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The effects of pentoxifylline on skeletal muscle contractility and neuromuscular transmission during hypoxia.

Simsek-Duran F, Ertunc M, Onur R - Indian J Pharmacol (2009)

Bottom Line: Re-oxygenation reduced contracture and indirect muscle contractions resumed.The rate of recovery of contractions was faster (P < 0.05) and the amplitude of contractions was greater (P < 0.01) in the PTX group.These results may implicate important clinical consequences for clinical usage of PTX in hypoxia-related conditions.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Faculty of Medicine, Hacettepe University, 06100 Sihhiye, Ankara, Turkey.

ABSTRACT

Objectives: The objective of this study was to investigate the effects of pentoxifylline (PTX), a drug that is mainly used for indications related to tissue hypoxia, on hypoxia-induced inhibition of skeletal muscle contractility and neuromuscular transmission in mice. We hypothesized that chronic PTX treatment alters skeletal muscle contractility and hypoxia-induced dysfunction.

Materials and methods: Mice were treated with 50 mg/kg PTX or saline intraperitoneally for a week. Following ether anesthesia, diaphragm muscles were removed; isometric muscle contractions and action potentials were recorded. Time to reach neuromuscular blockade and the rate of recovery of muscle contractility were assessed during hypoxia and re-oxygenation.

Results: The PTX group displayed 90% greater twitch amplitudes (P < 0.01). Hypoxia depressed twitch contractions and caused neuromuscular blockade in both groups. However, neuromuscular blockade occurred earlier in PTX-treated animals (P < 0.05). Muscle contractures developed during hypoxia were more pronounced in the PTX group (P < 0.05). Re-oxygenation reduced contracture and indirect muscle contractions resumed. The rate of recovery of contractions was faster (P < 0.05) and the amplitude of contractions was greater (P < 0.01) in the PTX group. PTX treatment increased amplitude (P < 0.05) and shortened action potential (P < 0.05) without altering resting membrane potential, excitation threshold, and neurotransmitter release.

Conclusion: Chronic PTX treatment increases diaphragm contractility, but amplifies hypoxia-induced contractile dysfunction in mice. These results may implicate important clinical consequences for clinical usage of PTX in hypoxia-related conditions.

No MeSH data available.


Related in: MedlinePlus

Effects of hypoxia on diaphragm muscles obtained from PTX-treated mice. After 15 min of the oxygenation period, hypoxia was instated by 95% N2 + 5% CO2 until neuromuscular blockade occurred (control, n = 6 and PTX, n = 12, *P < 0.01); P < 0.01, two-way ANOVA, post hoc Bonferroni
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Figure 0001: Effects of hypoxia on diaphragm muscles obtained from PTX-treated mice. After 15 min of the oxygenation period, hypoxia was instated by 95% N2 + 5% CO2 until neuromuscular blockade occurred (control, n = 6 and PTX, n = 12, *P < 0.01); P < 0.01, two-way ANOVA, post hoc Bonferroni

Mentions: PTX treatment increased contractility of the diaphragm muscles. Amplitudes of direct and indirect isometric muscle contractions in the PTX-treated group were greater than controls. Diaphragm muscles prepared from the control animals had twitch contraction amplitudes of 22.2 ± 4.5 g/g and 10.0 ± 1.4 g/g, upon direct and indirect stimulation, respectively. Muscles obtained from PTX-treated animals displayed about 90% greater contraction amplitudes for both types of stimulation [Figure 1, P < 0.01].


The effects of pentoxifylline on skeletal muscle contractility and neuromuscular transmission during hypoxia.

Simsek-Duran F, Ertunc M, Onur R - Indian J Pharmacol (2009)

Effects of hypoxia on diaphragm muscles obtained from PTX-treated mice. After 15 min of the oxygenation period, hypoxia was instated by 95% N2 + 5% CO2 until neuromuscular blockade occurred (control, n = 6 and PTX, n = 12, *P < 0.01); P < 0.01, two-way ANOVA, post hoc Bonferroni
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2812779&req=5

Figure 0001: Effects of hypoxia on diaphragm muscles obtained from PTX-treated mice. After 15 min of the oxygenation period, hypoxia was instated by 95% N2 + 5% CO2 until neuromuscular blockade occurred (control, n = 6 and PTX, n = 12, *P < 0.01); P < 0.01, two-way ANOVA, post hoc Bonferroni
Mentions: PTX treatment increased contractility of the diaphragm muscles. Amplitudes of direct and indirect isometric muscle contractions in the PTX-treated group were greater than controls. Diaphragm muscles prepared from the control animals had twitch contraction amplitudes of 22.2 ± 4.5 g/g and 10.0 ± 1.4 g/g, upon direct and indirect stimulation, respectively. Muscles obtained from PTX-treated animals displayed about 90% greater contraction amplitudes for both types of stimulation [Figure 1, P < 0.01].

Bottom Line: Re-oxygenation reduced contracture and indirect muscle contractions resumed.The rate of recovery of contractions was faster (P < 0.05) and the amplitude of contractions was greater (P < 0.01) in the PTX group.These results may implicate important clinical consequences for clinical usage of PTX in hypoxia-related conditions.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Faculty of Medicine, Hacettepe University, 06100 Sihhiye, Ankara, Turkey.

ABSTRACT

Objectives: The objective of this study was to investigate the effects of pentoxifylline (PTX), a drug that is mainly used for indications related to tissue hypoxia, on hypoxia-induced inhibition of skeletal muscle contractility and neuromuscular transmission in mice. We hypothesized that chronic PTX treatment alters skeletal muscle contractility and hypoxia-induced dysfunction.

Materials and methods: Mice were treated with 50 mg/kg PTX or saline intraperitoneally for a week. Following ether anesthesia, diaphragm muscles were removed; isometric muscle contractions and action potentials were recorded. Time to reach neuromuscular blockade and the rate of recovery of muscle contractility were assessed during hypoxia and re-oxygenation.

Results: The PTX group displayed 90% greater twitch amplitudes (P < 0.01). Hypoxia depressed twitch contractions and caused neuromuscular blockade in both groups. However, neuromuscular blockade occurred earlier in PTX-treated animals (P < 0.05). Muscle contractures developed during hypoxia were more pronounced in the PTX group (P < 0.05). Re-oxygenation reduced contracture and indirect muscle contractions resumed. The rate of recovery of contractions was faster (P < 0.05) and the amplitude of contractions was greater (P < 0.01) in the PTX group. PTX treatment increased amplitude (P < 0.05) and shortened action potential (P < 0.05) without altering resting membrane potential, excitation threshold, and neurotransmitter release.

Conclusion: Chronic PTX treatment increases diaphragm contractility, but amplifies hypoxia-induced contractile dysfunction in mice. These results may implicate important clinical consequences for clinical usage of PTX in hypoxia-related conditions.

No MeSH data available.


Related in: MedlinePlus