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Results for “Skeletal muscle dysfunction”

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At least 307 records · Page 17Linked to original sources

PubMed2000

Pelvic muscle exercise effect on pelvic muscle performance in women.

The aim of this study was to compare pelvic muscle (PM) characteristics (strength, endurance and contractability) before and after 12 weeks of pelvic muscle exercises in two groups of older women: the first composed of women with genuine stress incontinence, and the second made up of women with no symptoms of urinary incontinence or pelvic organ prolapse. This research also investigated the extent to which PM pressure and health-related characteristics could help discriminate between women with and without a clinical sign of PM dysfunction. Within a framework of skeletal muscle fitness, outcome measures were defined and compared. There was no significant difference in the baseline (P = 0.09) and post-PME (P = 0.63) strength, endurance and contractability of the two groups of women. The two groups did differ significantly on change scores (P = 0.05) following PME. A greater improvement in strength for women without a clinical sign of dysfunction was demonstrated. There was a probability of 91% that those with a history of gynecological surgery belonged to the group of women with SUI.

Adult↗

PubMed2005

Acute effects of N-acetylcysteine on skeletal muscle microcirculation following closed soft tissue trauma in rats.

Trauma-induced microcirculatory dysfunction, formation of free radicals and decreased endothelial release of nitric oxide (NO) contribute to evolving tissue damage following skeletal muscle injury. Administration of N-acetylcysteine (NAC) known to scavenge free radicals and generate NO is considered a valuable therapeutic approach. Thus, the objective of this study was to quantitatively analyze the acute effects of NAC on skeletal muscle microcirculation and leukocyte-endothelial cell interaction following severe standardized closed soft tissue injury (CSTI). Severe CSTI was induced in the hindlimbs of 14 male anesthetized Sprague-Dawley rats using the controlled impact injury technique. Rats were randomly assigned (n = 7) to high-dose intravenous infusion of NAC (400 mg/kg body weight) or isovolemic normal saline (NS). Non-injured, sham-operated animals (n = 7) were subjected to the same surgical procedures but did not receive any additional fluid. Creatin kinase (CK) activity was assessed at baseline, 1 h before and 2 h following posttraumatic NAC or NS infusion. Microcirculation of the extensor digitorum longus (EDL) muscle was analyzed using intravital microscopy and Laser-Doppler flowmetry (LDF). Edema index (EI) was calculated by measuring the EDL wet-to-dry weight ratio (EI=injured/contralateral limb). EDL-muscles were analyzed for desmin immunoreactivity and granulocyte infiltration. Microvascular deteriorations observed following NS-infusion were effectively reversed by NAC: Functional capillary density was restored to levels found in sham-operated animals and leukocyte adherence was significantly (p < 0.05) reduced compared to the NS group. NAC significantly (p < 0.05) increased erythrocyte flux determined by Laser-Doppler flowmetry. Posttraumatic serum CK levels and EI were significantly (p < 0.05) decreased by NAC. During the posttraumatic acute phase, single infusion of NAC markedly reduced posttraumatic microvascular dysfunction, attenuated both leukocyte adherence and tissue infiltration. NAC also decreased CSTI-induced edema formation and myonecrosis as reflected by attenuated serum CK levels and attenuated loss of desmin immunoreactivity. NAC may serve as an effective therapeutic strategy by supporting microvascular blood supply and tissue viability in the early posttraumatic period. Additional studies aimed at long-term analysis and investigation of injury severity--or dosage dependency are needed.

Acetylcysteine↗

PubMed1996

The effect of zidovudine on skeletal muscle mtDNA in HIV-1 infected patients with mild or no muscle dysfunction.

