Anti-Selectin Therapy Modifies Skeletal Muscle Ischemia and Reperfusion Injury

Mr, Weiser; Sa, Gibbs; Cr, Valeri; Shepro, David; Hb, Hechtman

doi:10.1097/00024382-199606000-00003

Cited by 35 publications

(23 citation statements)

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“…Immunological blockade of adhesion molecules and cytokines slows recruitment of neutrophils while their removal/inactivation is known to ameliorate IRI. 3,4,7,8 Antioxidants such as taurine, vitamin C and n-acetyl cysteine have been used to scavenge MPO-derived activated oxygen species. 9,10,28 Superoxide dismutase also preserves muscle function after IRI by way of a similar scavenging mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4] Endothelial dysfunction occurs as a result of tissue hypoxia and on subsequent reperfusion, cytokines and adhesion molecules are enhanced leading to chemotaxis and infiltration by neutrophils. Necrosis of damaged tissue by neutrophil myeloperoxidase (MPO) and other enzymes generates active oxygen species, which in turn can extend the ischaemic injury.…”

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confidence: 99%

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Oral vitamin C attenuates acute ischaemia-reperfusion injury in skeletal muscle

Kearns

Moneley

Murray

et al. 2001

The Journal of Bone and Joint Surgery. British volume

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I schaemia-reperfusion injury (IRI) is caused byendothelial and subendothelial damage by neutrophil-derived oxidants. Vitamin C is an antioxidant which attenuates endothelial injury after IRI. Our aim was to evaluate the effect of oral vitamin C in the prevention of IRI in skeletal muscle. We used a model of cross-clamping (3 hours) and reperfusion (1 hour) of the cremaster muscle in rats. Muscle function was assessed electrophysiologically by electrical field stimulation. Infiltration by neutrophils was determined by the activity of tissue myeloperoxidase (MPO) and tissue oedema by the wet-to-dry ratio. Neutrophil respiratory burst activity was measured in control animals and groups pretreated with vitamin C.IRI significantly decreased muscle function and increased muscle neutrophil MPO activity and muscle oedema. Pretreatment with vitamin C preserved muscle function and reduced tissue oedema and neutrophil infiltration. Neutrophil respiratory burst activity was reduced in the group treated with vitamin C compared with the control group.We conclude that pretreatment with oral vitamin C protects against acute muscle IRI, possibly by attenuating neutrophil respiratory burst activity.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Oral vitamin C attenuates acute ischaemia-reperfusion injury in skeletal muscle

Kearns

Moneley

Murray

et al. 2001

The Journal of Bone and Joint Surgery. British volume

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“…The selectin-family consists of three members, L-, P-and E-selectin of which L-selectin is constitutively expressed on the surface of leukocytes [40] whereas P-and E-selectins are expressed by endothelial cells in response to stimuli such as Interleukin-1b and TNF-a [41]. P-selectin antibody has been successfully used to reduce local skeletal muscle reperfusion injury in the rat [42] and pulmonary/hepatic injury in a mouse model of lower torso ischemia [43]. In a sheep model of ischemia-reperfusion, antibodies directed against both P-and L-selectin significantly reduced pulmonary leakage and neutrophil accumulation [44].…”

Section: Endothelial Cell-dysfunction and Leukocyte Adhesionmentioning

confidence: 99%

Ischemia-Reperfusion Injury

Dorweiler

Pruefer²,

Andrási³

et al. 2007

Eur J Trauma Emerg Surg

116

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The term ischemia-reperfusion injury describes the experimentally and clinically prevalent finding that tissue ischemia with inadequate oxygen supply followed by successful reperfusion initiates a wide and complex array of inflammatory responses that may both aggravate local injury as well as induce impairment of remote organ function. Conditions under which ischemia-reperfusion injury is encountered include the different forms of acute vascular occlusions (stroke, myocardial infarction, limb ischemia) with the respective reperfusion strategies (thrombolytic therapy, angioplasty, operative revascularization) but also routine surgical procedures (organ transplantation, free-tissue-transfer, cardiopulmonary bypass, vascular surgery) and major trauma/shock. Since the first recognition of ischemia-reperfusion injury during the 1970s, significant knowledge has accumulated and the purpose of this review is to present an overview over the current literature on the molecular and cellular basis of ischemia-reperfusion injury, to outline the clinical manifestations and to compile contemporary treatment and prevention strategies. Although the concept of reperfusion injury is still a matter of debate, it is corroborated by recent and ongoing clinical trials that demonstrated ischemic preconditioning, inhibition of sodium-hydrogen-exchange and administration of adenosine to be effective in attenuating ischemia-reperfusion injury.

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“…The primary target of the reperfusion injury is the microcirculation where the leukocyte-endothelium interaction results in transendothelial migration and tissue injury from the release of reactive oxygen species and elastases [16,17]. Although skeletal muscle has a relatively high tolerance to ischaemia, skeletal muscle dysfunction and infarction are wellrecognised complications of the reperfusion injury.…”

Section: Introductionmentioning

confidence: 99%

Activated protein C attenuates acute ischaemia reperfusion injury in skeletal muscle

Dillon¹,

Laing²,

Cahill³

et al. 2005

J. Orthop. Res.

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Activated protein C (APC) is an endogenous anti-coagulant with anti-inflammatory properties. The purpose of the present study was to evaluate the effects of activated protein C in the setting of skeletal muscle ischaemia reperfusion injury (IRI). IRI was induced in rats by applying rubber bands above the levels of the greater trochanters bilaterally for a period of 2 h followed by 12 h reperfusion. Treatment groups received either equal volumes of normal saline or activated protein C prior to tourniquet release. Following 12 h reperfusion, muscle function was assessed electrophysiologically by electrical field stimulation. The animals were then sacrificed and skeletal muscle harvested for evaluation.Activated protein C significantly attenuated skeletal muscle reperfusion injury as shown by reduced myeloperoxidase content, wet to dry ratio and electrical properties of skeletal muscle. Further in vitro work was carried out on neutrophils isolated from healthy volunteers to determine the direct effect of APC on neutrophil function. The effects of APC on TNF-u stimulated neutrophils were examined by measuring CD18 expression as well as reactive oxygen species generation. The in vitro work demonstrated a reduction in CD 18 expression and reactive oxygen species generation.We conclude that activated protein C may have a protective role in the setting of skeletal muscle ischaemia reperfusion injury and that this is in part mediated by a direct inhibitory effect on neutrophil activation.

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Anti-Selectin Therapy Modifies Skeletal Muscle Ischemia and Reperfusion Injury

Cited by 35 publications

References 0 publications

Oral vitamin C attenuates acute ischaemia-reperfusion injury in skeletal muscle

Oral vitamin C attenuates acute ischaemia-reperfusion injury in skeletal muscle

Ischemia-Reperfusion Injury

Activated protein C attenuates acute ischaemia reperfusion injury in skeletal muscle

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