High Colloid Oncotic Therapy for Contusional Brain Edema

Tomita, Hiroki; Ito, Umeo; Tone, Osamu; Masaoka, Hiroyuki; Tominaga, Ben

doi:10.1007/978-3-7091-9334-1_151

Cited by 27 publications

(29 citation statements)

References 6 publications

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“…In another study, 25% Alb was administered in moderate to high doses over a 2-week period to elevate plasma oncotic pressure in patients with brain contusion; this therapy safely and effectively reduced contusional edema. 51 Similarly, patients with putaminal hemorrhage treated with 12.5 to 25 g per day of Alb for 2 weeks showed reductions of cerebral edema and improved outcome. 52 In another study, patients with cirrhosis and spontaneous bacterial peritonitis were treated with intravenous Alb at an initial dose of 1.5 g/kg, followed by 1 g/kg on day 3; this treatment was tolerated and led to reduced renal impairment and lowered mortality rates.…”

Section: Clinical Applicationsmentioning

confidence: 91%

Human Albumin Therapy of Acute Ischemic Stroke

Belayev

Liu

Zhao

et al. 2001

Stroke

279

138

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Background and Purpose-We examined the neuroprotective efficacy of moderate-dose human albumin therapy in acute focal ischemic stroke and defined the therapeutic window after stroke onset, within which this therapy would confer neurobehavioral and histopathological neuroprotection. Methods-Sprague-Dawley rats were anesthetized with halothane/nitrous oxide and received 2-hour middle cerebral artery occlusion (MCAo) by a poly-L-lysine-coated intraluminal suture. Neurological status was evaluated during occlusion (60 minutes) and daily for 3 days after MCAo. In the dose-response study, human albumin doses of either of 0.63 or 1.25 g/kg or saline vehicle (5 mL/kg) were given intravenously immediately after suture removal. In the therapeutic window study, a human albumin dose of 1.25 g/kg was administered intravenously at 2 hours, 3 hours, 4 hours, or 5 hours after onset of MCAo. Three days after MCAo, brains were perfusion-fixed, and infarct volumes and brain swelling were determined. Results-Moderate-dose albumin therapy significantly improved the neurological score at 24 hours, 48 hours, and 72 hours and significantly reduced total infarct volume (by 67% and 58%, respectively, at the 1.25-and 0.63-g/kg doses). Cortical and striatal infarct volumes were also significantly reduced by both doses. Brain swelling was virtually eliminated by albumin treatment. Even when albumin therapy (1.25 g/kg) was initiated as late as 4 hours after onset of MCAo, it improved the neurological score and markedly reduced infarct volumes in cortex (by 68%), subcortical regions (by 52%), and total infarct (by 61%). Conclusions-Moderate-dose albumin therapy markedly improves neurological function and reduces infarction volume and brain swelling, even when treatment is delayed up to 4 hours after onset of ischemia. (Stroke. 2001;32:553-560.)

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Section: Clinical Applicationsmentioning

confidence: 91%

Human Albumin Therapy of Acute Ischemic Stroke

Belayev

Liu

Zhao

et al. 2001

Stroke

279

138

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“…Albumin is also a major antioxidant defense against oxidizing agents generated by either endogenous processes or exogenous agents (Halliwell, 1988). Albumin treatment may improve outcome after experimental and clinical TBI (Belayev et al, 1999;Tomita et al, 1994).After TBI, increased formation of RSNO could be anticipated because of increased production of NO by NOS isoforms and increased formation of peroxynitrite. We reported increased iNOS expression within first 2 days in experimental TBI in rats (Clark et al, 1996b).…”

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confidence: 99%

Increased S-Nitrosothiols and S-Nitrosoalbumin in Cerebrospinal Fluid after Severe Traumatic Brain Injury in Infants and Children: Indirect Association with Intracranial Pressure

Bayır

Kochanek

Liu

et al. 2003

J Cereb Blood Flow Metab

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Summary: Nitric oxide (NO) is implicated in both secondary damage and recovery after traumatic brain injury (TBI). Transfer of NO groups to cysteine sulfhydryls on proteins produces S-nitrosothiols (RSNO). S-nitrosothiols may be neuroprotective after TBI by nitrosylation of N-methyl-D-aspartate receptor and caspases. S-nitrosothiols release NO on decomposition for which endogenous reductants (i.e., ascorbate) are essential, and ascorbate is depleted in cerebrospinal fluid (CSF) after pediatric TBI. This study examined the presence and decomposition of RSNO in CSF and the association between CSF RSNO level and physiologic parameters after severe TBI. Cerebrospinal fluid samples (n ‫ס‬ 72) were obtained from 18 infants and children on days 1 to 3 after severe TBI (Glasgow Coma Scale score < 8) and 18 controls. Cerebrospinal fluid RSNO levels assessed by fluorometric assay peaked on day 3 versus control (1.42 ± 0.11 mol/L vs. 0.86 ± 0.04, P < 0.05). Snitrosoalbumin levels were also higher after TBI (n ‫ס‬ 8, 0.99 ± 0.09 mol/L on day 3 vs. n ‫ס‬ 6, 0.42 ± 0.02 in controls, P < 0.05). S-nitrosoalbumin decomposition was decreased after TBI. Multivariate analysis showed an inverse relation between CSF RSNO and intracranial pressure and a direct relation with barbiturate treatment. Using a novel assay, the presence of RSNO and S-nitrosoalbumin in human CSF, an ∼1.7-fold increase after TBI, and an association with low intracranial pressure are reported, supporting a possible neuroprotective role for RSNO. The increase in RSNO may result from increased NO production and/or decreased RSNO decomposition. Key Words: Nitric oxide-Nitrosative stress-Oxidative stressHead injury-Ascorbate-DAF-2.Although the primary event in traumatic brain injury (TBI) is direct disruption of brain parenchyma, a significant amount of damage results from a secondary cascade of biochemical, cellular, and molecular events (Kochanek et al., 2000). Secondary insults contribute to evolution of damage, protection, and repair, thus providing a variety of therapeutic targets.Nitric oxide (NO) is implicated in both injury (Dawson et al., 1994) and neurologic recovery (Holscher, 1997) after brain injury. The location, timing, and amount of NO production may determine its role, as well as the type of injury sustained (Iadocola et al., 1995;Lipton et al., 1993). Nitric oxide is synthesized by at least three known isoforms of NO synthase (NOS). Nitric oxide produced by endothelial NOS (eNOS) provides benefit in models of TBI (DeWitt et al., 1997). Nitric oxide produced by neuronal NOS (nNOS) contributes to neuronal damage after ischemic or excitotoxic insults (Huang et al., 1994;Schulz et al., 1995). Nitric oxide derived from inducible NOS (iNOS) may contribute to either secondary damage (Wada et al., 1998a) or recovery (Sinz et al., 1999) plasma, erythrocytes, platelets, and leukocytes, and in rat cerebellum (Stamler et al., 1992;Kluge et al., 1997;Gaston, 1999;Kelm, 1999;Gladwin et al., 2000). Steadystate concentrations of RSNO are tissue specific and depe...

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“…Several studies have indicated beneficial effects of albumin to head injury (Tomita et al, 1994;Belayev et al;1999;Bernard et al, 2008), and the post hoc SAFE-TBI study is the only study so far showing adverse effects. Its original database, however, was not designed to meet any specific set of TBI-related criteria and there was an unclear subgroup selection of TBI patients.…”

Section: Wahlström Et Al 2009)mentioning

confidence: 99%