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Biomedical subjects

A McArdle

Publications and source records attributed to A McArdle.

At least 37 records · Page 2Linked to original sources
PubMed1999

Free radical activity following contraction-induced injury to the extensor digitorum longus muscles of rats.

The purpose of the study was to investigate the role of free radicals in the injury induced by a protocol of repeated pliometric (lengthening) contractions to the extensor digitorum longus (EDL) muscle in situ in rats. Previous data have indicated that prior treatment with the antioxidant polyethylene glycol-superoxide dismutase reduced the damage that was apparent at 3 days following this type of exercise. Three hours and 3 days following the protocol, the magnitude of the semiquinone-derived free radical signal observed by electron spin resonance spectroscopy (ESR) was not different for exercised and non-exercised skeletal muscles. A reduction in the protein thiol content of muscle was evident at 3 h, and was still apparent at 3 days. Three hours after the protocol, the total muscle glutathione content and the percentage in the oxidized form were unchanged, but by 3 days the percentage of muscle glutathione present in the oxidized form was elevated. The susceptibility of muscle to lipid peroxidation in vitro was reduced 3 days after the pliometric contractions. These data indicate that oxidation of protein thiols and glutathione may be involved in the secondary damage following pliometric contractions, but provide no evidence that the species involved were derived from mitochondrial semiquinone radicals.

Animals↗
PubMed1999

Apoptosis in multinucleated skeletal muscle myotubes.

Several recent studies report endonuclease-mediated DNA degradation as evidence of apoptotic degeneration of skeletal muscle in the muscular dystrophies and other muscle disorders. Interpretation of the results of such studies is complicated by the ubiquitous presence of non-muscle cells within muscle in vivo and by a lack of knowledge concerning the nature of the process of apoptosis in postmitotic, multinucleated skeletal muscle and the potential mechanisms involved. Staurosporine treatment of C2C12 skeletal muscle myotubes induced several classic features of apoptosis, including cell and nuclear shrinkage with initial preservation of cellular membranes. Externalization of phosphatidylserine occurred within 2 hours of treatment, and myotubes contained procaspase 3, which seemed to be activated within 4 hours. DNA degradation was identified by transferase uridine triphosphate nick-end labeling within 4 hours, and DNA ladders were identified on agarose electrophoresis of genomic DNA within 8 hours. Thus, the process of apoptosis in postmitotic multinucleated skeletal muscle shares many of the characteristics of apoptosis in mononuclear mitotic cells. However, the pattern of degeneration does not seem to be compatible with that seen in the muscular dystrophies.

Animals↗
PubMed1998

Effect of propylthiouracil-induced hypothyroidism on the onset of skeletal muscle necrosis in dystrophin-deficient mdx mice.

1. Duchenne and Becker muscular dystrophies are X-linked disorders caused by defects in muscle dystrophin. The mdx mouse is an animal model for Duchenne muscular dystrophy which has a point mutation in the dystrophin gene, resulting in little (<3%) or no expression of dystrophin in muscle. Mdx mice show a characteristic pattern of muscle necrosis and regeneration. Muscles are normal until the third postnatal week when widespread necrosis commences. This is followed by muscle regeneration, with the persistence of centrally nucleated fibres. 2. This work has examined the hypothesis that the onset of this muscle necrosis is associated with postnatal maturation of the thyroid endocrine system and that pharmacological inhibition of thyroid hormone synthesis delays the onset of muscle necrosis. 3. Serum T4 and T3 concentrations of mice were found to rise immediately before the onset of muscle necrosis in the mdx mouse, and induction of hypothyroidism by treatment of animals with propylthiouracil was found to delay the onset of muscle necrosis. 4. The results provide the first demonstration of experimental delay of muscle necrosis by manipulation of the endocrine system in muscle lacking dystrophin, and provide a novel insight into the way in which a lack of dystrophin interacts with postnatal development to precipitate muscle necrosis in the mdx mouse.

Animals↗
PubMed1997

In vivo model of muscle pain: quantification of intramuscular chemical, electrical, and pressure changes associated with saline-induced muscle pain in humans.

