Temperature dependence of rat diaphragm muscle contractility and fatigue

Prezant, David J.; Richner, Beat; Valentine, D. E.; Aldrich, Thomas K.; Fishman, Charles L.; Nagashima, Hideo; Chaudhry, I.; Cahill, John

doi:10.1152/jappl.1990.69.5.1740

Cited by 25 publications

(26 citation statements)

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“…All contraction experiments were done at 37° C. Although this temperature deviates from previously established guidelines, it better reflects the physiological temperature for in vivo diaphragm contraction, and thus maximizes extrapolation of the data obtained to the physiological in vivo situation. Moreover, this temperature is inline with our own previous studies (2,25,26), and similar/ identical experiments have been done by other laboratories (27)(28)(29), indicating feasibility of bodytemperature experiments. The muscle was then stretched to the length where twitch contractions are optimal, and allowed to rest for 10 min.…”

Section: Diaphragm Force Measurementssupporting

confidence: 90%

Peptide-Based Inhibition of NF-κB Rescues Diaphragm Muscle Contractile Dysfunction in a Murine Model of Duchenne Muscular Dystrophy

Peterson

Kline

Canan

et al. 2011

Mol Med

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Deterioration of diaphragm function is one of the prominent factors that contributes to the susceptibility of serious respiratory infections and development of respiratory failure in patients with Duchenne Muscular Dystrophy (DMD). The NF-κB signaling pathway has been implicated as a contributing factor of dystrophic pathology, making it a potential therapeutic target. Previously, we demonstrated that pharmacological inhibition of NF-κB via a small NEMO Binding Domain (NBD) peptide was beneficial for reducing pathological features of mdx mice. Now, we stringently test the effectiveness and clinical potential of NBD by treating mdx mice with various formulations of NBD and use diaphragm function as our primary outcome criteria. We found that administering DMSO-soluble NBD rescued 78% of the contractile deficit between mdx and wild-type (WT) diaphragm. Interestingly, synthesis of a GLP NBD peptide as an acetate salt permitted its solubility in water, but as a negative consequence, also greatly attenuated functional efficacy. However, replacing the acetic acid counterion of the NBD peptide with trifluoroacetic acid retained the peptide's water solubility and significantly restored mdx diaphragm contractile function and improved histopathological indices of disease in both diaphragm and limb muscle. Together, these results support the feasibility of using a mass-produced, water-soluble NBD peptide for clinical use.

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Section: Diaphragm Force Measurementssupporting

confidence: 90%

Peptide-Based Inhibition of NF-κB Rescues Diaphragm Muscle Contractile Dysfunction in a Murine Model of Duchenne Muscular Dystrophy

Peterson

Kline

Canan

et al. 2011

Mol Med

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“…The in vitro diaphragm costal muscle strip preparation used in this study has been described previously [27]. The diaphragm and adjacent rib sections were removed en bloc in <5 min and placed in a dissection tray filled with modified Krebs-Ringer bicarbonate (KRB; pH 7.42) solution (in mM: glucose, 11.5; NaCl, 138; KCl, 5.9; CaCl 2 , 1.4; MgSO 4 , 0.9; NaH 2 PO 4 , 1.2; and NaHCO 3 , 25) and aerated continuously with 95% O 2 and 5% CO 2 .…”

Section: In Vitro Contractility/fatigue Protocolmentioning

confidence: 99%

“…Baseline single twitch (2-ms impulse duration at supramaximal voltage) and tetanic forces (400-ms trains of 2-ms impulses delivered at 2-min intervals at 10, 20, 60, and 100 Hz) were measured and then repeated to ensure reproducibility. At 37°C, a force plateau is reached after 400 ms of stimulation, and maximum tetanic force occurs at 100 Hz [27]. Time to peak contraction (CT) and half relaxation (RT-1/2) times were measured for single twitches.…”

Section: In Vitro Contractility/fatigue Protocolmentioning

confidence: 99%

Short Term vs Long Term Dexamethasone Treatment: Effects on Rat Diaphragm Structure and Function

Prezant

Richner

Maggiore

et al. 1998

Lung

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The effects of dexamethasone treatment duration (2.5 vs 10 weeks) on diaphragm myosin heavy chain isoforms, fiber types, and contractile characteristics were studied in male rats. Compared with ad libitum-fed and pair-fed controls, dexamethasone significantly decreased body weight, costal diaphragm weight, and the relative expression of myosin heavy chain isoform MHC-2B. Compared with pair-fed controls, the effect on MHC-2B expression was greater after 10 weeks than after 2.5 weeks. Type I and type II costal diaphragm fiber atrophy occurred, and type II fiber atrophy was greater after 10 weeks. Costal diaphragm-specific forces were not affected significantly by dexamethasone, regardless of the treatment duration or control group comparison. Fatigue resistance indexes were increased significantly after long term treatment compared with pair-fed controls and after both short-term and long-term treatment compared with ad libitum-fed controls. In conclusion, the effects of dexamethasone on MHC isoform phenotype expression, fiber type costal diaphragm atrophy, and fatigue resistance were dependent on treatment duration, with greater effects after long-term (10 weeks) treatment.

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“…The muscle strip was suspended vertically in a 100-ml organ bath filled with Krebs-Ringer bicarbonate solution at 30°C [14]and continuously aerated as described above. The central tendon was anchored to a fixed hook at the base of the organ bath using silk thread while the costal margin was sutured to a hook extending from a Washington polygraph (model 400MDI).…”

Section: Methodsmentioning

confidence: 99%

An Investigation into the Mechanism of Action of Almitrine on Isolated Rat Diaphragm Muscle Fatigue

Markos

Campion²,

Carey³

et al. 2002

Respiration

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Background: Previous studies have shown that almitrine bismesylate, a respiratory stimulant which acts on the mitochondrial electron transport chain, enhances recovery of rat diaphragm muscle from fatigue. Objectives: Our aim is to investigate if the enhanced recovery is due to an anti-oxidant property of almitrine, since the electron transport chain is a major site of intracellular free radical production. Methods: A low-frequency fatigue protocol was used (30 Hz; 250 ms; delivered once every 2 s for 5 min), and the effects of almitrine before and after fatigue onset were compared to those of the anti-oxidant compound N-acetylcysteine (NAC). Results: Almitrine (6 and 10 µg/ml) given before fatigue gave better recovery rates than postfatigue application. In contrast, NAC (100 µM) application before fatigue onset was not as effective as NAC given immediately after the cessation of the fatigue protocol. However, almitrine (6 µg/ml) completely reversed the reduction in baseline twitch tension brought about by a free-radical-producing mixture of FeCl₃ + ADP (1 mM + 2.5 mM, respectively). Conclusion: The results of this study confirm that almitrine enhances recovery from fatigue and, in contrast to NAC prefatigue application, is more effective. Also, almitrine was shown to have an anti-oxidant effect, but it does not act like a typical anti-oxidant.

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Temperature dependence of rat diaphragm muscle contractility and fatigue

Cited by 25 publications

References 0 publications

Peptide-Based Inhibition of NF-κB Rescues Diaphragm Muscle Contractile Dysfunction in a Murine Model of Duchenne Muscular Dystrophy

Peptide-Based Inhibition of NF-κB Rescues Diaphragm Muscle Contractile Dysfunction in a Murine Model of Duchenne Muscular Dystrophy

Short Term vs Long Term Dexamethasone Treatment: Effects on Rat Diaphragm Structure and Function

An Investigation into the Mechanism of Action of Almitrine on Isolated Rat Diaphragm Muscle Fatigue

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