The Effects of Hypothermia and L-Arginine on Skeletal Muscle Function in Ischemia–Reperfusion Injury

Stahl, Daniel; Souder, Nicholas; Probe, Robert A.; Sampson, Wayne; Tharakan, Binu; Ward, Russell

doi:10.1097/bot.0b013e31823dea55

Cited by 7 publications

(13 citation statements)

References 26 publications

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“…18 studies used rats in their experimental design. Of these 18 studies, nine articles used Sprague-Dawley rats [23][24][25][26][27][28][29][30][31], one used Wistar albino rats [32], seven studies used Lewis rats [33][34][35][36][37][38][39], and one study used Fisher rats [40]. Five of the 29 articles used mice in their experimental design.…”

Section: Study Characteristicsmentioning

confidence: 99%

“…Ischemia and I/R models were used for all the included studies (Table 1). These studies used either elastic non-pneumatic tourniquet [26,27,29,32,40,49], pneumatic tourniquet [23,31,33,34,[41][42][43], atraumatic clamps [24,25,28,[46][47][48]51], or ligation methods [30,39,44,45] to produce ischemia in the hind limbs. Specifically, four of the studies amputated the thigh sparing femoral vessels, later femoral vessels were occluded to avoid venous congestion and create ischemia [35][36][37][38].…”

Section: Study Characteristicsmentioning

confidence: 99%

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Efficacy of non-surgical interventions for promoting improved functional outcomes following acute compartment syndrome: A systematic review

et al. 2022

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Background Acute compartment syndrome (ACS) is a devastating complication which develops following a traumatic extremity injury that results in increased pressure within osteofascial compartments, thereby leading to ischemia, muscle and nerve necrosis, and creates a life-threatening condition if left untreated. Fasciotomy is the only available standard surgical intervention for ACS. Following fasciotomy the affected extremity is plagued by prolonged impairments in function. As such, an unmet clinical need exists for adjunct, non-surgical therapies which can facilitate accelerated functional recovery following ACS. Thus, the purpose of this systematic review was to examine the state of the literature for non-surgical interventions that aim to improve muscle contractile functional recovery of the affected limb following ACS. Methods English language manuscripts which evaluated non-surgical interventions for ACS, namely those which evaluated the function of the affected extremity, were identified as per PRISMA protocols via searches within three databases from inception to February 2022. Qualitative narrative data synthesis was performed including: study characteristics, type of interventions, quality, and outcomes. Risk of bias (RoB) was assessed using the Systematic Review Centre for Laboratory Animal Experimentation’s (SYRCLE) RoB tool and reported level of evidence for each article. Results Upon review of all initially identified reports, 29 studies were found to be eligible and included. 23 distinct non-surgical interventions were found to facilitate improved muscle contractile function following ACS. Out of 29 studies, 15 studies which evaluated chemical and biological interventions, showed large effect sizes for muscle function improvement. Conclusions This systematic review demonstrated that the majority of identified non-surgical interventions facilitated an improvement in muscle contractile function following pathological conditions of ACS.

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Section: Study Characteristicsmentioning

confidence: 99%

Section: Study Characteristicsmentioning

confidence: 99%

Efficacy of non-surgical interventions for promoting improved functional outcomes following acute compartment syndrome: A systematic review

et al. 2022

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“…In this study, the process of ischemia (I/R) was induced using an atraumatic femoral artery rubber band tourniquet that was applied on both hind roots of the limb. Ischemia was followed by a reperfusion period (20). To determine the contractility features and electrical characteristics of the muscles left and right EDL muscles were used in all groups.…”

Section: Animal Preparation and I/r Processmentioning

confidence: 99%

Effect of iloprost on contractile impairment and mitochondrial degeneration in ischemia-reperfusion of skeletal muscle

