Oxidative stress and nitric oxide synthase in skeletal muscles of rats with post‐infarction, compensated chronic heart failure

Rush, James W. E.; Green, H. J.; MacLean, David A.; Code, L. M.

doi:10.1111/j.1365-201x.2005.01479.x

Cited by 23 publications

(23 citation statements)

References 32 publications

(55 reference statements)

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“…Hill et al 22 showed that SOD activity was unchanged in mild and moderate heart failure stages, but significantly depressed during the chronic period (16 weeks) subsequent to myocardial infarction in rats. Rush et al 23 also showed that 12 weeks after coronary artery ligation-induced moderate congestive heart failure in rats, SOD activity was decreased. The importance of SOD in attenuating ischemic/reperfusion injury has been demonstrated clearly by the use of transgenic animal models.…”

Section: Discussionmentioning

confidence: 93%

Novel biomarkers of bladder decompensation after partial bladder obstruction

Güven

Önal

Whitbeck

et al. 2007

Neurourology and Urodynamics

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Section: Discussionmentioning

confidence: 93%

Novel biomarkers of bladder decompensation after partial bladder obstruction

Güven

Önal

Whitbeck

et al. 2007

Neurourology and Urodynamics

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“…Additionally, after myocardial infarction, the soleus muscle in rats contains decreased endothelial NO levels (Rush et al 2005). TU induces a rapid and sustained increase in NO production and release at the stimulated site (Miura et al 2001;Olesen et al 1988), contributing to the vasodilation.…”

Section: Discussionmentioning

confidence: 98%

Ultrasound Modulates Skeletal Muscle Cytokine Levels in Rats with Heart Failure

Rossato

Lago

Hentschke

et al. 2015

Ultrasound in Medicine & Biology

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“…36 Recently, it has been demonstrated that muscles in both humans with chronic heart failure and CHF rats have a decreased level of antioxidant enzymes. 37,38 Thus, we propose that the faster fatigue development in CHF soleus fibers may be attributable to impaired mitochondrial function resulting in both increased dependence on anaerobic ATP production and an increased ROS production. …”

Section: Effects Of Chf On Fatigue Developmentmentioning

confidence: 94%

Effects of Congestive Heart Failure on Ca ²⁺ Handling in Skeletal Muscle During Fatigue

Lunde

Sejersted

Thorud

et al. 2006

Circulation Research

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Abstract-Skeletal muscle weakness and decreased exercise capacity are major symptoms reported by patients with congestive heart failure (CHF). Intriguingly, these skeletal muscle symptoms do not correlate with the decreased heart function. This suggests that CHF leads to maladaptive changes in skeletal muscles, and as reported most markedly in slow-twitch muscles. We used rats at 6 weeks after infarction to measure expression of key proteins involved in SR Ca 2ϩ release and uptake in slow-twitch soleus muscles. We also measured force and myoplasmic free [Ca 2ϩ ] ([Ca 2ϩ ] i ) in intact single fibers of soleus muscles. CHF rats showed clear signs of severe cardiac dysfunction with marked increases in heart weight and left ventricular end-diastolic pressure compared with sham operated rats (Sham). There were small, but significant, changes in the content of proteins involved in cellular Ca 2ϩ handling in CHF muscles: slight increases in SR Ca 2ϩ release channels (ie, the ryanodine receptors) and in SR Ca 2ϩ -ATPase. Tetanic force and [Ca 2ϩ ] i were not significantly different between CHF and Sham soleus fibers under resting conditions. However, during the stimulation period there was a decrease in tetanic force without changes in [Ca 2ϩ ] i in CHF fibers that was not observed in Sham fibers. The fatigue-induced changes recovered rapidly. We conclude that CHF soleus fibers fatigue more rapidly than Sham fibers because of a reversible fatigue-induced decrease in myofibrillar function. Key Words: skeletal muscle Ⅲ congestive heart failure Ⅲ muscle fatigue Ⅲ Ca 2ϩ P atients with congestive heart failure (CHF) frequently report skeletal muscle weakness and decreased fatigue resistance. These skeletal muscle symptoms are not correlated with the observed decrease in heart function. 1 This suggests that CHF leads to intrinsic defects in skeletal muscles, and several authors have described important functional and biochemical changes in skeletal muscle cells (for recent reviews see references 2-4). Even so, the mechanism(s) underlying the impaired skeletal muscle function in CHF remains unclear.Impaired sarcoplasmic reticulum (SR) Ca 2ϩ handling has been observed in skeletal muscle cells of rats with CHF induced by myocardial infarction. [5][6][7] Using a rat CHF model at 6 weeks after infarction, we could only detect a subtle slowing of the SR Ca 2ϩ reuptake in single fast-twitch fibers isolated from a foot muscle. 8 However, in our rat model of CHF, changes in contractile function during stimulation are more pronounced in slow-twitch than in fast-twitch skeletal muscle; slow-twitch soleus muscles of CHF rats showed a marked slowing of relaxation followed by a decrease in force development that was not seen in control muscles. 8,9 The aim of the present study was to determine whether skeletal muscle Ca 2ϩ handling and force production in CHF animals were changed at an early time point when changes in protein expression were minimal. Therefore we measured the expression of key proteins involved in SR Ca 2ϩ release ...

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Oxidative stress and nitric oxide synthase in skeletal muscles of rats with post‐infarction, compensated chronic heart failure

Abstract: These observations suggest a heretofore unreported muscle fibre-type-specific response of oxidative stress and NOS isoforms to CHF is of importance in understanding the cellular mechanisms of skeletal muscle dysfunction in CHF.

Cited by 23 publications

References 32 publications

Novel biomarkers of bladder decompensation after partial bladder obstruction

Novel biomarkers of bladder decompensation after partial bladder obstruction

Ultrasound Modulates Skeletal Muscle Cytokine Levels in Rats with Heart Failure

Effects of Congestive Heart Failure on Ca ²⁺ Handling in Skeletal Muscle During Fatigue

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Oxidative stress and nitric oxide synthase in skeletal muscles of rats with post‐infarction, compensated chronic heart failure

Abstract: These observations suggest a heretofore unreported muscle fibre-type-specific response of oxidative stress and NOS isoforms to CHF is of importance in understanding the cellular mechanisms of skeletal muscle dysfunction in CHF.

Cited by 23 publications

References 32 publications

Novel biomarkers of bladder decompensation after partial bladder obstruction

Novel biomarkers of bladder decompensation after partial bladder obstruction

Ultrasound Modulates Skeletal Muscle Cytokine Levels in Rats with Heart Failure

Effects of Congestive Heart Failure on Ca 2+ Handling in Skeletal Muscle During Fatigue

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Effects of Congestive Heart Failure on Ca ²⁺ Handling in Skeletal Muscle During Fatigue