Effect of steroid on ischemic brain edema. Analysis of cytotoxic and vasogenic edema occurring during ischemia and after restoration of blood flow.

Ito, Umeo; Ohno, Kikuo; Suganuma, Y; Suzuki, Kenichi; Inaba, Yutaka

doi:10.1161/01.str.11.2.166

Cited by 35 publications

(7 citation statements)

References 35 publications

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“…Gerbils without neurologic deficits (during ischemia) had minimal amounts of brain edema and brain H202 levels (after reperfusion); gerbils with mild neurologic deficits (during ischemia) had intermediate levels of brain edema and brain H202 (after reperfusion); and gerbils with severe neurologic deficits (during ischemia) had the greatest brain edema and brain H202 levels (after reperfusion). Gerbils were used for these studies because they commonly lack the posterior communicating artery (incomplete Circle of Willis), and therefore, occlusion of one carotid artery provides a model that is similar to human stroke (33)(34)(35)(36)(37)(38). Although the severity of neurologic deficit in each gerbil was not predictable, large groups of gerbils were always tested and the proportions of gerbils that developed either no, mild, or severe neurologic deficits during carotid occlusion (ischemia) were always similar in each test group.…”

Section: Discussionmentioning

confidence: 99%

Xanthine oxidase-derived hydrogen peroxide contributes to ischemia reperfusion-induced edema in gerbil brains.

Patt¹,

Harken²,

Burton³

et al. 1988

J. Clin. Invest.

205

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The contribution of toxic 02 metabolites to cerebral ischemia reperfusion injury has not been determined. We found that gerbils subjected to temporary unilateral carotid artery occlusion (ischemia) consistently developed neurologic deficits during ischemia with severities that correlated with increasing degrees of brain edema and brain H202 levels after reperfusion. In contrast, gerbils treated just before reperfusion (after ischemia) with dimethylthiourea (DMTU), but not urea, had decreased brain edema and brain H202 levels. In addition, gerbils fed a tungsten-rich diet for 4, 5, or 6 wk developed progressive decreases in brain xanthine oxidase (XO) and brain XO + xanthine dehydrogenase (XD) activities, brain edema, and brain H202 levels after temporary unilateral carotid artery occlusion and reperfusion. In contrast to tungsten-treated gerbils, allopurinol-treated gerbils did not have statistically significant decreases in brain XO or XO + XD levels, and reduced brain edema and brain H202 levels occurred only in gerbils developing mild but not severe neurologic deficits during ischemia. Finally, gerbils treated with DMTU or tungsten all survived, while > 60% of gerbils treated with urea, allopurinol, or saline died by 48 h after temporary unilateral carotid artery occlusion and reperfusion. Our findings indicate that H202 from XO contributes to reperfusion-induced edema in brains subjected to temporary ischemia.

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Section: Discussionmentioning

confidence: 99%

Xanthine oxidase-derived hydrogen peroxide contributes to ischemia reperfusion-induced edema in gerbil brains.

Patt¹,

Harken²,

Burton³

et al. 1988

J. Clin. Invest.

205

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“…The muscle was dried at 60°C in a convection oven for 72 h, and then the dry weight was measured. The wet-to-dry weight ratio was calculated as an indicator of muscle edema (11).…”

Section: Methodsmentioning

confidence: 99%

“…Next, we evaluated the edema of muscular tissue at track 2 because tissue edema has been reported as an important indicator of I/R injury (11).…”

Section: Local Concentration Of Fgf-2mentioning

confidence: 99%

A free radical scavenger but not FGF-2-mediated angiogenic therapy rescues myonephropathic metabolic syndrome in severe hindlimb ischemia