Zidovudine (ZDV), a nucleoside analogue which inhibits viral replication, is currently used in the treatment of type 1 human immunodeficiency virus (HIV-1) infection. It has been considered to be the cause of an acquired form of myopathy associated with a depletion of mitochondrial DNA (mtDNA) in muscle fibres, although the fact that the patients previously studied were clearly symptomatic, and the theoretical difficulty in differentiating on HIV-related myopathy from the effects of ZDV, led to a controversy on the possible deleterious effect of ZDV on muscle fibres. We studied the muscle biopsy taken from 42 HIV-1 infected patients, regardless of their medical complaints, and two series of controls: 12 HIV-negative patients suffering from diverse neuromuscular diseases and 10 normal patients who underwent orthopaedic surgery. Whole DNA was extracted following standard procedures and analysed by means of Southern blotting and polymerase chain reaction (PCR). We found that mtDNA was only depleted in HIV-1 infected patients treated with ZDV, but not in controls or patients untreated with this antiretroviral drug. Moreover, the depletion was more marked in patients who either presented weakness, myalgia, raised serum creatine kinase (CK), or ragged-red fibres. Mitochondrial DNA deletions were found in low proportion in all groups of patients, regardless of their HIV infection or ZDV status, but not in normal controls. We conclude that ZDV treatment in HIV-1 positive patients produces depletion of muscle mtDNA. The depletion can be demonstrated even in asymptotic patients, but is more marked in patients with clinical symptoms or abnormalities in their muscle biopsies. Other mtDNA abnormalities such as deletions seemed to be more related to other circumstances concurring in HIV-1 infected patients than to the effects of ZDV.

Adult↗

PubMed2006

Understanding the importance of selenium and selenoproteins in muscle function.

Selenium is an essential trace element. In cattle, selenium deficiency causes dysfunction of various organs, including skeletal and cardiac muscles. In humans as well, lack of selenium is associated with many disorders, but despite accumulation of clinical reports, muscle diseases are not generally considered on the list. The goal of this review is to establish the connection between clinical observations and the most recent advances obtained in selenium biology. Recent results about a possible role of selenium-containing proteins in muscle formation and repair have been collected. Selenoprotein N is the first selenoprotein linked to genetic disorders consisting of different forms of congenital muscular dystrophies. Understanding the muscle disorders associated with selenium deficiency or selenoprotein N dysfunction is an essential step in defining the causes of the disease and obtaining a better comprehension of the mechanisms involved in muscle formation and maintenance.

Animals↗

PubMed1995

Increased urinary zinc excretion in cancer patients is linked to immune activation and renal tubular cell dysfunction.

Urinary zinc excretion is known to be increased in cancer patients, but the pathogenesis of this phenomenon remains uncertain. Both skeletal muscle catabolism and renal tubular cell dysfunction have been proposed to explain this observation. We have investigated urinary zinc and N-acetyl-beta-D-glucosaminidase (NAG), an indicator of renal tubular cell dysfunction, as well as serum neopterin, an index of systemic immune activation, in 22 patients with cancer and seven controls. Both serum neopterin and urinary zinc were significantly elevated in cancer patients (15.8 +/- 12.7 versus 7.3 +/- 2.3 nmol l-1 and 1.77 +/- 0.80 versus 1.21 +/- 0.41 mmol mol-1 creatinine, P < 0.02 and P < 0.05, respectively), while NAG was similar in cancer patients and the controls (13.58 +/- 13.80 versus 13.68 +/- 12.19 mu kat mol-1 creatinine). A significant correlation was observed between serum neopterin and urine zinc (rs = 0.5119, P < 0.02), serum neopterin and urine NAG (rs = 0.6761, P < 0.002), and urinary zinc and NAG (rs = 0.6348, P < 0.002). In conclusion, the present data indicate a link between urinary zinc excretion and immune activation as well as renal tubular cell dysfunction. In addition, renal tubular cell dysfunction appears to be linked to immune activation.

Acetylglucosaminidase↗

PubMed2005

Microcirculatory effects of melatonin in rat skeletal muscle after prolonged ischemia.

