NOS upregulation attenuates vascular endothelial dysfunction in the late phase of ischemic preconditioning in skeletal muscle

Wang, Wei Z.; Fang, Xiaojie; Stepheson, Linda L.; Khiabani, Kayvan T.; Zamboni, WA

doi:10.1016/j.orthres.2003.10.004

Cited by 28 publications

(4 citation statements)

References 33 publications

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“…The surgical preparation for vascular pedicle isolated cremaster model has been described in our previous published papers [23–27]. Briefly, an incision was made on the ventral aspect of the animal from the anterior iliac spine to the pubic nodus without opening the scrotum.…”

Section: Methodsmentioning

confidence: 99%

“…The method for cremaster muscle observation in vivo were described in our previously published papers [23–27]. Briefly, right cremaster muscle was surgically opened on day 2 (after 24 hr of reperfusion) and carefully spread on a glass slide secured to a plexiglas observation platform with 5–0 silk sutures.…”

Section: Methodsmentioning

confidence: 99%

“…The methods to determine endothelial‐dependent and ‐independent vasodilatation in the terminal arteriole of cremaster muscle were described in our previous published papers [23–27]. Briefly, one terminal arteriole with a diameter of 10–12 μ m was chosen from each cremaster muscle.…”

Section: Methodsmentioning

confidence: 99%

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Melatonin reduces ischemia/reperfusion‐induced superoxide generation in arterial wall and cell death in skeletal muscle

Wang

Fang

Stephenson

et al. 2006

Journal of Pineal Research

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The purpose of this study was to determine the effect of melatonin on superoxide generation in arterial wall at an early phase of reperfusion and on endothelial dysfunction of microvasculature and cell viability of cremaster muscle at late phase of reperfusion (24 hr) after prolonged ischemia. Bilateral vascular pedicles which supply blood flow to the cremaster muscle were exposed. After surgical preparation, microvascular clamps were applied on the right iliac, femoral and spermatic arteries to create 4 hr of ischemia in both feeding vessels and the unexposed cremaster muscle. The vascular clamping was omitted on the left iliac, femoral and spermatic arteries and served as an internal control. Melatonin or Vehicle was via by intravenous injection at 10 min prior to reperfusion and 10 min after reperfusion. In the first experiment, the vascular pedicle was harvested after reperfusion to measure superoxide generation in real time by lucigenin-derived chemiluminescence. In the second experiment, endothelial-dependent and -independent vasodilatation was examined in the terminal arteriole of cremaster muscle which was then harvested to examine cell viability by WST-1 assay on day 2. Superoxide generation in arterial wall peaked at first 5-min of reperfusion and declined to near baseline after 60 min of reperfusion. Melatonin treatment significantly reduced superoxide generation in arterial walls and improved cell viability in cremaster muscles. Melatonin treatment also significantly reduced microvascular endothelial dysfunction which was still observable in the microcirculation of cremaster muscle after 24 hr of reperfusion. Melatonin reduces superoxide generation in the early phase of reperfusion resulting in attenuating endothelial dysfunction and muscle cell death in the late phase of reperfusion.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Melatonin reduces ischemia/reperfusion‐induced superoxide generation in arterial wall and cell death in skeletal muscle

Wang

Fang

Stephenson

et al. 2006

Journal of Pineal Research

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“…Ischemic conditioning may stimulate angiogenesis within ischemic myocardium via release of various biochemical factors [96] and thereby improve perfusion at the microvessel level [97] but these findings remain controversial [98]. Improved availability of nutrients and oxygen within ischemic myocardium of conditioned hearts may be advantageous for tissue regenerative therapies.…”

Section: Remote Cardiac Conditioningmentioning

confidence: 99%

Myocardial Infarction: Perspectives on Cardiac Regeneration and Cardiac Remote Conditioning Interventions to Limit Cellular Injury

