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Results for “Skeletal muscle dysfunction”

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PubMed1991

Activated neutrophils increase microvascular permeability in skeletal muscle: role of xanthine oxidase.

To determine the role of xanthine oxidase in the microvascular dysfunction produced by activated granulocytes, we examined the effect of xanthine oxidase depletion or inhibition on the increase in microvascular permeability produced by infusion of the neutrophil activator phorbol myristate acetate (PMA). Changes in vascular permeability were assessed by measurement of the solvent drag reflection coefficient for total plasma proteins (sigma) in rat hindquarters subjected to PMA infusion in xanthine oxidase-replete and -depleted animals, in animals pretreated with the xanthine oxidase inhibitor oxypurinol, and in animals depleted of circulating neutrophils by pretreatment with antineutrophil serum (ANS). Xanthine oxidase depletion was accomplished by administration of a tungsten-supplemented (0.7 g/kg diet) molybdenum-deficient diet. In animals fed the tungsten diet, muscle total xanthine dehydrogenase plus xanthine oxidase activity was decreased to less than 10% of control values. Estimates of sigma averaged 0.84 +/- 0.04 in control hindquarters, whereas PMA infusion was associated with a marked increase in microvascular permeability (decrease in sigma to 0.68 +/- 0.03). PMA infusion also caused an increase in the amount of the radical-producing oxidase form of xanthine oxidase (from 3.9 +/- 0.05 to 5.6 +/- 0.4 mU/g wet wt). ANS pretreatment attenuated this permeability increase (sigma = 0.77 +/- 0.04) and diminished the rise in xanthine oxidase activity (4.9 +/- 0.5 mU/g wet wt). Xanthine oxidase depletion with the tungsten diet or pretreatment with oxypurinol had no effect on this neutrophil-mediated microvascular injury (sigma = 0.69 +/- 0.06 and 0.67 +/- 0.03, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

Enhancing the response to parenteral nutrition in critical care.

Parenteral nutrition (PN) is an essential component in the support of critically ill patients with gastrointestinal dysfunction. Although PN cannot fully reverse hypermetabolism and accelerated skeletal muscle breakdown observed during periods of critical illness, it can prevent the adverse effects associated with malnutrition. The use of PN is not without complications, so care must be taken to ensure successful clinical outcomes with this complex therapy. Strategies have been developed by practitioners to promote safe practices with implementation of PN therapy and optimize a patient's response to PN. Identification of appropriate patient populations, strict glucose control, and manipulation of macro- and micronutrients are techniques being used to augment a patient's response to PN administration. This article will review the novel methods used to enhance benefits received from PN during critical illness.

Journal Article↗

PubMed2002

[An exercise program for the hypertensive patient. Leaving hypertension behind].

Today, regular exercise is considered an important therapeutic principle in arterial hypertension. Apart from weight reduction, the positive effects of sports (moderately practiced) include a reduction in peripheral resistance, improvement of endothelial dysfunction, and an increase in insulin sensitivity of the skeletal muscles. Training programs should be tailored to the physical and mental status of the patient, in particular to the severity of the hypertension, where indicated, with consideration being given to the hypertensive drugs used. In the case of marked hypertension or already existing secondary complications, training should be started only when the patient's blood pressure has been brought under pharmacological control. Ideally, training should be applied as 20-60 minute sessions at least twice weekly, with exercise keeping within aerobic capacity.

Antihypertensive Agents↗

PubMed1990

[Mechanisms of exertion dyspnea in cardiac insufficiency].