The purpose of this study was to determine microcirculatory effects and response of nitric oxide synthase (NOS) to melatonin in skeletal muscle after prolonged ischemia. A vascular pedicle isolated rat cremaster muscle model was used. Each muscle underwent 4 hr of zero-flow warm ischemia followed by 2 hr of reperfusion. Melatonin (10 mg/kg) or saline as a vehicle was given by intraperitoneal injection at 30 min prior to reperfusion and the same dose was given immediately after reperfusion. After reperfusion, microcirculation measurements including arteriole diameter, capillary perfusion and endothelial-dependent and -independent vasodilatation were performed. The cremaster muscle was then harvested to measure endothelial NOS (eNOS) and inducible NOS (iNOS) gene expression and enzyme activity. Three groups of rats were used: sham-ischemia/reperfusion (I/R), vehicle + I/R and melatonin + I/R. As compared with vehicle + I/R group, administration of melatonin significantly enhanced arteriole diameter, improved capillary perfusion, and attenuated endothelial dysfunction in the microcirculation of skeletal muscle after 4 hr warm ischemia. Prolonged warm ischemia followed by reperfusion significantly depressed eNOS gene expression and constitutive NOS activity and enhanced iNOS gene expression. Administration of melatonin did not significantly alter NOS gene expression or activity in skeletal muscle after prolonged ischemia and reperfusion. Melatonin provided a significant microvascular protection from reperfusion injury in skeletal muscle. This protection is probably attributable to the free radical scavenging effect of melatonin, but not to its anti-inflammatory effect.

Adjuvants, Immunologic↗

PubMed2004

The effects of aging and exercise training on endothelin-1 vasoconstrictor responses in rat skeletal muscle arterioles.

OBJECTIVES: The incidence of cardiovascular disease increases with advancing age. Vascular dysfunction has been linked to cardiovascular disease and aging, although most research has focused on endothelium-dependent vasodilator dysfunction. Another possible mechanism for this vascular dysfunction with aging is enhanced vasoconstrictor responsiveness of the resistance vasculature, and in particular, reactivity of arterioles to endothelin-1 (ET-1). We hypothesized that vasoreactivity to ET-1 would be greater in skeletal muscle arterioles from old rats, and that endurance exercise training would abolish differences in ET-1 responsiveness between young and old animals. METHODS: Young sedentary (YS; 4 months; n=18), old sedentary (OS; 24 months; n=17), young trained (YT; n=9) and old trained (OT; n=7) male Fischer 344 rats were used. Training modality was treadmill exercise at 15 m/min up a 15 degrees incline, 1 h/day, 5 days/week, for 12 weeks. Soleus and white gastrocnemius muscle first-order arterioles were isolated for in vitro experimentation. Intraluminal diameter was measured in response to increasing concentrations of ET-1 (10(-11) to 10(-8) M) or KCl (10-100 mM) in arterioles with an intact or denuded endothelium and with and without an ETA (BQ-123 [10(-6) M]) or ETB (BQ-788 [10(-8) M]) receptor antagonist present. RESULTS: There was an age-associated increase in gastrocnemius vasoconstrictor responsiveness and sensitivity to ET-1 in arterioles with intact endothelium (ET-1 EC50: YS, 5.2 E(-9)+/-1.1 E(-9) M; OS, 2.0 E(-9)+/-0.8 E(-9) M); neither removal of the endothelium nor ETB blockade abolished this difference in arteriolar sensitivity to ET-1 between old and young rats. In contrast, ETA inhibition abolished the greater sensitivity (EC50) of arterioles from old animals (ET-1 EC50: YS, 10 E(-9)+/-0.7 E(-9) M; OS, 10 E(-9)+/-1.5 E(-9) M). Gastrocnemius muscle arterioles exhibited an age-related reduction in KCl-induced vasoconstriction which was abolished with the removal of the endothelium. Soleus muscle arteriolar responses to ET-1 and KCl were unaffected by aging. Additionally, exercise training had no effect on ET-1 vasoconstriction of soleus or gastrocnemius muscle arterioles. CONCLUSIONS: Aging results in an augmented gastrocnemius muscle arteriolar vasoconstriction to ET-1 which is mediated through an enhanced ETA receptor signaling pathway and not through an ETB receptor mechanism associated with either the endothelium or vascular smooth muscle. These findings suggest that enhanced vascular ET-1 sensitivity in fast-twitch skeletal muscles may play a role in the vascular dysfunction that is often associated with old age.

