Ischemia-reperfusion-induced muscle damage: Protective effect of corticosteroids and antioxidants in rabbits

Bushell, Alison J.; Klenerman, L.; Davies, Helen M.S.; Grierson, Ian; Jackson, Malcolm J.

doi:10.3109/17453679609002338

Cited by 41 publications

(19 citation statements)

References 13 publications

(6 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Muscle tissue has been thought to be insensitive to ischemia/reperfusion-induced damage, but a number of recent papers have suggested that oxygen free radical species may be produced during reperfusion of skeletal muscle [15]. In this study, 3-hour-hypoxia did not cause any increase in the lipid peroxidation in the newborn rat muscles.…”

Section: Discussionmentioning

confidence: 52%

Role of Nitric Oxide in Hypoxia-Induced Changes in Newborn Rats

Kılıç

Kiliç²,

Güven³

et al. 2000

Neonatology

View full text Add to dashboard Cite

In order to investigate the role of nitric oxide (NO) in hypoxic tissue damage in newborns, we studied the effects of systemic administration of an inhibitor of NO synthase, N^G-nitro-L-arginine (L-NNA), and the precursor for the synthesis of NO, L-arginine (L-ARG), on the biochemical and histological changes in brain, heart, lung, liver, kidney, intestine, and skeletal muscle tissues. Four groups of 1-day-old Wistar rat pups were used: control, hypoxic, L-ARG, and L-NNA groups. L-ARG 100 mg/kg or L-NNA 2 mg/kg was administered as a bolus intraperitoneally 1.5 h before hypoxia. Hypoxia increased lipid peroxidation in all tissues except muscle; this increase was prevented by L-NNA and L-ARG in brain, heart, lung, kidney, and liver tissues. L-NNA in intestine and L-ARG in muscle tissue increased lipid peroxidation. The tissue-associated myeloperoxidase activity was decreased in the liver by L-NNA and L-ARG. Histopathological changes in intestines were villous epithelial separation and hyperemia in hypoxic and L-NNA groups which were not observed in control and L-ARG groups. In lungs, pulmonary hemorrhage was observed only in the hypoxic group. These data suggest that NO acts both as a destructive and a protective agent in the pathogenesis of hypoxia-reoxygenation injuries.

show abstract

Section: Discussionmentioning

confidence: 52%

Role of Nitric Oxide in Hypoxia-Induced Changes in Newborn Rats

Kılıç

Kiliç²,

Güven³

et al. 2000

Neonatology

View full text Add to dashboard Cite

show abstract

“…There are reports of HR formation in ischemicreperfusion injury models of cerebrum, peripheral nerve and skeletal muscle (20)(21)(22), in a muscle necrosis model induced by bupivacaine hydrochloride (23), in amyotrophic lateral sclerosis (24), and in Parkinson's disease (25). This is the first report to measure HR formation in SM.…”

Section: Discussionmentioning

confidence: 86%

Hydroxyl Radical Formation in Skeletal Muscle of Rats with Glucocorticoid-Induced Myopathy

Konno

2005

Neurochem Res

View full text Add to dashboard Cite

Steroid myopathy is a well-known adverse effect of glucocorticoids that causes muscle weakness and atrophy; however, its pathogenic mechanism is still unclear. Recently, oxidative stress was reported to contribute to steroid myopathy, but there is no report that actually attempts to measure hydroxyl radical. I developed an animal model of steroid myopathy in rat with dexamethasone (9-Fluoro-11beta,17, 21-trihydroxy-16alpha-methylpregna-1,4-diene-3,20-dione), and measured hydroxyl radical using the salicylate trapping method. There was significant dose-dependent relation between both 2,5- and 2,3-dihydroxybenzoic acids and dexamethasone in the treated group, compared to the control group. These results suggest that hydroxyl radical plays a role in the pathogenesis of steroid myopathy.

show abstract

“…One example of this type of mechanism is the degenerative process seen following prolonged tissue ischaemia and subsequent reperfusion. In this situation antioxidant supplementation may offer some protection against tissue damage, but blockers of cellular Ca uptake and inhibitors of neutrophil activation or sequestration have equivalent protective effects (Bushell et al 1996).…”

mentioning

confidence: 99%

Free radicals in skin and muscle: damaging agents or signals for adaptation?

Jackson

1999

Proc. Nutr. Soc.

View full text Add to dashboard Cite

Much of the current literature regarding the biological effects of antioxidant nutrients has concentrated on their potential role in inhibiting or preventing tissue damage induced by free radical species produced during metabolism. Recent findings indicate that antioxidants may also have more subtle roles, regulating changes in gene expression induced by oxidizing free radical species. There is increasing evidence that free radicals act as signals for cell adaptation in a variety of cell types and the nature of the mechanisms by which free radical species influence gene expression is the subject of much current research. Processes such as these may be particularly important in tissues regularly exposed to varying amounts of oxidative stress as part of their normal physiological functions. Examples of such tissues include skin exposed to u.v. light and skeletal muscle subjected to repeated bouts of exercise.

show abstract

Ischemia-reperfusion-induced muscle damage: Protective effect of corticosteroids and antioxidants in rabbits

Cited by 41 publications

References 13 publications

Role of Nitric Oxide in Hypoxia-Induced Changes in Newborn Rats

Role of Nitric Oxide in Hypoxia-Induced Changes in Newborn Rats

Hydroxyl Radical Formation in Skeletal Muscle of Rats with Glucocorticoid-Induced Myopathy

Free radicals in skin and muscle: damaging agents or signals for adaptation?

Contact Info

Product

Resources

About