Kingma¹

2020

WJCD

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Acute myocardial infarction initiates a cascade of events including loss of protein homeostasis and chronic inflammation that affect overall cellular repair and senescence. This contributes to loss of cardiomyocytes and consequent formation of fibrotic scar. In certain vertebrate species, the heart can completely self-repair or regenerate after myocardial injury; however, this does not appear to be the case for humans. Despite this limitation, studies using novel non-pharmacologic interventions designed to protect against ischemic damage and to improve patient outcomes are ongoing. Remote ischemic conditioning stratagems are used to attenuate ischemia-reperfusion injury in clinical and animal studies; endogenous protective factors that stimulate complex signal transduction pathways are deemed responsible. Some of these factors could conceivably act in concert with those involved in regulating cardiovascular regeneration. Numerous studies have focused on cardiac regenerative interventions using stem-cell based therapies and transplantation of cardiomyocyte (or other cell types) or biocompatible matrices. This review discusses recent progress of pre-clinical and clinical translational studies for cardiac regeneration. In addition, we submit that interventions using cellular adjunctive therapies combined with remote ischemic conditioning may prove to be of interest in the battle to find novel strategies for protection against cardiac injury. are described in the scientific literature; myocardial stunning, i.e. viable cardiomyocytes that exhibit prolonged post-ischemic contractile dysfunction even after reperfusion, and myocardial hibernation, i.e. viable, but chronically contractile dysfunctional cardiomyocytes. While the pathogenesis of cell death in non-cardiac cells is less considered in most studies, it is clear that vascular endothelial and smooth muscle cells along with nervous system components within the ischemic zone are negatively affected by coronary occlusion; this contributes significantly to overall loss of cardiac contractile function and limits recovery potential. Loss of these myocardial components probably renders the affected tissue non-salvageable for a number of reasons including no-reflow, or disrupted electrical conduction, etc. Timely reperfusion of the infarct-related artery by various clinical strategies (just enumerate them as reperfusion therapy which may be pharmacological, primary percutaneous coronary intervention, primary PCI, urgent coronary artery bypass graft, appears to limit overall myocardial damage; however, reperfusion itself may exacerbate injury via apoptosis or autophagy [19]. While patient survival after ischemia has markedly improved over the last forty years, the prevalence of chronic heart failure due, in part, to remodeling of the damaged left ventricle has also increased [20] [21]. Cardiac repair is a complex, tightly regulated process between innate and immune systems [22] that includes inflammation and infiltration of the infarct area by immune cell subtypes (neutro...

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Ischemia/reperfusion‐induced necrosis and apoptosis in the cells isolated from rat skeletal muscle

Wang

Fang

Stephenson

et al. 2007

Journal Orthopaedic Research

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Necrosis was considered to be the solo mechanism for ischemia/reperfusion (I/R)-induced cell death. Recent evidence from I/R models of the heart, liver, kidney, and brain indicates that apoptosis is a major contributor to I/R-induced cell death. However, evidence of I/R-induced apoptosis in skeletal muscle is sparse and divided. The purpose for the present study was to investigate I/R-induced necrosis and apoptosis in the cells isolated from rat skeletal muscle. A rat gracilis muscle model was used. After surgical preparation, clamps were applied on the vascular pedicle to create 4 h of ischemia and released for 24 h of reperfusion (I/R, n ¼ 10). Clamping was omitted in sham I/R rats (sham I/R, n ¼ 10). The muscle samples were harvested after 24 h of reperfusion for the process of cell isolation. Cells were stained by Propidium Iodide (PI) or Annexin V-FITC or both. Twenty thousand cells from each muscle sample were scanned and analyzed by flow cytometry. The average percentage of live cells was 45 AE 2% in the I/R group versus 65 AE 3% in the sham I/R group (p < 0.01). The average percentage of necrotic cells was 18 AE 1% in I/R versus 12 AE 1% in sham I/R (p < 0.01). The average percentage of apoptotic cells was 40 AE 3% in I/R versus 27 AE 3% in sham I/R (p < 0.01). Our results clearly demonstrated that I/R not only causes necrosis, but also accelerates apoptosis in the cells isolated from rat skeletal muscle.ß

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NOS upregulation attenuates vascular endothelial dysfunction in the late phase of ischemic preconditioning in skeletal muscle

Cited by 28 publications

References 33 publications

Melatonin reduces ischemia/reperfusion‐induced superoxide generation in arterial wall and cell death in skeletal muscle

Melatonin reduces ischemia/reperfusion‐induced superoxide generation in arterial wall and cell death in skeletal muscle

Myocardial Infarction: Perspectives on Cardiac Regeneration and Cardiac Remote Conditioning Interventions to Limit Cellular Injury

Ischemia/reperfusion‐induced necrosis and apoptosis in the cells isolated from rat skeletal muscle

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