Aging↗

PubMed2001

Dilated cardiomyopathy of Becker-type muscular dystrophy with exon 4 deletion--a case report.

The authors report a 47-year-old man with Becker-type muscular dystrophy presenting with dilated cardiomyopathy. Left ventriculography showed diffuse severe hypokinesia: left ventricular end-diastolic volume index 193 mL/m2, left ventricular end-systolic volume index 143 mL/m2, and left ventricular ejection fraction 26%. Skeletal muscle biopsy demonstrated a dystrophic process. Genetic analysis revealed a deletion of exon 4. There was a difference in immunostaining pattern between skeletal muscles and cardiac muscles. Severe cardiac dysfunction in this case may be associated with the damage in dystrophin-deficient fibers.

Cardiomyopathy, Dilated↗

PubMed1997

[Immunohistochemical localization of chymase; a mast cell marker and clinical significance in diseased human skeletal muscle].

UNLABELLED: In the advanced stage of dystrophinopathy, cardiac dysfunction is a serious complication for prognosis. Recently, an angiotensin converting enzyme (ACE), which converts angiotensin (A) 1 to A 2, has been reported to be effective for cardiac insufficiency. The A 2 is produced more dominantly in the path via the production of a neutral serine protease, chymase (MW 25,000), secreted from the mast cell. We have observed localization of chymase in diseased human skeletal muscle tissues, and evaluated its clinical significance. The frozen muscle biopsied specimens from 91 neuromuscular disorders (muscular dystrophies, inflammatory myopathies and neurogenic muscular disorders) were stained by using monoclonal antibody against the chymase, and the positive cells in a whole sectional field were counted. In the serial sections, we also performed routine histochemistry and immunostainings of immunological markers (CD4, CD8 and others) as well as the apoptotic proteins for comparison. RESULTS: The chymase-positive mast cells were scattered mainly in the endomysium, partly in the perimysium and around small vessels. Although the positivity was not disease specific, more numerous strongly positive cells were observed in dystrophinopathy and inflammatory myopathies, but less in myotonic dystrophy and neurogenic muscle disorders. In the normal control muscle, however, strongly positive cells appeared less frequently than in the above mentioned diseased muscles. The chymase-positive cells partly corresponded to the ubiquitin-positive ones, but perforin, granzyme A, Fas and Bcl-2 did not. In conclusion, the chymase-positive mast cell may play a primary or secondary role in the diseased muscle, and their more abundant appearance in dystrophinopathy and some other myopathies suggest the effectiveness of an ACE blocker, an anti-chymase drug.

Biomarkers↗

PubMed1999

Decreased blood flow but unaltered insulin sensitivity of glucose uptake in skeletal muscle of chronic smokers.