Intramuscular injection of hypertonic saline is a good model to study human muscle pain (Kellgren 1938). The present study concerns the intramuscular (i.m.) pain mediators in saline-induced muscle pain. In experiment 1, the diffusion of infused hypertonic and isotonic saline (0.5 ml) in m. tibialis anterior was illustrated by magnetic resonance imaging (MRI) in one subject. In experiment 2, six volunteers received four sequential infusions (0.5 ml given at 5 min intervals) of isotonic saline and thereafter four sequential infusions (0.5 ml given at 5 min intervals) of hypertonic saline into m. tibialis anterior. The isotonic and hypertonic saline infusions were computer-controlled and separated by 20 min. The muscle pain intensity was assessed by continuous recordings on a visual analogue scale (VAS). One microdialysis probe was inserted 1 cm from the infusion needle in m. tibialis anterior and another probe in the other m. tibialis anterior. Concentrations of the i.m. sodium, potassium, magnesium, and prostaglandin E2 (PGE2) were assessed from the dialysates. Intramuscular electromyography (EMG) and pressure were assessed in the area of the infused saline. In experiment 1, the infusion of hypertonic and isotonic saline created a visible saline-pool on the MRI scans. These saline-pool volumes were stable and not correlated to the pain scores. In experiment 2, infusion of isotonic saline produced little pain compared to infusion of hypertonic saline. Maximal pain was reported after the first infusion of hypertonic saline and thereafter the pain gradually decreased with subsequent infusions of hypertonic saline. During infusion of hypertonic saline the i.m. sodium and potassium concentrations increased significantly, i.m. magnesium concentration tended to be increased, and the i.m. PGE2 concentration tended to be decreased although these changes were not significant. The i.m. EMG was smaller during and after infusions of hypertonic saline compared with isotonic saline. The i.m. pressure was not different during the infusions of hypertonic and isotonic saline but was increased between the infusions of hypertonic saline. This study has shown that i.m. infusion of hypertonic saline produced a saline-pool, causing the i.m. pressure to increase. Possibly, pain activation and cessation are related to increased intramuscular sodium and potassium content respectively.

Adult↗
PubMed1997

Contraction-induced injury to the extensor digitorum longus muscles of rats: the role of vitamin E.

Three days after a protocol of 225 pliometric (lengthening) contractions was administered to in situ extensor digitorum longus muscles of rats, the force deficit was 64 +/- 7% and the percentage of damaged muscle fibers was 38 +/- 5% of the control values. We then tested the hypothesis that at 3 h and 3 days after the protocol an elevation in the muscle vitamin E content would decrease the force deficit, the percentage of damaged muscle fibers, and the serum activities of creatine kinase and pyruvate kinase. The 5-8 days of intravenous injections of alpha-tocopherol increased muscle vitamin E content threefold compared with vehicle (ethanol)-treated rats. Despite the difference in vitamin E content, the force deficit and number of damaged fibers were not different. After the contraction protocol, the serum creatine kinase and pyruvate kinase activities of the vehicle-treated rats increased fourfold at 3 h and twofold at 3 days, whereas the vitamin E-treated rats showed no change. We conclude that vitamin E treatment did not ameliorate either the induction of the injury or the more severe secondary injury at 3 days. Despite the absence of evidence for an antioxidant function, the lack of any increase in serum enzyme activities for vitamin E-treated rats at 3 h and 3 days supported a role for vitamin E in the prevention of enzyme loss after muscle damage.

Animals↗
PubMed1996

Reported blood exposure rates and staff nurse satisfaction with a closed surgical drainage system.

BACKGROUND: The purposes of this investigation were (1) to describe performance characteristics, incidence of exposure, and staff satisfaction with a closed drainage system, the Kendall Tru-Close, and (2) to compare performance, incidence of exposure, and satisfaction between the closed drainage system and a currently used surgical drainage system (the Hemovac). METHODS: Subjects were 40 adult male and female patients who had undergone selective orthopedic joint surgery. Twenty patients received the Hemovac drainage system, and 20 patients received the Tru-Close drainage system. Data collection instruments included a patient demographic data form, a daily assessment form, a nurses' bedside survey (self-report), and a satisfaction questionnaire. RESULTS: There were significantly fewer exposures with the closed drainage system when compared with the Hemovac system. An odds ratio of 5.09 indicated that the odds of exposure to fluids with the Hemovac system were five times greater than for the closed system. Nursing satisfaction scores were higher for the Tru-Close system than the Hemovac system for items that related to protection from exposure to self or environment. However, overall nursing satisfaction with the new device was mixed. CONCLUSIONS: Although nurses liked the increased protection from exposure afforded by the Tru-Close drainage system, other patient management issues emerged related to the increased weight of the reservoir bag.

Adult↗
PubMed1996

Exposure risks related to the management of three wound drainage systems.

