Noninvasive remote ischemic preconditioning for global protection of skeletal muscle against infarction

Addison, Patrick; Neligan, Peter C.; Ashrafpour, Homa; Khan, Asim Ali; Zhong, Anguo; Moses, Michael A.; Forrest, Christopher R.; Pang, Cho Y.

doi:10.1152/ajpheart.00106.2003

Cited by 148 publications

(166 citation statements)

References 43 publications

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“…The use of limbs is one of the most promising possibilities of evolving both pre-and postconditioning ischemic tolerance. 28,29 The major beneficiary of these approaches is the heart, 29 but the kidney, 30 distant muscle, 31 liver, 32 lung, 15 or CNS 33 can also be targeted. With respect to remote preconditioning, the present study has two messages.…”

Section: Discussionmentioning

confidence: 99%

Ischemic limb preconditioning downregulates systemic inflammatory activation

Szabó

Varga

Keresztes

et al. 2008

Journal Orthopaedic Research

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We examined local and systemic antiinflammatory consequences of ischemic preconditioning (IPC) in a rat model of limb ischemia-reperfusion (I-R) by characterizing the leukocyte-endothelial interactions in the periosteum and the expression of adhesion molecules playing a role in leukocyte-mediated inflammatory processes. IPC induction (2 cycles of 10 min of complete limb ischemia and 10 min of reperfusion) was followed by 60 min of ischemia/180 min of reperfusion or sham-operation. Data were compared with those on animals subjected to I-R and sham-operation. Neutrophil leukocyte-endothelial cell interactions (intravital videomicroscopy), intravascular neutrophil activation (CD11b expression changes by flow cytometry), and soluble and tissue intercellular adhesion molecule-1 (ICAM-1; ELISA and immunohistochemistry, respectively) expressions were assessed. I-R induced enhanced leukocyte rolling and adherence in the periosteal postcapillary venules after 120 and 180 min of reperfusion. This was associated with a significantly enhanced CD11b expression (by $80% and 72%, respectively) and moderately increased soluble and periosteal ICAM-1 expressions. IPC prevented the I-R-induced increases in leukocyte adherence and CD11b expression without influencing the soluble and tissue ICAM-1 levels. The results show that limb IPC exerts not only local, but distant antiinflammatory effects through significant modulation of neutrophil recruitment. ß

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Section: Discussionmentioning

confidence: 99%

Ischemic limb preconditioning downregulates systemic inflammatory activation

Szabó

Varga

Keresztes

et al. 2008

Journal Orthopaedic Research

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“…This energy is provided by ATP molecules, for which storage is limited (ϳ35-55 mol/mg protein) (2,64,66).…”

Section: Mitochondria the "Powerhouse" Of The Cellsmentioning

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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“…Another potential explanation might be an improvement in metabolic efficiency via activation of KATP channels. In animal experiments, prolonged ischemia of the skeletal muscle demonstrates that IPC attenuates ATP depletion [50][51][52][53] , secondary to the activation of KATP channels [53][54][55][56][57] . Previous work showed that the activation of KATP channels may contribute to more effective blood flow redistribution during exercise 58,59) .…”

Section: Potential Factorsmentioning

confidence: 99%

Ischemic preconditioning: Potential impact on exercise performance and underlying mechanisms

Horiuchi

2017

JPFSM

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Originally, in clinical settings, ischemic preconditioning (IPC) has been used to delay cardiac cell injury and protect against myocardial and vascular damage. Furthermore, as this manipulation is relatively easy and noninvasive, previous studies have examined how IPC may have beneficial effects on exercise performance. However, because of various factors, such as different populations, exercise modes and intensities, and IPC protocols, not enough evidence is available to achieve a consensus on the impact of IPC on exercise performance, e.g., time to failure during exercise, time trial performance, and peak power. Existing evidence suggests that IPC seems not to impair exercise performance, though one study found an impairment. However, about half of the previous studies showed beneficial effects of IPC on exercise performance. Similarly, the physiological responses from IPC are varied. It is still possible that various factors, such as exercise mode and intensity, heterogeneous population and IPC protocol may affect exercise performance. Previous studies showed that effective blood flow via an increase in nitric oxide and the improvement of metabolic efficiency might be candidate factors that can explain the effect of IPC on exercise performance, although no direct evidence has been obtained. This review aims to identify potential sources of variation in these effects on exercise performance with IPC.

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Noninvasive remote ischemic preconditioning for global protection of skeletal muscle against infarction

Cited by 148 publications

References 43 publications

Ischemic limb preconditioning downregulates systemic inflammatory activation

Ischemic limb preconditioning downregulates systemic inflammatory activation

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

Ischemic preconditioning: Potential impact on exercise performance and underlying mechanisms

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