Chronic cigarette smoking is associated with dysfunction of the vascular endothelium. Smokers have also been shown to be insulin-resistant, at least in some studies. Since insulin-induced vasodilation is dependent on endothelial cell nitric oxide (NO) synthesis, we tested the hypothesis that decreased skeletal muscle blood flow causes insulin resistance in smokers. We studied 37 young normotensive normolipidemic nondiabetic men, of which 14 were smokers and 23 lifelong nonsmokers. The groups were similar with respect to age, body mass index (BMI), and maximal oxygen uptake (VO2max). Basal and insulin-stimulated femoral muscle blood flow was measured using [(15)O]H2O and insulin-stimulated muscle glucose uptake using [18F]fluoro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET). Whole-body glucose uptake was measured using the hyperinsulinemic (insulin infusion 5 mU/kg x min)-euglycemic clamp technique. In the basal state, muscle blood flow was 51% lower in smokers (17 +/- 3 mL/kg muscle x min) versus nonsmokers (35 +/- 17 mL/kg x min, P < .0001). Insulin increased muscle blood flow comparably in both groups; the mean rate of insulin-stimulated blood flow was 30 +/- 10 and 55 +/- 38 mL/kg x min (P = .049), respectively. Whole-body and skeletal muscle glucose uptake were similar in both groups during insulin infusion. We conclude that muscle blood flow is lower in chronic smokers compared with nonsmokers under both fasting and hyperinsulinemic conditions. The insulin-induced increase in muscle blood flow and insulin-stimulated glucose uptake appear normal, suggesting that the vasodilatory and metabolic effects of insulin are intact in smokers and the reduced muscle blood flow per se does not cause insulin resistance in these subjects.

Adult↗

PubMed2006

Exercise and skeletal muscle glucose transporter 4 expression: molecular mechanisms.

1. Skeletal muscle is a highly plastic tissue that has a remarkable ability to adapt to external demands, such as exercise. Many of these adaptations can be explained by changes in skeletal muscle gene expression. A single bout of exercise is sufficient to induce the expression of some metabolic genes. We have focused our attention on the regulation of glucose transporter isoform 4 (GLUT-4) expression in human skeletal muscle. 2. Glucose transporter isoform 4 gene expression is increased immediately following a single bout of exercise, and the GLUT-4 enhancer factor (GEF) and myocyte enhancer factor 2 (MEF2) transcription factors are required for this response. Glucose transporter isoform enhancer factor and MEF2 DNA binding activities are increased following exercise, and the molecular mechanisms regulating MEF2 in exercising human skeletal muscle have also been examined. 3. These studies find possible roles for histone deacetylase 5 (HDAC5), adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) and p38 mitogen-activated protein kinase (MAPK) in regulating MEF2 through a series of complex interactions potentially involving MEF2 repression, coactivation and phosphorylation. 4. Given that MEF2 is a transcription factor required for many exercise responsive genes, it is possible that these mechanisms are responsible for regulating the expression of a variety of metabolic genes during exercise. These mechanisms could also provide targets for the treatment and management of metabolic disease states, such as obesity and type 2 diabetes, which are characterized by mitochondrial dysfunction and insulin resistance in skeletal muscle.

Exercise↗

PubMed2001

The skeletal muscle channelopathies: basic science, clinical genetics and treatment.

The human neurological channelopathies are a rapidly expanding group of mainly genetic conditions that are characterized by dysfunction of membrane-bound glycoproteins (ion channels). The skeletal muscle channelopathies were the first to be characterized in this group. In recent years significant progress has been made in our understanding of the molecular genetic and cellular electrophysiological bases of these disorders. DNA-based diagnosis is now a reality for many of the channelopathies. The advances made have implications for both genetic counselling and for tailoring treatment to specific channelopathies.

Humans↗

PubMed2006

Platelet-derived growth factor B retention is essential for development of normal structure and function of conduit vessels and capillaries.