BACKGROUND: In response to the Occupational Safety and Health Administration regulations and Centers for Disease Control and Prevention guidelines, health care employers must explore and incorporate new methods to protect staff and patients from blood-borne pathogens. An area directly affected by the new OSHA standards is the postoperative management of surgical drainage systems. This study compared three surgical wound drainage systems: a "closed" system (Tru-Close) and two currently used drainage systems (Hemovac, and Mini-Snyder) for nursing practices and risk of exposure to blood or body fluids in a simulated setting. METHODS: Fifty-eight volunteer registered nurses were asked to choose appropriate personal protection equipment and use recommended universal precautions while measuring and emptying fluid and reactivating each of the drainage systems and to complete a satisfaction questionnaire. Each postoperative wound drainage system was filled with simulated wound drainage and connected to a manikin in an empty patient room. Exposure/contamination was defined as spilling, dripping, or splashing of simulated drainage fluid anywhere in the patient's room or bathroom. RESULTS: Forty-five percent of nurses who emptied bulb evacuator systems and 40% of nurses who emptied Hemovac systems had resulting contamination to the environment or exposure to self. There were no contaminations with the Tru-Close system. Most contaminations were droplets of fluid on environmental surfaces rather than on the nurses themselves. Most nurses chose gloves for personal protection regardless of the system used. Gowns and face shields were rarely used. Most contaminations were due to emptying simulated fluid (27%) or emptying rinse water (29%) into the patient's toilet. Twenty-three percent (23%) of contaminations occurred while simulated fluid was poured into a container at the bedside. The most common object contaminated was the toilet seat (67%). The bed linen was contaminated 16% of the time. Nurse's gloves were exposed in 6% of the trials. CONCLUSIONS: As administrators and researchers explore new methods to protect patients, health care providers, and the environment from blood-borne pathogens, changes should be balanced with the impact on patient care and user satisfaction.

Adult↗
PubMed1996

Investigation by polymerase chain reaction of enteroviral infection in patients with chronic fatigue syndrome.

1. Chronic fatigue syndrome is characterized by muscle fatigue and pain at rest, symptoms which are usually exacerbated with exercise. Although various studies have shown minor, non-specific morphological and biochemical changes in muscle of patients with chronic fatigue syndrome, no consistent defect has been identified. Some have suggested that an enteroviral infection in muscle may cause the chronic muscle fatigue seen in patients with chronic fatigue syndrome, with acute infection directly and irreversibly impairing mitochondrial function, and persistent infection depressing muscle protein synthesis and metabolism. 2. To clarify the involvement of enterovirus infection in chronic fatigue syndrome, muscle biopsies from a group of patients with chronic fatigue syndrome were examined for the presence of enteroviral RNA by reverse transcriptase-polymerase chain reaction techniques in relation to functional studies of muscle mitochondria and the muscle RNA/DNA ratio. 3. Fifty-eight percent of patients reported an uncharacterized 'viral infection' before the onset of their illness, but none of the muscle samples from 34 patients contained detectable amounts of enteroviral RNA. Muscle tissue had a general reduction in the RNA/DNA ratio and mitochondrial enzyme activities with no specific abnormality in the activity of enzymes encoded partially on the mitochondrial genome (cytochrome-c oxidase) or nuclear genome (citrate synthase, succinate reductase). 4. These data provide no evidence of an enteroviral infection in muscle of patients with chronic fatigue syndrome, although this does not exclude a role of enterovirus in initiating the disease process. The general reduction in RNA/DNA ratio and mitochondrial enzyme activities is consistent with a general reduction in habitual activity.

Adult↗
PubMed1996

Fasting increases the extent of muscle necrosis in the mdx mouse.

1. The effects of fasting for 48 h were investigated in C57BL/10 (wild type) and age-matched C57BL/10 dystrophin-deficient (mdx) mice. 2. Fasting resulted in an increased percentage of necrotic fibres in muscles from the hindlimb and lumbar regions of mdx mice. The percentage of necrotic fibres of forelimb and chest muscles of mdx mice was unaltered by fasting. In wild-type mice, very few necrotic fibres were observed after fasting. 3. The necrotic changes in fasted mdx muscle were not accompanied by altered energy status as evaluated by muscle ATP and phosphocreatine concentrations. 4. A significantly decreased rectal temperature was observed in mdx but not in wild-type mice after fasting. 5. Fasting would normally be expected to cause a reduction in muscle fibre size. The high prevalence of necrosis in fasted mdx mice is therefore an unusual response that may be related to disturbance of the mechanisms which, in the fed state, compensate for the dystrophin deficiency in these animals.

Animals↗
PubMed1995

Effects of cocaine on leakage of creatine kinase from skeletal muscle: in vitro and in vivo studies in mice.

