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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

Reappearance of indirect muscle twitches in PTX-treated mice during re-oxygenation (control, n = 6, PTX-treated, n = 12, *P < 0.05); P < 0.05, the Mann-Whitney U-test
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Figure 0004: Reappearance of indirect muscle twitches in PTX-treated mice during re-oxygenation (control, n = 6, PTX-treated, n = 12, *P < 0.05); P < 0.05, the Mann-Whitney U-test

Mentions: Re-oxygenation was instated in all preparations after completion of neuromuscular transmission failure. During 30 min of re-oxygenation, indirect muscle twitches reappeared, hypoxic contracture returned to the baseline, and muscle contractility partially recovered [Figure 3]. Indirect muscle twitches reappeared 1.4 ± 0.2 min after re-oxygenation in the control group and 1.8 ± 0.2 min later in the PTX group [P < 0.05, Figure 4]. In this period, amplitudes of direct and indirect contractions of the diaphragm muscles prepared from the PTX-treated mice were significantly greater [P < 0.01, Figure 3]. However, the rate of recovery of muscle contractility upon re-oxygenation was slower in the PTX group. At the end of the re-oxygenation period, direct muscle contractions in the control group recovered to 82% of the baseline values and indirect contractions recovered to 65%. These ratios in the PTX group were 63% for direct contractions and 61% for indirect contractions.


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

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

Reappearance of indirect muscle twitches in PTX-treated mice during re-oxygenation (control, n = 6, PTX-treated, n = 12, *P < 0.05); P < 0.05, the Mann-Whitney U-test
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 0004: Reappearance of indirect muscle twitches in PTX-treated mice during re-oxygenation (control, n = 6, PTX-treated, n = 12, *P < 0.05); P < 0.05, the Mann-Whitney U-test
Mentions: Re-oxygenation was instated in all preparations after completion of neuromuscular transmission failure. During 30 min of re-oxygenation, indirect muscle twitches reappeared, hypoxic contracture returned to the baseline, and muscle contractility partially recovered [Figure 3]. Indirect muscle twitches reappeared 1.4 ± 0.2 min after re-oxygenation in the control group and 1.8 ± 0.2 min later in the PTX group [P < 0.05, Figure 4]. In this period, amplitudes of direct and indirect contractions of the diaphragm muscles prepared from the PTX-treated mice were significantly greater [P < 0.01, Figure 3]. However, the rate of recovery of muscle contractility upon re-oxygenation was slower in the PTX group. At the end of the re-oxygenation period, direct muscle contractions in the control group recovered to 82% of the baseline values and indirect contractions recovered to 65%. These ratios in the PTX group were 63% for direct contractions and 61% for indirect contractions.

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