Effort dyspnea in cardiac failure corresponds to a subjective perception of difficulty in breathing which is itself secondary to a disproportion between the central bulbar respiratory regulation and the level of pulmonary ventilation attained. In cardiac failure, this situation is the result of dysfunction of both the respiratory apparatus and the skeletal striated muscle during exercise. During exercise a rise in left ventricular end diastolic pressure causes: a reduction in pulmonary compliance. The bronchial and alveolar capillaries drain into the pulmonary veins. The congestion of these capillaries and the resulting oedema makes the lung "stiffer"; an increase in the resistances of the small airways due to direct compression by congested bronchial vessels. The physiological dead space increases: the respiratory muscles ventilate pulmonary zones which are not perfused to no benefit. The reduction of pulmonary compliance, the increased resistances of the airways and of the physiological dead space all contribute to increase the work of the respiratory muscles. In addition to these mechanical phenomena, there is greater stimulation of the respiratory centre in the brain stem by the metabolic abnormalities of the skeletal striated muscles. During effort, they rapidly function under anaerobic conditions and the resulting hyperproduction of lactate and carbon dioxide stimulates the respiratory centres.

Anaerobic Threshold↗

PubMed1990

[Myoglobin release and renal function in polytraumatized patients in intensive care].

The excessive release of myoglobin following extensive skeletal muscle trauma, burns, and myopathies may result in renal dysfunction. Due to its molecular size, myoglobin is filtered through the glomerulus and is in part reabsorbed by the tubular system. intraluminal deposition of myoglobin following renal hypoperfusion and the impact of endogenous mediators on cell function contribute to the pathogenesis of acute renal failure. The present study was aimed to investigate the relation between myoglobin and renal function in polytraumatized patients. Thirty-four patients with an Injury Severity Score (ISS) of 28 +/- 3.1 (SEM) and a mean age of 39.5 years (range 18-70) were studied prospectively. Myoglobin, sodium, and creatinine concentrations in plasma and urine were determined 8-hourly. Myoglobin excretion, fractional myoglobin excretion, myoglobin clearance, creatinine clearance, and fractional excretion of sodium were calculated. The mean concentration of plasma myoglobin on the 1st day post-trauma was 3087 ng/ml. A continuous decrease in plasma myoglobin concentration could be observed, with a mean value of 497 ng/ml on day 7. The myoglobin concentration in urine showed marked fluctuations: the mean values were 3.37-4.12 mg/ml on day 1 and 0.78-1.34 mg/ml on day 7. There was no correlation between plasma and urine myoglobin concentrations. The myoglobin concentration increased during the period of observation, but there was no correlation with the creatinine clearance. The fractional excretion of myoglobin was in the range of 1% to 14%. There was no correlation between the fractional excretions of myoglobin and sodium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Discrepancy between systolic and diastolic dysfunction of the left ventricle in patients with Duchenne muscular dystrophy.

To assess the systolic and diastolic dysfunction of the left ventricle (LV) in relation to age and the severity of impairment in Duchenne muscular dystrophy (DMD), we performed M-mode, two-dimensional and pulsed-wave Doppler echocardiography in 45 male subjects with DMD aged 8 to 25 years and in 40 age-matched healthy controls. Systolic dysfunction started in the first decade of life, with some patients showing severe systolic dysfunction in their early teens. This dysfunction, however, did not always depend on the severity of the skeletal muscle disease. No patients with DMD showed an increase in peak atrial velocity and time-velocity integrals of the atrial contraction velocity curve, findings frequently reported to precede the abnormalities in many cardiac diseases; it was thought therefore that these patients had no increase in left atrial compensation. Diastolic dysfunction may not routinely precede or accompany the systolic dysfunction in DMD, in contrast with what is reported in patients with ischaemic or hypertensive heart disease. DMD patients usually show a predominant systolic dysfunction.

Adolescent↗

PubMed1989

Possible systemic smooth muscle layer dysfunction due to a deficiency of dystrophin in Duchenne muscular dystrophy.