OBJECTIVE: Extracellular retention of PDGF-B has been proposed to play an important role in PDGF-B signalling. We used the PDGF-B retention motif knockout mouse (RetKO) to study the effects of retention motif deletion on development of micro- and macrovascular structure and function. METHODS: Passive and active properties of conduit vessels were studied using myograph techniques and histological examination. Capillary structure and function was studied using measurements of capillary density in skeletal muscle and by assessing aerobic physical performance in a treadmill setup. Cardiac function was assessed using echocardiography. RESULTS: Myograph experiments revealed an increased diameter and stiffness of the aorta in RetKO. Histological examination showed increased media collagen content and a decreased number of aortic wall layers, however with a similar number of vascular smooth muscle cells. This outward eutrophic remodelling of the aorta was accompanied by endothelial dysfunction. RetKO showed decreased capillary density in skeletal muscle and signs of a defective delivery of capillary oxygen to skeletal muscle, as shown by a decreased physical performance. In RetKO mice, echocardiography revealed an adaptive eccentric cardiac hypertrophy. CONCLUSION: We conclude that retention of PDGF-B during development is essential for a normal conduit vessel function in the adult mouse. Furthermore, PDGF-B retention is also necessary for the development of an adequate capillary density, and thereby for a normal oxygen delivery to skeletal muscle. The lack of primary effects on cardiac function supports the redundant role of PDGF-B in cardiac development.

Animals↗

PubMed2004

Effects of whole-body exercise training on body composition and functional capacity in normal-weight patients with COPD.

BACKGROUND: Skeletal muscle wasting is related to muscle dysfunction, exercise intolerance, and increased mortality risk in patients with COPD. STUDY OBJECTIVES: The aims of this study were to investigate the effects of whole-body exercise training on body composition in normal-weight patients with COPD, and to study the relationship between changes in body composition and functional capacity. SETTING AND PARTICIPANTS: Fifty patients with COPD (FEV(1), 39% of predicted [SD, 16]) admitted to the pulmonary rehabilitation center at Hornerheide, and 36 healthy age-matched control subjects (for baseline comparison) were included. INTERVENTIONS: Patients participated in a standardized inpatient exercise training program consisting of daily submaximal cycle ergometry, treadmill walking, weight training, and gymnastics during 8 weeks. MEASUREMENTS: Fat-free mass (FFM) was measured by bioelectrical impedance analysis. None of the patients met the criteria for nutritional supplementation (body mass index </= 21, or FFM index </= 15 kg/m(2) in women and </= 16 kg/m(2) in men). Exercise capacity was measured using incremental cycle ergometry. Isokinetic quadriceps strength was measured with a Biodex dynamometer (Biodex Medical Corporation; Shirley, NY). RESULTS: At baseline, patients were characterized by a significantly lower FFM than the control subjects. Age and FFM were independent predictors of skeletal muscle function and exercise capacity in patients. After rehabilitation, weight (72.4 +/- 9.8 to 73.0 +/- 9.4 kg, p < 0.05) significantly increased, as a result of increased FFM (52.4 +/- 7.3 to 53.4 +/- 7.7 kg, p < 0.05), while fat mass (20.0 +/- 6.1 to 19.6 +/- 5.7 kg) tended to decrease. Peak work rate (63 +/- 29 to 84 +/- 42 W, p < 0.001), maximal oxygen consumption (O(2)max) [1,028 +/- 307 to 1,229 +/- 421 mL/min, p < 0.001], and isokinetic quadriceps strength (82.5 +/- 36.4 to 90.3 +/- 34.9 Newton-meters, p < 0.05) all improved. Changes in FFM were proportionally smaller than functional improvements, and were related to changes in O(2)max (r = 0.361, p < 0.05), but not to other changes in functional capacity. CONCLUSIONS: Intensive exercise training per se is able to induce an anabolic response in normal-weight patients with COPD classified into Global Initiative for Chronic Obstructive Lung Disease stages III-IV. Improvements in exercise performance and muscle function are proportionally larger than increases in FFM.

Aged↗

PubMedDate not supplied

Apoptosis induced by proteasome inhibition in human myoblast cultures.

Dysfunction of the ubiquitin-proteasome system has recently been implicated in the pathogenesis of some untreatable myodegenerative diseases characterized by the formation of ubiquitinated inclusions in skeletal muscles. We have developed an in vitro model of proteasomal dysfunction by applying inhibitors of the proteasome to primary adult human skeletal muscle cultures. Our data show that proteasome inhibition causes both cytoplasmic accumulation of ubiquitinated inclusions and apoptotic death, the latter through accumulation of active caspase-3.