et al. 2018

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Purpose Acute lower extremity ischemia is still a main cause of mortality and morbidity in orthopedic traumatology and reconstructive surgery. In acute lower extremity ischemia, the skeletal muscles are the tissues that are the most vulnerable to ischemia. The aim of this study was to evaluate the effects of iloprost (IL) therapy on skeletal muscle contractile impairment and mitochondrial degeneration in an acute lower extremity ischemia-reperfusion rat model. Main Methods Forty Wistar albino rats were randomly divided into a control group and four experimental groups. Experimental groups were either subjected to 2 h of lower extremity ischemia followed by a 4-h reperfusion period or to 4 h of ischemia followed by an 8-h reperfusion period. Except for the animals in the control group, all animals received IL (1 ng/kg/min) or saline (1 ml/kg) by intraperitoneal infusion for 10 min immediately before reperfusion. At the end of the recording of skeletal muscle electrical activity and contractility, all rats were sacrificed by decapitation and muscle samples of lower extremity were immediately harvested for histopathologic analyses. Results After ischemia-reperfusion, a breakdown in the force-frequency curves of extensor digitorum longus muscle was observed, showing the diminished muscle contractility. However, IL significantly improved muscle contractility following injury induced by 2 h of ischemia followed by a 4-h reperfusion period. In addition, IL partially ameliorated mitochondrial degeneration in the muscle cells of ischemia groups. Conclusion This study indicates that immediate IL therapy repairs muscle damage especially after 2 h of ischemia and 4 h of reperfusion and therefore that IL improves contractile function.

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“…Researchers have reported that antioxidants such as vitamin E, l -arginine, curcumin, and mitochondrion-targeted peptide protect skeletal muscle against I/R injury. 11 –14…”

Section: Introductionmentioning

confidence: 99%

“…Researchers have reported that antioxidants such as vitamin E, L-arginine, curcumin, and mitochondrion-targeted peptide protect skeletal muscle against I/R injury. [11][12][13][14] Our previous study showed that edaravone (3-methy-1-pheny1-2-pyrazolin-5-one), a potent systemic scavenger of free radicals, protects the hind limb skeletal muscles of mice against I/R injury induced by application of a tourniquet for 1.5 h. 15 Edaravone inhibits both nonenzymatic lipid peroxidation and the lipoxygenase pathway, in addition to exhibiting potent antioxidant effects against I/R injury-induced vascular endothelial cell injury, delayed neuronal death, brain edema, and concomitant neurologic deficits. Edaravone was approved for use in treating acute brain infarctions in Japan in 2002; in 2015, it was approved for treating amyotrophic lateral sclerosis based on its neuroprotective effects.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of edaravone on systemic inflammation and local damage in skeletal muscles following long-term ischemia to murine hind limb

Yokoyama

Tsujii

Iino

et al. 2019

J Orthop Surg (Hong Kong)

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Purpose: The purpose of this study was to evaluate local and systemic pathology in a murine model of ischemia–reperfusion (I/R) injury induced by long-term application of a tourniquet on the hind limbs and to assess the protective effects of edaravone, a potent systemic scavenger of free radicals, using this model. Methods: Sixty C57BL6 mice were divided in two groups, with one group receiving a 3 mg/kg intraperitoneal injection of edaravone and the other group receiving an identical amount of saline 30 min before ischemia under deep anesthesia. The left thigh of each animal was constricted for 4 h with a 4.5-oz. orthodontic rubber band to induce ischemia; 4 h was the critical duration for skeletal muscles. After ischemia, specimens of skeletal muscles, both kidneys, and plasma were collected at 0, 2, 12, 24, 48, and 72 h. Injury to the skeletal muscles and vacuolar degeneration of the kidneys were histologically assessed. Additionally, apoptosis of skeletal muscle cells was assessed by analysis of caspase 3/7 activity and TUNEL staining. Plasma tumor necrosis factor (TNF)-α levels were measured using an enzyme-linked immunosorbent assay kit. Results: Skeletal muscles exhibited prominent injury of myofibers at 12 h after I/R injury, with clear upregulation of plasma TNF-α expression and histologic evidence of tubular dysfunction of the kidneys. Plasma TNF-α levels declined and histologic renal damage was ameliorated in edaravone-treated mice, but treatment did not protect skeletal muscle following ischemia for 4 h. Nonetheless, compared with group S, expression of the apoptosis marker caspase 3/7 was significantly inhibited in the skeletal hind limb muscles of Ed-group mice affected by reperfusion injury following ischemia for 4 h. Conclusion: The present study demonstrated that edaravone is a potentially useful drug for systemic or local treatment of reperfusion injury resulting from long-term ischemia.

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The Effects of Hypothermia and L-Arginine on Skeletal Muscle Function in Ischemia–Reperfusion Injury

Cited by 7 publications

References 26 publications

Efficacy of non-surgical interventions for promoting improved functional outcomes following acute compartment syndrome: A systematic review

Efficacy of non-surgical interventions for promoting improved functional outcomes following acute compartment syndrome: A systematic review

Effect of iloprost on contractile impairment and mitochondrial degeneration in ischemia-reperfusion of skeletal muscle

Inhibitory effect of edaravone on systemic inflammation and local damage in skeletal muscles following long-term ischemia to murine hind limb

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