The localization of dystrophin was examined immunohistochemically in various tissues from mice and rats as well as from biopsied human muscle specimens, using polyclonal antibodies against dystrophin. Although dystrophin was completely absent in biopsied muscle specimens from 3 male DMD patients, it was faintly observed in the surface membrane of almost all muscle fibers examined in a female DMD patient. In all controls, human and animal, a strong dystrophin reaction was observed in the surface membrane of intrafusal muscle fibers and at the neuromuscular junctions, rather than in the surface membrane of skeletal and cardiac muscle fibers. In addition, dystrophin was clearly localized in the surface membrane of smooth muscle fibers in the viscera, bronchial system, ureter, and tunica media of blood vessels, including arteries and veins, in all examined animal tissues. In mdx mice, dystrophin was absent in almost all muscle and smooth muscle fibers in various tissues and blood vessels. These results suggested a possible systemic dysfunction of smooth muscle layers, especially those of blood vessels, as well as skeletal muscle fibers, due to a deficiency of dystrophin in Duchenne muscular dystrophy.

Animals↗

PubMed2003

Somatic dysfunction during carisoprodol cessation: evidence for a carisoprodol withdrawal syndrome.

Carisoprodol is a commonly used skeletal muscle relaxant with potential for abuse because of its active metabolite, meprobamate, and several reports have suggested that patients abruptly stopping intake of carisoprodol may have a withdrawal syndrome. The authors studied changes in the occurrence of somatic dysfunctions in five patients during an 8-day period following discontinuation from large doses of carisoprodol. Results showed that the number of somatic dysfunctions changed significantly during the withdrawal period. Each patient had an increase in the number of somatic dysfunctions during the first 3 days after cessation of carisoprodol with return to at or near baseline by the eighth day. This was reflected statistically in a significant-within-subjects effect for time. Results of supplemental analyses revealed a significant component of the effect and a trend for the quadratic component to be significant. Increases in the number of somatic dysfunctions during carisoprodol discontinuation support the existence of a carisoprodol withdrawal syndrome.

Adult↗

PubMed2013

Delivery of recombinant adeno-associated virus vectors to rat diaphragm muscle via direct intramuscular injection.

The diaphragm is the most important inspiratory muscle in all mammals, and ventilatory insufficiency caused by diaphragm dysfunction is the leading cause of morbidity and mortality in many genetic and acquired diseases affecting skeletal muscle. Currently, pharmacological inhibitors, genetically modified animals, and invasive procedures are used to study disorders affecting the diaphragm. However, these methodologies can be problematic because of off-target drug effects and the possible nonphysiological consequences of lifelong genetic alterations. Therefore, alternative methods to study this important respiratory muscle are needed. To resolve this, we have developed a methodology to deliver recombinant adeno-associated virus (rAAV) vectors to the rat diaphragm via direct intramuscular injection. We hypothesized that by direct injection of rAAV into the muscle we can selectively target the diaphragm and establish a novel experimental method for studying signaling pathways and also provide a strategy for effectively using rAAV to protect the diaphragm against disease. This report describes the methods and evidence to support the use of rAAV as a therapeutic intervention to study rat diaphragm biology during conditions that promote diaphragm dysfunction.

Animals↗

PubMed2003

Satellite cell depletion in degenerative skeletal muscle.

Adult skeletal muscle has the striking ability to repair and regenerate itself after injury. This would not be possible without satellite cells, a subpopulation of cells existing at the margin of the myofiber. Under most conditions, satellite cells are quiescent, but they are activated in response to trauma, enabling them to guide skeletal muscle regeneration. In degenerative skeletal muscle states, including motor nerve denervation, advanced age, atrophy secondary to deconditioning or immobilization, and Duchenne muscular dystrophy, satellite cell numbers and proliferative potential significantly decrease, contributing to a diminution of skeletal muscle's regenerative capacity and contractility. This review will highlight the fate of satellite cells in several degenerative conditions involving skeletal muscle, and will attempt to gauge the relative contributions of apoptosis, senescence, impaired proliferative potential, and host factors to satellite cell dysfunction.

Aging↗

PubMed1996

Skeletal muscle metabolism as a target for drug therapy in peripheral arterial disease.