Kaneko

Yonemitsu

Fujii

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. A free radical scavenger but not FGF-2-mediated angiogenic therapy rescues myonephropathic metabolic syndrome in severe hindlimb ischemia. Am J Physiol Heart Circ Physiol 290: H1484 -H1492, 2006. First published November 23, 2005 doi:10.1152/ajpheart.01006.2005The therapeutic use of angiogenic factors shows promise in the treatment of critical limb ischemia; however, its potential for myonephropathic metabolic syndrome (MNMS), a fatal complication caused by arterial reconstruction, has not been elucidated. The objective of this study was to evaluate the effectiveness of recombinant Sendai virus-mediated gene transfer of fibroblast growth factor-2 (FGF-2) directly compared with that of a radical scavenger, MCI-186, in a rat model of MNMS. MNMS was surgically induced by aortic occlusion below renal arteries for 4 h, followed by 6 h of reperfusion. Administration of MCI-186 (twice; iv 5 min before induced ischemia and ip 5 min before reperfusion; 10 mg/kg, respectively), but not FGF-2 gene transfer (once, 48 h before induced ischemia), dramatically prevented the increase of serum biochemical markers as well as the edema of the gastrocnemius muscle. The effect of MCI-186 was accompanied by the marked suppression of the neutrophilic infiltration into the local (muscle) and remote (lung) organs. Although serum and muscular levels of a neutrophil-chemoattractant (growth-related oncogene/cytokine-induced neutrophil chemoattractant-1) were not affected by any treatment, the serum level of soluble intercellular adhesion molecule-1 was decreased by treatment with MCI-186 but not by treatment with FGF-2. These results suggest the distinct mechanism of MNMS from critical limb ischemia without reperfusion. Therefore, radical scavenging should be paid more attention than therapeutic angiogenesis when arterial circulation is reconstructed. fibroblast growth factor-2; free radicals; critical limb ischemia; neutrophils IN THE LAST DECADE, a number of experimental studies have suggested the possible utility of angiogenic growth factors ("therapeutic angiogenesis") to treat limb ischemia, as well as ischemic heart diseases (30,31,36). Emerging evidence in clinical trials for limb ischemia, however, has shown a relatively limited outcome of therapeutic angiogenesis, in both protein and gene therapies, in double-blinded placebo-controlled studies (17,23,26). Therefore, further effort should be put into the clinical evaluation of the potentials of therapeutic angiogenesis, including the choice of the angiogenic factors, optimized dose and local level of the dose, and indications for clinical stages (4, 5).In a recent series of experimental studies, we demonstrated that intramuscularly boosted expression of basic fibroblast growth factor (bFGF or FGF-2), which is a prototype polypeptide for angiogenesis, by a highly efficient gene transfer vector, recombinant Sendai virus (SeV) (37), constantly showed efficient therapeutic effects in acute severe hindlimb ischemia of mice (19,21,25,32), as well as chronic limb ischemia of rabbits (2...

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“…Lastly, it can also be discussed if stress-induced modulation of edema is causally related to glucocorticoids. Treatment with the corticosteroid dexamethasone failed to influence edema formation after stroke in humans (Ito et al, 1980;Ogun and Odusote, 2001). It is therefore possible that stress influences edema formation through a mechanism independently of glucocorticoid receptor activation.…”

Section: Post-lesion Restraint Stress Exacerbates Infarct Sizementioning

confidence: 99%

“…The brains were then dried in an oven (VWR Scientific Products, Batavia, IL) at 100 °C for 24 h. The dry weights of each hemisphere were measured. Edema levels were determined using the wet/dry method (Ito et al, 1980;MacLellan et al, 2004) and the following formula: Brain water content (%)=[(Wet weight−Dry weight)/wet weight]×100.…”

Section: Edema Measurementmentioning

confidence: 99%

Delayed recovery and exaggerated infarct size by post-lesion stress in a rat model of focal cerebral stroke

et al. 2008

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Stress might be one of the most salient intrinsic factors influencing the risk of stroke and its outcome. Previous studies have linked stress to increased infarct size and exaggerated cognitive deficits in rodent models of stroke. This study compares the effects of chronic restraint stress, representing a psychological stressor, prior to or after motor cortex devascularization lesion on motor recovery in rats. Daily testing in a skilled reaching task revealed initially exaggerated deficits in limb use caused by pre-lesion stress in the absence of increased infarct size. Both preand post-lesion stresses affected movement by delaying recovery and limiting compensation of lesion-induced deficits. Nevertheless, only rats that experienced post-lesion stress showed enlarged infarct size. This was accompanied by enlarged edema formation in the lesion hemisphere of poststress animals on day 2 post-lesion. There were no significant differences in infarct size between post-lesion day 2 and day 15. The data demonstrate that both pre-and post-lesion chronic restraint stresses affect motor recovery after ischemic lesion. Lesion volume, however, is influenced by the timing of a stressful experience relative to the lesion. These findings suggest that stress represents a critical variable determining the outcome after stroke.

show abstract

Effect of steroid on ischemic brain edema. Analysis of cytotoxic and vasogenic edema occurring during ischemia and after restoration of blood flow.

Cited by 35 publications

References 35 publications

Xanthine oxidase-derived hydrogen peroxide contributes to ischemia reperfusion-induced edema in gerbil brains.

Xanthine oxidase-derived hydrogen peroxide contributes to ischemia reperfusion-induced edema in gerbil brains.

A free radical scavenger but not FGF-2-mediated angiogenic therapy rescues myonephropathic metabolic syndrome in severe hindlimb ischemia

Delayed recovery and exaggerated infarct size by post-lesion stress in a rat model of focal cerebral stroke

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