The mechanism of cocaine-induced rhabdomyolysis and/or muscle damage has not been elucidated. To determine if cocaine has a direct effect on muscle, isolated soleus and EDL muscles were incubated in the presence of 1 mM and 0.2 mM cocaine using a pulse and continuous exposure protocol. The release of creatine kinase from the isolated EDL muscle was statistically significant only when muscles were exposed to 1 mM cocaine for a period of 30 minutes. These findings suggest that cocaine-induced creatine kinase release could be mediated by a direct action on the fibers. It is also possible, however, that cocaine-induced muscle damage and creatine kinase release may be mediated via an indirect effect. It is possible that cocaine's vasoconstrictor effects could lead to muscle damage via an ischemia-reperfusion injury leading to free radical formation and lipid peroxidation. This study, therefore, also investigated the possibility that cocaine-induced cytosolic enzyme release may be mediated via the formation of free radicals leading to lipid peroxidation. To test this hypothesis, muscle total glutathione levels, a free radical scavenger, and muscle thiobarbituric acid reactive substances (TBARS), a measurement of lipid peroxidation, were examined following an acute IV cocaine dose in mice. Sedentary BalbC mice were injected with cocaine (40 mg/kg) or normal saline via the tail vein. Creatine kinase levels in serum and total glutathione and TBARS in liver and muscle were determined at 4, 8, and 24 hrs. Serum creatine kinase levels were significantly elevated 5-fold, while TBARS were elevated 100% in the gastrocnemius muscle of cocaine-treated animals at 4 hrs compared to normal saline controls. However, serum creatine kinase levels, total glutathione and TBARS in the gastrocnemius muscle were not statistically different at 8 or 12 hrs; or in the liver and anterior tibialis muscle at 4, 8, or 24 hrs. The present findings suggests that lipid peroxidation may be occurring in skeletal muscle after a single IV cocaine dose in mice.

Animals↗
PubMed1995

Demonstration of three-dimensional vector flow estimation using bandwidth and two transducers on a flow phantom.

A method of performing three-dimensional (3-D) velocity vector estimation with two transducers is demonstrated on a flow phantom using the Doppler spectra's mean frequencies and bandwidths. The results are compared with 3-D vector estimates computed from Doppler mean frequencies obtained with a five-transducer system. It is shown that the two-transducer vector Doppler system which uses bandwidth can improve on the accuracy of a three-transducer vector Doppler system which relies only on Doppler mean frequencies.

Blood Flow Velocity↗
PubMed1995

How does dystrophin deficiency lead to muscle degeneration?--evidence from the mdx mouse.

The mdx mouse has a defect in the same gene as boys with Duchenne muscular dystrophy, which results in the absence of the protein product, dystrophin. A large number of recent studies have used the mdx mouse model to examine the potential role of dystrophy in normal muscle and the mechanisms by which dystrophin-deficiency leads to myopathy. This review discusses critically the results of these studies and their relevance to understanding the mechanisms by which dystrophin-deficiency leads to muscle necrosis.

Animals↗
PubMed1994

Time course of changes in plasma membrane permeability in the dystrophin-deficient mdx mouse.

Control C57Bl/10 and mutant, dystrophin-deficient mdx mice of different ages were used to study the permeability of the plasma membrane to cytosolic components, to a vital stain (procion orange) and to extracellular 45calcium. Prenecrotic, 14 +/- 2-day-old mdx mice had normal serum activities of creatine kinase (CK) and pyruvate kinase (PK). Muscles from these animals also had no increased permeability to procion orange or extracellular 45calcium. Serum activities of CK and PK had risen acutely in the 21-day-old mdx mouse compared with control and remained elevated up to 6 months of age. The influx of procion orange and 45calcium content were abnormally elevated in the 40 +/- 4-day-old mdx mouse. These data provide no evidence for an increase in muscle plasma membrane permeability as a primary pathogenic effect of a lack of dystrophin, but results suggest that some factor expressed or de-expressed during mouse development may be necessary for the full expression of the dystrophic process.

Aging↗
PubMed1994

Release of creatine kinase and prostaglandin E2 from regenerating skeletal muscle fibers.

To study the effect of regeneration on the release of creatine kinase (CK) and prostaglandin E2 from muscle, extensor digitorum longus muscles of mice were injected with 50 microliters of BaCl2 solution in saline (1.2% wt/vol). Injected muscles showed almost complete degeneration at 3 days postinjection but had regenerated to approximately the same fiber cross-sectional area as contralateral control muscles by 12 days postinjection. These muscles released reduced amounts of intracellular CK compared with contralateral control muscles in response to excessive isometric contractile activity or treatment with the calcium ionophore A-23187 (20 microM) in vitro. However, regenerating muscles contained a lower total CK activity than contralateral control muscles, which accounted for the reduced CK efflux after experimental damage. Regenerating muscles released an increased amount of prostaglandin E2 compared with control muscles after both damaging stimuli. We conclude that regenerated muscles show no reduced susceptibility to contraction-induced damage (as assessed by CK release) but show an elevated release of prostaglandin E2 in response to contractile activity or an increase in intracellular calcium.

Animals↗