Peripheral arterial disease (PAD) is an atherosclerotic disease which modifies lower extremity hemodynamics. There is considerable evidence that skeletal muscle metabolism is altered in PAD. Several studies have demonstrated altered mitochondrial enzyme content in PAD muscle as compared with controls, and enzyme activity may not increase normally in PAD with exercise training. A variety of metabolic intermediates, including acylcarnitines, accumulate in muscle of PAD patients, suggesting incomplete oxidative metabolism. Studies employing 31P-NMR (nuclear magnetic resonance) also suggest a metabolic myopathy in PAD. Strikingly, while hemodynamics do not predict claudication-limited performance, metabolic injury as evidenced by acylcarnitine accumulation is strongly correlated with patients' functional status in PAD. Further, exercise rehabilitation improves claudication-limited performance without modifying large vessel hemodynamics. The stress placed on skeletal muscle during exercise in PAD and the observed evidence of metabolic dysfunction is similar to ischemia/reperfusion injury in cardiac muscle. Recognition of the role of cellular metabolic injury and function in PAD has formed the basis for novel therapeutic strategies in this disease.

Adenosine Triphosphate↗

PubMed1998

Exercise training in the treatment of heart failure: what is achieved and how?

Exercise intolerance is present in most patients with left ventricular dysfunction. Factors affecting the central and peripheral circulation, ventilatory system and skeletal muscles limit the exercise capacity in varying degrees within each patient. Exercise training is now being applied with growing enthusiasm to patients with heart failure. Improvements in the peripheral circulation and skeletal muscle structure and function appear to account for the observed benefit in exercise tolerance after training. Exercise programmes in these patients should be initially conducted with close supervision and tailored to the individual patient.

Exercise↗

PubMed1979

Electromyographic abnormalities in osteosarcoma arising in Paget disease of the vertebral column.

The case of a patient with low back pain and Paget disease of the L5, S1 vertebrae is presented. Electromyography revealed dysfunction in both the paraspinal and gluteal muscles. Postmortem examination showed sarcomatous transformation of the vertebrae with nerve root compression and skeletal muscle infiltration by tumor. The electromyographic abnormalities are correlated with the pathologic findings. The clinical features of neurologic dysfunction in Paget disease of the vertebral column and in osteosarcoma arising in Paget disease of the vertebral column are reviewed. Electromyography can provide valuable information in the evaluation of the patient with Paget disease of the vertebral column who is suspected of having neurologic dysfunction.

Electromyography↗

PubMedDate not supplied

Muscle functional deficits after tourniquet ischemia.

The contractile properties of the rabbit tibialis anterior muscle were studied 48 hours after an ischemic episode induced by pneumatic tourniquet compression of the thigh. Forty animals were divided into five groups, each of which had continuous ischemia of either 1, 2, or 4 hours, or a total of 2 or 4 hours of ischemia interrupted by 10 minutes of reperfusion at 1-hour intervals. Contralateral limbs served as controls. Muscle contractile properties were tested by stimulation of the peroneal nerve distal to the site of tourniquet compression. Peak tetanic tension in the 1-hour group did not differ significantly from controls. In the 2- and 4-hour groups, peak tetanic tensions were 31% and 2% of controls, respectively, and twitch tensions were 25% and 1% of controls, respectively. Hourly reperfusion intervals had no significant effect on maximum tetanic or twitch tension compared with continuous ischemia for either 2 or 4 hours. Clinically significant muscle dysfunction may be induced by 2 or more hours of pneumatic tourniquet application. Hourly reperfusion intervals may not improve skeletal muscle function distal to the tourniquet. However, reperfusion intervals could still affect muscle that is compressed beneath the cuff. Tourniquet-induced contractile deficits may interfere with postoperative functional recovery.

Animals↗

PubMed2007

Non-cultured cell transplantation in an ovine model of non-ischemic heart failure.

