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Peripheral Muscle (peripheral + muscle)
Selected AbstractsLow-dose metformin improves hyperglycaemia related to myotonic dystrophyDIABETIC MEDICINE, Issue 3 2005T. Kouki Abstract Background One of the clinical features of myotonic dystrophy is insulin resistance with non-obese diabetes mellitus (DM). Recently, the mechanism of insulin resistance in patients with myotonic dystrophy was revealed. The optimal treatment of DM with myotonic dystrophy has not been established. We report the effect of metformin in a patient with myotonic dystrophy without obesity. Case report A 58-year-old woman (BMI = 22.1 kg/m2) with myotonic dystrophy and DM was followed at our clinic. She had been treated with glimepiride for DM for the last 6 months, without achieving good control (HbA1c 9.3%). She was admitted with congestive heart failure and cholecystitis. She was treated with diuretics, antibiotics and insulin. As her blood glucose fell, we discontinued insulin and started glimepiride, but her glycaemic control had worsened. We started metformin instead of glimepiride. After 4 weeks of metformin, HbA1c was decreased to 7.4%, while HOMA-IR during glimepiride treatment was 4.9, and 3.7 with metformin. Three months later, HbA1c was maintained (7.5%). Conclusion It is important to choose the optimal treatment for DM in myotonic dystrophy, because the patients have hyperinsulinemia caused by specific mechanism and could not reduce the insulin resistance. Metformin improved hyperglycemia through increased insulin-independent glucose uptake in peripheral muscle. We believe metformin is the optimal agent for these patients. [source] Electroporation-mediated interleukin-10 overexpression in skeletal muscle reduces acute rejection in rat cardiac allograftsTHE JOURNAL OF GENE MEDICINE, Issue 2 2006Reza Tavakoli Abstract Objectives Human interleukin 10 (hIL-10) may reduce acute rejection after organ transplantation. Our previous data shows that electroporation-mediated transfer of plasmid DNA to peripheral muscle enhances gene transduction dramatically. This study was designed to investigate the effect of electroporation-mediated overexpression of hIL-10 on acute rejection of cardiac allografts in the rat. Methods The study was designed to evaluate the effect of hIL-10 gene transfer on (a) early rejection pattern and (b) graft survival. Gene transfer was achieved by intramuscular (i.m.) injection into the tibialis anterior muscle of Fischer (F344) male recipients followed by electroporation 24 h prior to transplantation. Heterotopic cardiac transplantation was performed from male Brown Norway rat to F344. Four groups were studied (n = 6). Treated animals in groups B1 and B2 received 2.5 µg of pCIK hIL-10 and control animals in groups A1 and A2 distilled water. Graft function was assessed by daily palpation. Animals from group A1 were sacrificed at the cessation of the heart beat of the graft and those in group B1 were sacrificed at day 7; blood was taken for ELISA measurement of hIL-10 and tissue for myeloperoxidase (MPO) measurement and histological assessment. To evaluate graft survival, groups A2 and B2 were sacrificed at cessation of the heart beat of the graft. Results Histological examination revealed severe rejection (IIIB-IV) in group A1 in contrast to low to moderate rejection (IA-IIIA) in group B1 (p = 0.02). MPO activity was significantly lower in group B1 compared to group A1 (18 ± 7 vs. 32 ± 14 mU/mg protein, p = 0.05). Serum hIL-10 levels were 46 ± 13 pg/ml in group B1 vs. 0 pg/ml in group A1. At day 7 all heart allografts in the treated groups B1 and B2 were beating, whereas they stopped beating at 5 ± 2 days in groups A1 and A2 vs. 14 ± 2 days in group B2 (p = 0.0012). Conclusions Electroporation-mediated intramuscular overexpression of hIL-10 reduces acute rejection and improves survival of heterotopic heart allografts in rats. This study demonstrates that peripheral overexpression of specific genes in skeletal muscle may reduce acute rejection after whole organ transplantation. Copyright © 2006 John Wiley & Sons, Ltd. [source] Influence of chronic hypoxemia on peripheral muscle function and oxidative stress in humansCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 2 2004Marion Faucher Summary Transient re-oxygenation of humans suffering from chronic obstructive pulmonary disease (COPD) allows the assessment of the consequences of chronic hypoxemia on peripheral muscle and metabolism apart from the effects of de-conditioning. The subjects performed maximal voluntary contractions (MVC) of flexor digitorum and vastus lateralis muscles and sustained infra-maximal contractions. COPD patients repeated the whole challenge during a 50-min oxygen breathing period and after recovery to baseline hypoxemia. We measured the compound evoked muscle mass action potential (M-wave) and the medium frequency (MF) of surface electromyography (EMG) power spectrum. Blood lactate (LA) and potassium (K+), erythrocyte-reduced glutathione (GSH), and plasma thiobarbituric acid reactive substances (TBARS) were also measured. Compared with a control group, COPD patients had lower MVCs, an attenuated decrease in MF during exercise, lower resting level of GSH, no posthandgrip TBARS increase and no GSH consumption. Reoxygenation (1) increased MVCs, (2) accentuated the MF decline and (3) elicited a posthandgrip TBARS increase and GSH consumption. Thus, we conclude that chronic hypoxemia exerts specific muscular effects: a reduced force production, an attenuated ,muscle wisdom', and the suppression of the exercise oxidative stress. [source] Effects of SZ1677, a new non-depolarizing steroidal neuromuscular blocking drug, and rocuronium on two laryngeal muscles and the anterior tibial muscle in guinea pigsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2006A. Michalek-Sauberer Background:, SZ1677 is a new neuromuscular blocking drug structurally related to rocuronium. We compared the effect of an ED90 of SZ1677 (25 ,g/kg) with that of rocuronium (100 ,g/kg) in guinea pig laryngeal and peripheral muscles. Methods:, Electromyography was used to quantify neuromusc-ular blockade at the posterior cricoarytenoid muscle, the thyroarytenoid muscle and the anterior tibial muscle after SZ1677 (n = 10) and rocuronium (n = 9). Results:, Maximum neuromuscular blockade was similar after SZ1677 and rocuronium (83 ± 11% vs. 89 ± 11%; thyroarytenoid muscle: 91 ± 8% vs. 97 ± 3%; anterior tibial muscle: 91 ± 15% vs. 96 ± 3%, respectively). Onset time of neuromuscular blockade at the laryngeal muscles was similar for the two neuromuscular blocking drugs; it was shorter at the thyroarytenoid muscle (67 ± 32 s vs. 42 ± 40 s) than at the posterior cricoarytenoid muscle (101 ± 26 s vs. 102 ± 108 s). Onset time at the anterior tibial muscle was longer after SZ1677 (114 ± 34 s) than after rocuronium (68 ± 46 s); P < 0.05. Neuromuscular recovery was faster after SZ1677 (interval 25%,75%: posterior cricoarytenoid muscle: 222 ± 66 s; thyroarytenoid muscle: 192 ± 92 s; tibial muscle 149 ± 55 s) than after rocuronium (450 ± 148 and 464 ± 183 s, 292 ± 86 s, respectively); P < 0.05. Conclusions:, In guinea pigs, SZ1677 offers a rapid onset of neuromuscular blockade at a laryngeal adductor muscle with a shorter duration than rocuronium. Regardless of the drug used, the course of neuromuscular blockade differs not only between peripheral muscles and the larynx but also between antagonistic laryngeal muscles. The differences seem to be species specific. [source] Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemiaCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2009Tessa A. C. Nizet Summary Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO2). Acute metabolic acidosis was induced by administration of ammonium chloride (NH4Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33·2 ± 11·5 years; FEV1 108·3 ± 16·2% predicted), 14 asthma patients (5 male; age 48·1 ± 16·1 years; FEV1 101·6 ± 15·3% predicted), and 15 moderate to severe COPD patients (9 male; age 62·8 ± 6·8 years; FEV1 50·0 ± 11·8% predicted). An acute metabolic acidemia of BE ,3·1 mmol.L,1 was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference ,0·1 kPa.sec.L,1 [95%-CI: ,0·1 ,,0·02]. In COPD patients PaCO2 was significantly lowered during metabolic acidemia (mean difference ,1·73 mmHg [,3·0 ,,0·08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure. [source] | ||||||||||