Role of neutrophil-endothelial adhesion in skeletal muscle reperfusion injury

Crinnion, J. N.; Homer‐Vanniasinkam, Shervanthi; Parkin, SM; Gough, Michael

doi:10.1002/bjs.1800830234

Cited by 34 publications

(11 citation statements)

References 23 publications

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“…Although the pathophysiology of ischaemia reperfusion injury is complex, there is increasing evidence that neutrophil adhesion to the activated microvascular endothelium is a key step in this process [2]. Activation of circulating PMNs leads to the up-regulation of surface adhesion molecules (CD1 ldCDl8 and CD1 lb/CD18) with their adherence to and migration across the endothelium.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…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%

“…Studies have confirmed the key role of neutrophilic infiltration in IRI. [1][2][3] Depletion of the numbers of neutrophils by haemofiltration or adhesion by immunological means can moderate IRI to a considerable extent. [5][6][7][8] Similarly, in various models of IRI, the administration of antioxidants limits the injury caused by neutrophil-derived oxygen free radicals, including systemic injury after ischaemia of the lower torso.…”

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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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“…Locally, after reperfusion, activated neutrophils cause additional injury to the already ischemic striated muscle through the release of reactive oxygen species (ROS) and proteolytic enzymes [12,37,55,57]. Systemic neutrophil infiltration after IRI manifests as sequestration in distant organs, such as lungs and kidneys [26,59].…”

Section: Introductionmentioning

confidence: 99%