OBJECTIVE: Cell therapy may be a promising alternative or adjunct to current treatment modalities for ischemic heart failure. But little is known on the impact of myogenic cell transplantation in large animal models of non-ischemic cardiomyopathy. The aim of the present study was to explore whether an ovine model of toxin-induced heart disease could benefit from non-cultured skeletal muscle cell transplantation. METHODS: Sequential intracoronary injections of doxorubicin (0.75 mg/kg) were carried out every 2 weeks until echocardiographic detection of myocardial dysfunction. Sheep were then randomly assigned to either non-cultured cell transplantation (n=8) or placebo injection (n=5). For the cell therapy group, a skeletal muscle biopsy (about 10 g) was explanted from each animal approximately 3h before grafting. After thoracotomy, 20 epicardial injections were carried out. The animals were assessed one last time before sacrifice, 2 months after the thoracotomy. Cells were tracked with cmDiI (red fluorescence) and characterized with immunohistochemistry with monoclonal antibodies to a fast skeletal isoform of myosin heavy chain. RESULTS: Two months after intramyocardial grafting, tissue Doppler imaging and conventional echocardiographic assessment of the groups showed a marked improvement in the non-cultured cell therapy group. Ejection fraction (EF) (p<0.05) as well as systolic endocardial velocities (p<0.01) improved versus the placebo group. CmDiI and skeletal myosin heavy chain expression was detected in all animals at 2 months after implantation confirming engraftment of skeletal muscle cells. CONCLUSIONS: In conclusion, our data indicate that non-cultured muscle cell transplantation is feasible and may translate into a functional benefit in an ovine model of dilated heart failure.

Animals↗

PubMed1996

Regional blood flow alterations after bovine fumaryl beta beta-crosslinked hemoglobin transfusion and nitric oxide synthase inhibition.

OBJECTIVES: a) To determine whether isovolemic exchange transfusion with cell-free, bovine fumaryl beta beta-crosslinked hemoglobin results in a different pattern of regional blood flow distribution than transfusion with a poor oxygen-carrying, colloidal solution. b) Because of potential nitric oxide scavenging by plasma-based hemoglobin, to determine whether blood flow differences are reduced after nitric oxide synthase inhibition. DESIGN: A prospective, randomized design with repeated blood flow measurements within groups. SETTING: Experimental physiology laboratory in a university medical center. SUBJECTS: Pentobarbital-anesthetized female cats. INTERVENTIONS: Three groups of eight cats were studied: a) a control group with no transfusion (hematocrit of 32%); b) an anemia group in which exchange transfusion with an albumin-containing solution reduced hematocrit to 18% over a 40- to 50-min period; and c) a group in which cell-free hemoglobin was exchanged transfused to reduce hematocrit to 18%, without a proportional reduction in oxygen-carrying capacity. Bovine hemoglobin was covalently crosslinked intramolecularly between the 81-lysine residues on the beta-subunits to stabilize the tetramer. Regional blood flow was measured by the radiolabeled microsphere technique before transfusion and at 10, 100, and 180 mins from the start of transfusion. At 190 mins, N omega-nitro-L-arginine methyl ester (L-NAME; 10mg/kg) was infused to inhibit nitric oxide synthase and blood flow was measured 30 mins later. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure was unchanged in the control and albumin-transfused groups. However, mean arterial pressure increased rapidly in the hemoglobin-transfused group. With hemoglobin transfusion, there were marked reductions in blood flow to the intestines, kidneys and adrenal glands. Administration of L-NAME after hemoglobin transfusion failed to increase arterial pressure or cause further reductions in intestinal, renal, or adrenal blood flow. Administration of L-NAME to the control and albumin-transfused groups increased arterial pressure and reduced intestinal, renal, and adrenal blood flows to values attained with hemoglobin transfusion. In contrast, in skeletal muscle and left ventricle, blood flow rates increased in the albumin-transfused group and were greater than those values found in the control group and hemoglobin-transfused group. The greater flow in the albumin-transfused group persisted after L-NAME administration. There was no difference in renal sodium, potassium, or osmolar excretion, or in urine flow between groups. CONCLUSIONS: Transfusion with cell-free, bovine crosslinked hemoglobin in cats can selective reductions in blood flow in the intestines, kidneys, and adrenal glands without evidence of renal dysfunction by a mechanism consistent with nitric oxide scavenging. In skeletal and cardiac muscle, the increase in blood flow persisted after nitric oxide inhibition in the albumin group relative to the hemoglobin-transfused group at equivalent hematocrit values. This finding is consistent with compensatory vasoconstriction with hemoglobin transfusion due to improved oxygenation by this oxygen carrier.

