Nitric oxide is not involved in the endotoxemia-induced alterations in Ca 2+ and ryanodine responses in mouse diaphragms

Liu, Shing‐Hwa; Lai, J L; Yang, Rong‐Sen; Lin‐Shiau, Shoei‐Yn

doi:10.1007/s00210-002-0597-z

Cited by 11 publications

(10 citation statements)

References 44 publications

(44 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A reduced ryanodineinduced contracture in diaphragm from septic mice (7.5 mg/kg LPS ip) that was reversed by the LPS inhibitor polymyxin B confirmed the involvement of LPS signaling on the sarcoplasmic reticulum regulation (433). This was explained by a similarly reduced SR Ca 2ϩ release by LPS.…”

Section: ؉ Transients In Critical Illnessmentioning

confidence: 54%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

293

329

View full text Add to dashboard Cite

Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. Some ICUAW forms require stringent diagnostic features; CIM is marked by membrane hypoexcitability, severe atrophy, preferential myosin loss, ultrastructural alterations, and inadequate autophagy activation while myopathies in pure sepsis do not reproduce marked myosin loss. Reduced membrane excitability results from depolarization and ion channel dysfunction. Mitochondrial dysfunction contributes to energy-dependent processes. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Myosin loss is more pronounced than actin loss in CIM. Protein quality control is altered by inadequate autophagy. Ca 2ϩ dysregulation is present through altered Ca 2ϩ homeostasis. We highlight clinical hallmarks, trigger factors, and potential mechanisms from human studies and animal models that allow separation of risk factors that may trigger distinct mechanisms contributing to weakness. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. Future challenges include identification of primary/secondary events during the time course of critical illness, the interplay between membrane excitability, bioenergetic failure and differential proteolysis, and finding new therapeutic targets by help of tailored animal models.

show abstract

Section: ؉ Transients In Critical Illnessmentioning

confidence: 54%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

293

329

View full text Add to dashboard Cite

show abstract

“…For example, Benson et al showed that Ca ++ uptake and content in limb skeletal muscle are increased during sepsis and that these high Ca ++ concentrations are critically involved in regulation of muscle protein breakdown in sepsis (91). On the other hand, Liu investigated the in vivo effects of lipopolysaccharide on the Ca ++ -dependent mechanical activity and ryanodine response in isolated sarcoplasmic reticulum membrane vesicles from the mouse diaphragm, demonstrating that Ca ++ release and [3H]ryanodine binding in sarcoplasmic reticulum membrane vesicles of lipopolysaccharide-treated animals were significantly depressed (92) (Fig. 5).…”

Section: Sarcoplasmic Reticulummentioning

confidence: 99%

“…* p < .05 as compared with control; ** p < .05 as compared with LPS group. Reproduced with permission from Liu et al (92). …”

Section: Figurementioning

confidence: 99%

Sepsis-induced myopathy

Callahan

Supinski²

2009

Critical Care Medicine

228

194

View full text Add to dashboard Cite

Sepsis is a major cause of morbidity and mortality in critically ill patients, and despite advances in management, mortality remains high. In survivors, sepsis increases the risk for the development of persistent acquired weakness syndromes affecting both the respiratory muscles and the limb muscles. This acquired weakness results in prolonged duration of mechanical ventilation, difficulty weaning, functional impairment, exercise limitation, and poor health-related quality of life. Abundant evidence indicates that sepsis induces a myopathy characterized by reductions in muscle force-generating capacity, atrophy (loss of muscle mass), and altered bioenergetics. Sepsis elicits derangements at multiple subcellular sites involved in excitation contraction coupling, such as decreasing membrane excitability, injuring sarcolemmal membranes, altering calcium homeostasis due to effects on the sarcoplasmic reticulum, and disrupting contractile protein interactions. Muscle wasting occurs later and results from increased proteolytic degradation as well as decreased protein synthesis. In addition, sepsis produces marked abnormalities in muscle mitochondrial functional capacity and when severe, these alterations correlate with increased death. The mechanisms leading to sepsis-induced changes in skeletal muscle are linked to excessive localized elaboration of proinflammatory cytokines, marked increases in free-radical generation, and activation of proteolytic pathways that are upstream of the proteasome including caspase and calpain. Emerging data suggest that targeted inhibition of these pathways may alter the evolution and progression of sepsis-induced myopathy and potentially reduce the occurrence of sepsis-mediated acquired weakness syndromes.

show abstract

“…In skeletal muscle, the sarcoplasmic reticulum contributes to calcium homeostasis and is the organelle responsible in muscle for calcium binding and release. Sepsis has marked effects on calcium homeostasis, increasing intracellular calcium in limb skeletal muscle [86], reducing calcium binding in isolated sarcoplasmic reticular membrane [90], decreasing release of calcium from the sarcoplasmic reticulum and increasing the sensitivity of contractile proteins to calcium [91]. Several of these activities (e.g.…”

Section: Altered Function Of the Sarcoplasmic Reticulummentioning

confidence: 99%

Molecular mechanisms of intensive care unit-acquired weakness

Bloch¹,

Polkey²,

Griffiths³

et al. 2011

Eur Respir J

View full text Add to dashboard Cite

Intensive care unit-acquired weakness (ICUAW) is an increasingly recognised and important clinical consequence of critical illness. It is associated with significant morbidity and mortality. The aetiology of this disease is not well understood. The purpose of this article is to review our understanding of the molecular pathogenesis of ICUAW in the context of current knowledge of clinical risk factors and aetiology.Key features of the disease are loss of muscle mass resulting from a shift in the dynamic balance of muscle protein synthesis and breakdown and a reduction in force-generating capacity. These alternations are secondary to neuropathy, disruption of the myofilament structure and function, a disrupted sarcoplasmic reticulum, electrical inexcitability and bioenergenetic failure.As knowledge and understanding of ICUAW grows, potential therapeutic targets will be identified, hopefully leading to multiple strategies for prevention and treatment of this important condition.

show abstract

Nitric oxide is not involved in the endotoxemia-induced alterations in Ca 2+ and ryanodine responses in mouse diaphragms

Cited by 11 publications

References 44 publications

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Sepsis-induced myopathy

Molecular mechanisms of intensive care unit-acquired weakness

Contact Info

Product

Resources

About