Adult↗

PubMed2003

Deficit in cytochrome c oxidase activity induced in rat sperm mitochondria by in vivo exposure to zidovudine.

A decreased sperm motility has been reported in men treated with nucleoside analog reverse transcriptase inhibitors (NRTI). Sperm motility is correlated with enzymatic activities of the sperm mitochondrial respiratory chain (MRC), which may be impaired by NRTI. We compared sperm and skeletal muscle MRC and citrate synthase (CS) activities, sperm adenosine triphosphate (ATP) content and sperm motility between rats exposed to zidovudine (AZT) for 10 weeks and controls. Decreased levels of CS-normalized cytochrome c oxidase (COX, the MRC complex IV) activity were observed in the spermatozoa from AZT-treated rats, with no significant decrease in ATP content or motility. In muscle absolute COX activity increased after exposure to AZT but CS-normalized COX activity remained unchanged. These results suggest that exposure to NRTI can induce MRC dysfunction earlier in spermatozoa than in skeletal muscle.

Adenosine Triphosphate↗

PubMed2001

Impaired oxidative metabolism in exercising muscle from ALS patients.

The pathogenic mechanism of selective loss of motor neurones in amyotrophic lateral sclerosis (ALS) is still poorly understood. Recently, research evidence has suggested that mitochondrial dysfunction occurs in central nervous system as well as in peripheral tissues from ALS patients. The aim of our study was to indirectly investigate in vivo oxidative metabolism of exercising muscle in a case history of patients affected by ALS. To this purpose 11 patients, 8 male and 3 female, mean age+/-SD: 52.4+/-11.1 years, performed a bicycle incremental test for the assessment of lactate production. At rest, there was increased lactate concentration in patients: 2.77+/-0.79 vs. 1.48+/-0.49 mmol/l in normal controls (normal range: 0.67-2.47 mmol/l). Analysis of lactate curve during exercise showed a lactate production increase compared to controls. Furthermore, anaerobic lactate threshold was detected at 40-50% of the predicted normal power output, anticipated with respect to both normal subjects and non-ALS chronically denervated controls with comparable motor impairment (60-70%), suggesting that mitochondrial dysfunction can occur in exercising skeletal muscle from ALS patients.

Adult↗

PubMed2006

Differential myolysis of myocardium and skeletal muscle in hamsters with dilated cardiomyopathy: beneficial protective effect of diltiazem.

BACKGROUND: Although dilated cardiomyopathic hamsters (TO-2) with mutation of the delta-sarcoglycan gene exhibit histological features of muscular dystrophy, it remains to be elucidated whether both myocardium and skeletal muscle are injured in a similar manner. METHODS AND RESULTS: The progression of myolysis in both myocardium and skeletal muscle were assessed biochemically and pathologically in TO-2 and F1B control hamsters. Left ventricular (LV) function was assessed by echocardiography and cardiac catheterization. Both the plasma concentration of cardiac troponin T and the plasma activity of alpha-hydroxybutyrate dehydrogenase (HBD) peaked at 8 weeks of age, and thereafter reduced greatly in TO-2 hamsters. Activity of creatine kinase (CK) in TO-2 hamsters was significantly greater than in controls throughout the observation period. Pathological findings of both nuclear chain and central nuclei in skeletal muscles were observed in TO-2 hamsters throughout the observation period, suggesting regeneration. LV dysfunction was first evident at 8 weeks of age and deteriorated thereafter in TO-2 hamsters. Treatment of TO-2 hamsters with diltiazem from 5 to 8 weeks of age could avert the LV functional deterioration and the increment in alpha-HBD activity, but CK activity was unchanged. CONCLUSIONS: Despite myolysis in skeletal muscle occurring consistently throughout the observation period, cardiac myolysis occurred predominantly in the early phase. These initial cardiac events might involve coronary spasm and/or calcium overload in the myocardium.

Animals↗