Animals↗

PubMed1998

Regular physical exercise corrects endothelial dysfunction and improves exercise capacity in patients with chronic heart failure.

BACKGROUND: The purpose of this study was to determine the effects of systemic exercise training on endothelium-mediated arteriolar vasodilation of the lower limb and its relation to exercise capacity in chronic heart failure (CHF). Endothelial dysfunction is a key feature of CHF, contributing to increased peripheral vasoconstriction and impaired exercise capacity. Local handgrip exercise has previously been shown to enhance endothelium-dependent vasodilation in conduit and resistance vessels in CHF. METHODS AND RESULTS: Twenty patients were prospectively randomized to a training group (n=10, left ventricular ejection fraction [LVEF] 24+/-4%) or a control group (n=10, LVEF 23+/-3%). At baseline and after 6 months, peak flow velocity was measured in the left femoral artery using a Doppler wire; vessel diameter was determined by quantitative angiography. Peripheral blood flow was calculated from average peak velocity (APV) and arterial cross-sectional area. After exercise training, nitroglycerin-induced endothelium-independent vasodilation remained unaltered (271% versus 281%, P=NS). Peripheral blood flow improved significantly in response to 90 microg/min acetylcholine by 203% (from 152+/-79 to 461+/-104 mL/min, P<0.05 versus control group) and the inhibiting effect of L-NMMA increased by 174% (from -46+/-25 to -126+/-19 mL/min, P<0.05 versus control group). Peak oxygen uptake increased by 26% (P<0.01 versus control group). The increase in peak oxygen uptake was correlated with the endothelium-dependent change in peripheral blood flow (r=0.64, P<0. 005). CONCLUSIONS: Regular physical exercise improves both basal endothelial nitric oxide (NO) formation and agonist-mediated endothelium-dependent vasodilation of the skeletal muscle vasculature in patients with CHF. The correction of endothelium dysfunction is associated with a significant increase in exercise capacity.

Blood Flow Velocity↗

PubMed1993

Myopathy with mitochondrial alterations in patients with primary biliary cirrhosis and antimitochondrial antibodies.

OBJECTIVE: To describe a syndrome of severe progressive myopathy, cardiomyopathy, and gastrointestinal dysmotility in 2 patients with asymptomatic primary biliary cirrhosis (PBC) and circulating antimitochondrial autoantibodies, and to review pertinent literature concerning this syndrome. METHODS: Clinical, electrophysiologic, serologic, and pathologic studies of the 2 affected patients were conducted. RESULTS: Skeletal muscle involvement was manifested by progressive weakness of the proximal muscles, marked diaphragmatic dysfunction with consequent hypoventilation and respiratory failure, and moderately elevated levels of muscle-associated enzymes. Serum from both patients contained antimitochondrial antibodies that reacted with components of the mitochondrial keto acid dehydrogenase enzyme complex. Results of electromyography were consistent with a myopathic process. The microscopic and ultrastructural changes in the skeletal muscles were distinct from those of typical myositis, and were notable for striking subsarcolemmal aggregation of abnormal mitochondria in the absence of significant inflammation. CONCLUSION: Severe skeletal muscle, cardiac, and gastrointestinal pathology with abnormalities of the muscle mitochondria develops in a subset of patients with mild PBC and antimitochondrial antibodies. The pathogenesis of this syndrome is unclear, but may be related to the presence of the antimitochondrial autoantibodies.

Adult↗