{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T15:26:18Z","timestamp":1791559578949,"version":"4.3.4"},"reference-count":71,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,3]]},"abstract":"<jats:p content-type=\"fine-print\"><jats:italic>Object.<\/jats:italic> The authors have recently demonstrated that high-dose human albumin is markedly neuroprotective in experimental traumatic brain injury (TBI) and cerebral ischemia. The pathophysiology of TBI involves acute uncoupling of cerebral glucose utilization and blood flow. The intent of this study was to establish whether the use of human albumin therapy in a model of acute TBI would influence this phenomenon.<\/jats:p>\n<jats:p content-type=\"fine-print\"><jats:italic>Methods.<\/jats:italic> Anesthetized, physiologically regulated rats received moderate (1.5\u20132 atm) fluid-percussion injury to the parietal lobe. Fifteen minutes after trauma or sham injury, rats in one group received human albumin (2.5 g\/kg) administered intravenously and those in another group received 0.9% saline vehicle. At 60 minutes and 24 hours posttrauma, autoradiographic studies of local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCMRglu) were conducted, and the LCMRglu\/LCBF ratio was determined. Sham-injured rats had normal levels of LCBF and LCMRglu, and no differences between vehicle- and albumin-treated rats were evident. Sixty minutes after TBI, LCBF was moderately reduced bilaterally in vehicle-treated rats, whereas in albumin-treated animals, the LCBF contralateral to the side of injury was generally normal. Despite acutely depressed LCBF, LCMRglu in vehicle-treated rats at 60 minutes was paradoxically normal bilaterally, and foci of elevated LCMRglu were noted in the ipsilateral hippocampus and thalamus. By contrast, in albumin-treated rats studied 60 minutes post-TBI, reduced LCMRglu values were measured in the ipsilateral caudoputamen and parietal cortex, whereas LCMRglu in other ipsilateral and contralateral sites did not differ from that measured in sham-injured animals. The metabolism\/blood flow ratio was normal in sham-injured rats, but became markedly elevated in vehicle-treated rats 60 minutes post-TBI (on average, by threefold ipsilaterally and 2.1-fold contralaterally). By contrast, the mean metabolism\/blood flow ratio in albumin-treated animals was elevated by only 1.6-fold ipsilaterally and was normal contralaterally. Twenty-four hours after TBI, LCBF contralateral to the side of injury had generally returned to normal levels in the albumin-treated group.<\/jats:p>\n<jats:p content-type=\"fine-print\"><jats:italic>Conclusions.<\/jats:italic> These results demonstrate that human albumin therapy benefits the posttraumatic brain by diminishing the pronounced metabolism &gt; blood flow dissociation that would otherwise occur within the 1st hour after injury. Viewed together with our previous evidence of histological neuroprotection, these findings indicate that human albumin therapy may represent a desirable treatment modality for acute TBI.<\/jats:p>","DOI":"10.3171\/jns.2001.94.3.0499","type":"journal-article","created":{"date-parts":[[2009,5,13]],"date-time":"2009-05-13T17:42:13Z","timestamp":1242236533000},"page":"499-509","source":"Crossref","is-referenced-by-count":39,"title":["Diminution of metabolism\/blood flow uncoupling following traumatic brain injury in rats in response to high-dose human albumin treatment"],"prefix":"10.3171","volume":"94","author":[{"given":"Myron D.","family":"Ginsberg","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weizhao","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ludmila","family":"Belayev","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ofelia F.","family":"Alonso","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yitao","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judith Y.","family":"Loor","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raul","family":"Busto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"key":"b1","series-title":"J Cereb Blood Flow Metab","doi-asserted-by":"publisher","first-page":"202","DOI":"10.1097\/00004647-199603000-00004","article-title":"Induction of spreading depression in the ischemic hemisphere following experimental middle cerebral artery occlusion: effect on infarct morphology.","volume":"16","author":"Back","year":"1996"},{"key":"b2","series-title":"Neurol Res","doi-asserted-by":"publisher","first-page":"643","DOI":"10.1080\/01616412.1998.11740577","article-title":"Ritanserin, a 5-HT2 receptor antagonist, increases subcortical blood flow following photothrombotic occlusion in rats.","volume":"20","author":"Back","year":"1998"},{"key":"b3","series-title":"J Cereb Blood Flow Metab","doi-asserted-by":"publisher","first-page":"566","DOI":"10.1038\/jcbfm.1995.70","article-title":"Three-dimensional image analysis of brain glucose metabolism-blood flow uncoupling and its electrophysiological correlates in the acute ischemic penumbra following middle cerebral artery occlusion.","volume":"15","author":"Back","year":"1995"},{"key":"b4","series-title":"J Neurotrauma","doi-asserted-by":"publisher","first-page":"791","DOI":"10.1089\/neu.1995.12.791","article-title":"Mediators of injury in neurotrauma: intracellular signal transduction and gene expression.","volume":"12","author":"Bazan","year":"1995"},{"key":"b5","series-title":"J Neurotrauma","doi-asserted-by":"publisher","first-page":"445","DOI":"10.1089\/neu.1999.16.445","article-title":"Posttreatment with high-dose albumin reduces histopathological damage and improves neurological deficit following fluid percussion brain injury in rats.","volume":"16","author":"Belayev","year":"1999"},{"key":"b6","series-title":"J Neurosurg","doi-asserted-by":"publisher","first-page":"595","DOI":"10.3171\/jns.1997.87.4.0595","article-title":"Effect of delayed albumin hemodilution on infarction volume and brain edema after transient middle cerebral artery occlusion in rats.","volume":"87","author":"Belayev","year":"1997"},{"key":"b7","series-title":"Brain Res","doi-asserted-by":"publisher","first-page":"107","DOI":"10.1016\/S0006-8993(99)01952-6","article-title":"Neuroprotective effect of high-dose albumin therapy against global ischemic brain injury in rats.","volume":"845","author":"Belayev","year":"1999"},{"key":"b8","series-title":"J Cereb Blood Flow Metab","doi-asserted-by":"publisher","first-page":"1266","DOI":"10.1097\/00004647-199712000-00002","article-title":"Transient middle cerebral artery occlusion by intraluminal suture: I. 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