-4684-4616-6_1","volume-title":"Recent progress in the study of brain edema","author":"Klatzo","year":"1984","unstructured":", , et al. Pathogenesis of ischemic brain edema. In: , eds. Recent progress in the study of brain edema. New York: Plenum Press, 1984: 1\u201310."},{"key":"10.1002\/hep.1840070616-BIB8","first-page":"207","volume-title":"Advances in neurology, Vol. 28. Brain edema","author":"Fishman","year":"1980","unstructured":". Metabolic basis of brain edema. In: , eds. Advances in neurology, Vol. 28. Brain edema. New York: Raven Press, 1980: 207\u2013215."},{"key":"10.1002\/hep.1840070616-BIB9","first-page":"83","volume-title":"Advances in Neurology, Vol. 28. Brain edema","author":"Hirano","year":"1980","unstructured":"Fine structure of edematous encephalopathy. In: , eds. Advances in Neurology, Vol. 28. Brain edema. New York: Raven Press, 1980: 83\u201397."},{"key":"10.1002\/hep.1840070616-BIB10","doi-asserted-by":"crossref","first-page":"756","DOI":"10.1177\/27.3.39099","volume":"27","author":"Norenberg","year":"1979","journal-title":"J Histochem Cytochem"},{"key":"10.1002\/hep.1840070616-BIB11","first-page":"303","volume-title":"Advances in cellular neurobiology","author":"Norenberg","year":"1981","unstructured":"The astrocyte in liver disease. In: , eds. Advances in cellular neurobiology. 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