Xanthine Oxidase Released From Reperfused Hind Limbs Mediate Küpffer Cell Activation, Neutrophil Sequestration, and Hepatic Oxidative Stress in Rats Subjected to Tourniquet Shock

Vega, Virginia L.; Mardones, Lorena; Maldonado, Mauricio; Nicovani, Sandra; Manríquez, Veronica; Roa, Jorge; Ward, Pamela

doi:10.1097/00024382-200014050-00012

Cited by 31 publications

(25 citation statements)

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“…We have recently shown an elevation of serum TNF-␣ levels following gut I/R, and kidney tissue TNF-␣ levels following renal I/R, and blockade of these increased levels to I/R by the same C5a antagonist used in the present study [29,30]. In the present study, we found that the C5a antagonist significantly blocked the rise in liver TNF-␣, indicating that C5a is also involved in the elevation of TNF-␣ following limb I/R, perhaps through the direct activation of Kupffer cells located in the liver [9,10]. This inhibition of circulating and tissue levels of TNF-␣ by C5a antagonists has been shown by us and others in a variety of inflammatory disease models where complement activation is involved [27][28][29][30][31]48].…”

Section: Discussionsupporting

confidence: 70%

Protective effects of a potent c5a receptor antagonist on experimental acute limb ischemia-reperfusion in rats

Woodruff¹,

Shiels²,

Reid³

et al. 2004

Journal of Surgical Research

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Section: Discussionsupporting

confidence: 70%

Protective effects of a potent c5a receptor antagonist on experimental acute limb ischemia-reperfusion in rats

Woodruff¹,

Shiels²,

Reid³

et al. 2004

Journal of Surgical Research

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“…XO levels also increase in plasma and liver after reperfusion of hindlimb ischemia and parallel an increase in TNFα and KC activation [ 40 ]. Pretreatment with allopurinol, a XO inhibitor and antioxidant, inhibits KC activation and liver leukocyte infi ltration, supporting the conclusion that neutrophil recruitment requires KC activation [ 40 ]. XO inhibition has also been shown to reduce the production of cytokineinduced neutrophil chemoattractant (CINC) by KCs, identifi ed through their ED2 expression, during hepatic IRI in rats [ 41 ].…”

Section: Ischemia-reperfusion Injurymentioning

confidence: 96%

Section: Ischemia-reperfusion Injurymentioning

confidence: 96%

“…Exogenous administration of XO to rats results in increased oxidative stress (quantifi ed by measurement of LPO using thiobarbituric acid reactive substances, TBARS) and neutrophil infi ltration (measured by MPO activity) in the liver [ 40 ]. XO levels also increase in plasma and liver after reperfusion of hindlimb ischemia and parallel an increase in TNFα and KC activation [ 40 ].…”

Section: Ischemia-reperfusion Injurymentioning

confidence: 99%

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Oxidative Stress and Liver Inflammation

Greenhalgh

Thompson

Henderson

et al. 2015

Oxidative Stress in Applied Basic Research and Clinical Practice

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“…Kocman et al (88) demonstrated an increase in malondialdehyde, an oxidative stress marker, after ischemia. During ischemia, xanthine dehydrogenase, which is found in the microvascular endothelial cells of skeletal muscle, is converted to XO (189), which, in turn, catalyzes the conversion of hypoxanthine to xanthine by producing O 2 ·Ϫ . Thus the primary sources of ROS during ischemia seem to be XO and mitochondrial complexes I and III (8,154,184).…”

Section: Chronology Of Events At the Level Of Skeletal Muscle Fiber Cmentioning

confidence: 99%

Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion

Paradis

Charles

Meyer

et al. 2016

American Journal of Physiology-Cell Physiology

103

127

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Peripheral artery disease (PAD) is a common circulatory disorder of the lower limb arteries that reduces functional capacity and quality of life of patients. Despite relatively effective available treatments, PAD is a serious public health issue associated with significant morbidity and mortality. Ischemia-reperfusion (I/R) cycles during PAD are responsible for insufficient oxygen supply, mitochondriopathy, free radical production, and inflammation and lead to events that contribute to myocyte death and remote organ failure. However, the chronology of mitochondrial and cellular events during the ischemic period and at the moment of reperfusion in skeletal muscle fibers has been poorly reviewed. Thus, after a review of the basal myocyte state and normal mitochondrial biology, we discuss the physiopathology of ischemia and reperfusion at the mitochondrial and cellular levels. First we describe the chronology of the deleterious biochemical and mitochondrial mechanisms activated by I/R. Then we discuss skeletal muscle I/R injury in the muscle environment, mitochondrial dynamics, and inflammation. A better understanding of the chronology of the events underlying I/R will allow us to identify key factors in the development of this pathology and point to suitable new therapies. Emerging data on mitochondrial dynamics should help identify new molecular and therapeutic targets and develop protective strategies against PAD.peripheral artery disease; ischemia-reperfusion; skeletal muscle; mitochondria; oxidative stress PERIPHERAL ARTERY DISEASE (PAD) refers to a common circulatory disorder of the lower limb caused by chronic narrowing of the arteries (e.g., stenosis and occlusion) or atherosclerosis. PAD represents a broad spectrum of disease severity, ranging from asymptomatic disease to frequent pain when walking (i.e., intermittent claudication or limping) or critical limb ischemia associated with decubitus pain and/or ulcers (114,126).PAD is known to be associated with reduced functional capacity and quality of life. It is a major cause of limb amputation, as well as an increased risk factor for myocardial infarction, stroke, and death. The incidence of PAD varies with age, from 3-10% in young people to 15-20% in people Ͼ70 yr of age, and is asymptomatic in 40% of the cases (1), with greater prevalence among men. The major PAD risk factors, including smoking, diabetes mellitus, dyslipidemia, hypertension, and obesity, are the same as those for cardiovascular and cerebrovascular diseases (35).Three main complementary treatment options improve the functional status and other clinical outcomes in PAD patients (54). 1) Optimization of medical therapy (i.e., pharmacotherapy) reduces the risk of cardiac ischemia, increases the distance a patient can walk, and improves the functional capacity of patients. 2) When possible, exercise training, a noninvasive and nonpharmacological therapy, improves walking ability and has protective effects in patients with PAD characterized by intermittent claudication and infrainguinal lesions...

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Xanthine Oxidase Released From Reperfused Hind Limbs Mediate Küpffer Cell Activation, Neutrophil Sequestration, and Hepatic Oxidative Stress in Rats Subjected to Tourniquet Shock

Cited by 31 publications

References 0 publications

Protective effects of a potent c5a receptor antagonist on experimental acute limb ischemia-reperfusion in rats

Protective effects of a potent c5a receptor antagonist on experimental acute limb ischemia-reperfusion in rats

Oxidative Stress and Liver Inflammation

Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion

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