Involvement of nitric oxide in the in vivo effects of lipopolysaccharide on the contractile and electrical properties of mouse diaphragm

Liu, Shing‐Hwa; Lai, J L; Lin, Ruey-Hseng; Lin, Min-Jon; Lin‐Shiau, Shoei‐Yn

doi:10.1007/pl00005083

Cited by 5 publications

(6 citation statements)

References 31 publications

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“…Perhaps the differences between Liu et al (who report increases in force, Ref. 129) and Comtois et al (who show protection from a decrease, Ref. 50) can be explained by the endotoxin concentrations they used, which were four times higher (25 mg/kg) in the animals exhibiting the decline in force.…”

Section: E Cytokinesmentioning

confidence: 87%

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Physiology of Nitric Oxide in Skeletal Muscle

Stamler

Meissner

2001

Physiological Reviews

931

773

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In the past five years, skeletal muscle has emerged as a paradigm of "nitric oxide" (NO) function and redox-related signaling in biology. All major nitric oxide synthase (NOS) isoforms, including a muscle-specific splice variant of neuronal-type (n) NOS, are expressed in skeletal muscles of all mammals. Expression and localization of NOS isoforms are dependent on age and developmental stage, innervation and activity, history of exposure to cytokines and growth factors, and muscle fiber type and species. nNOS in particular may show a fast-twitch muscle predominance. Muscle NOS localization and activity are regulated by a number of protein-protein interactions and co- and/or posttranslational modifications. Subcellular compartmentalization of the NOSs enables distinct functions that are mediated by increases in cGMP and by S-nitrosylation of proteins such as the ryanodine receptor-calcium release channel. Skeletal muscle functions regulated by NO or related molecules include force production (excitation-contraction coupling), autoregulation of blood flow, myocyte differentiation, respiration, and glucose homeostasis. These studies provide new insights into fundamental aspects of muscle physiology, cell biology, ion channel physiology, calcium homeostasis, signal transduction, and the biochemistry of redox-related systems.

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Section: E Cytokinesmentioning

confidence: 87%

“…Liu et al (129) suggest that endotoxin (7.5 mg/kg) may even increase twitch and tetanic force (of mouse diaphrgam) in a NO-dependent manner (129). These effects were attributed to decreases in chloride conductance that depolarize and thereby activate muscle.…”

Section: E Cytokinesmentioning

confidence: 99%

Physiology of Nitric Oxide in Skeletal Muscle

Stamler

Meissner

2001

Physiological Reviews

931

773

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“…In another mouse LPSinduced sepsis model, Liu et al (432) observed a marked depolarization in the diaphragm and increased input resistance due to an endotoxin-induced shutdown of sarcolemmal chloride conductance while K ϩ conductance was unaltered. NO synthase (NOS) inhibitors reversed the observed effects arguing in favor of an NO-mediated alteration of chloride conductance that was also confirmed by the fact that in vitro application of LPS by itself to diaphragm was not able to reproduce the membrane effects seen in the septic mouse, whereas addition of an NO donor was (432). In the CIM model of steroid denervation (SD), a downregulation of Cl Ϫ conductance was not seen with SD but only following denervation alone (582).…”

Section: Membrane Depolarization In Muscle In Critical Illnessmentioning

confidence: 97%

“…rate coma in patients with acute neurologic injury: by decreasing metabolic demand during a period of cell stress, it might increase cell survival to improve long-term outcome (319,432,604).…”

Section: Are Electrically Active Tissues Other Than Skeletal Muscle Amentioning

confidence: 99%

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

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

293

329

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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.

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“…Expression of inducible NO synthase in diaphragm during endotoxemia has been identified (Thompson et al 1996;Hussain et al 1997). Recently, some studies have also shown that NO may be involved in the endotoxin-induced sarcolemmal damage and altered electrical properties in diaphragm (Liu et al 1997;Lin et al 1998). The role of NO in the regulation of Ca 2+ release from sarcoplasmic reticulum of skeletal muscle during endotoxemia remains unclear.…”

Section: Introductionmentioning

confidence: 97%

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

Liu

Lai

Yang

et al. 2002

Naunyn-Schmiedeberg's Archives of Pharmacology

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Lipopolysaccharide (LPS, endotoxin)-induced diaphragmatic contractile dysfunction and sarcolemmal injury in animals has been identified. However, the precise nature of sepsis-related alterations in diaphragm myofiber function and the activity of Ca(2+) release from sarcoplasmic reticulum of skeletal muscle remain unclear. The present study investigated the in vivo effects of LPS on the Ca(2+)-dependent mechanical activity and ryanodine response in mouse diaphragm and Ca(2+) release from isolated sarcoplasmic reticulum membrane vesicles, and aimed to examine the role of nitric oxide (NO) in these responses. When diaphragms were bathed in a solution that was Cl(-)-free, Na(+)-free, but contained high K(+), a Ca(2+)-induced contracture was elicited. Increases in external Ca(2+) concentration produced increases in peak tension of Ca(2+)-induced contracture in control diaphragm, while a decrease was seen in endotoxemic diaphragm. Ryanodine induced a marked contracture in control diaphragms, which was diminished after endotoxemia. This finding is correlated with the decrease of ryanodine-induced Ca(2+) release and the suppression of [(3)H]ryanodine binding on the isolated SR of the skeletal muscle from LPS-treated rats. In mice treated with LPS significantly increased levels of plasma nitrite and serum TNF-alpha were observed, changes inhibited by aminoguanidine [an inhibitor of inducible NO synthase (iNOS)] and pentoxifylline (an inhibitor of tumor necrosis factor-alpha formation), respectively. Moreover, LPS treatment resulted in a significant expression of mRNA for iNOS in mouse diaphragms. The inhibitory effects on Ca(2+)- and ryanodine responses by LPS could be prevented by treatment with polymyxin B (LPS neutralizer) and pentoxifylline, but not by treatment with dexamethasone, N(G)-nitro- L-arginine or aminoguanidine (NOS inhibitors). These results imply that the NO-related pathway may not be involved in the dysfunction of the Ca(2+) release mechanism in the sarcoplasmic reticulum of mouse diaphragm during endotoxemia.

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Involvement of nitric oxide in the in vivo effects of lipopolysaccharide on the contractile and electrical properties of mouse diaphragm

Cited by 5 publications

References 31 publications

Physiology of Nitric Oxide in Skeletal Muscle

Physiology of Nitric Oxide in Skeletal Muscle

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

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

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