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PubMedDate not supplied

Association of sternal wound infection with parasternal muscle sutures.

BACKGROUND: Sternal wound infection complicating open-heart surgery is a potentially devastating complication that has been associated with a number of risk factors. We recently consulted on three consecutive patients with this complication who had heavy nonabsorbable parasternal sutures placed in muscle tissue adjacent to the sternum. The aim of this report is to document our findings and caution that this technique to control bleeding from the parasternal intercostal muscles my increase risk of infection. METHODS: The pathology, surgical findings, and microbiology of these three cases are analyzed for similarity and possible cause of infection. RESULTS: By surgical observation and culture reports, each infection appeared to have originated at the site of nonabsorbable suture in devascularized parasternal muscle tissue. Sinus tracts could be probed to a similar site in each patient. CONCLUSION: Placement of sutures in the parasternal muscles where the sternal wires wrap around the bone leads to compression and necrosis of muscle tissue. We caution that this technique to control bleeding may cause a nidus of infection and increase the risk of deep sternal wound infection.

Adult↗
PubMed1986

[Localization of binding sites in rat muscles and brain for cobra neurotoxin and serum immunoglobulins from patients with myasthenia].

Using the immunohistochemical technique, it was revealed that serum immunoglobulins of patients with myasthenia gravis (Ig) were irreversibly attached to the myoneuronal connections of the rat intercostal muscles like the marker of the nicotin cholinireceptors--the cobra venom neurotoxin (CT). In addition, Ig differs from CT in the binding to nervous cells of the claustrum and diencephalon reticular formation and with certain cells of the nucleus caudatus and hemispheric cerebral cortex. It is suggested that the autoimmune processes in patients with myasthenia gravis do not only involve myoneuronal connection but also participate in central mechanisms of the disease genesis.

Animals↗
PubMedDate not supplied

Severe neonatal nemaline myopathy with delayed maturation of muscle.

A Japanese infant with a severe neonatal form of nemaline myopathy showed features of muscle immaturity as well as rods in the biopsied quadriceps femoris muscle, and involvement of diaphragm was first confirmed at autopsy. The biopsied muscle showed numerous rods in 80% of muscle fibers, and an increased number of type 2C fibers (23.2%). Electron microscopic findings were characterized by the presence of many small, immature round fibers with central nuclei and sparse myofibrils, and an increased number of satellite cells in close association with the small muscle fibers, as well as numerous rod structures. These microscopic and electron microscopic findings are interpreted as immature muscle fibers. Maturational delay or arrest implies deprivation of a development promoting factor such as a neuronal signal. Severe involvement with numerous rods was demonstrated in both diaphragm and intercostal muscles at the time of the postmortem examination, compatible with the patient's respiratory failure.

Fatal Outcome↗
PubMed1979

The effects of abdominal loading on rib cage distortion in premature infants.

The action of the diaphragm in inspiration is to decrease intrathoracic pressure and raise abdominal pressure, which elevates the rib cage. In the supine position, the rise in abdominal pressure is smaller because of the lack of abdominal muscle tone. In premature infants the inward pull of the diaphragm on the very compliant ribs causes inward movement on inspiration (ie, distortion) which is exacerbated by the lack of intercostal muscle activity during rapid eye movement (REM) sleep, their predominant state. We raised abdominal pressure by means of an inflatable cuff in 12 newborn infants (gestation 28 to 40 weeks) to try to improve inspiratory coupling of the rib cage and diaphragm. There was no significant change in minute ventilation, indicating no ventilatory impairment. In all studies in which there was distortion, abdominal loading produced a reduction or abolition of distortion (P less than .01). Abdominal loading may be useful in reducing diaphragmatic activity in premature infants.

Abdomen↗
PubMed1981

Importance of inspiratory muscle tone in maintenance of FRC in the newborn.

The importance of inspiratory muscle tone in the maintenance of functional residual capacity (FRC) in newborns was studied in eight premature infants with birth weights of 1,166 +/- 217 g and gestational age 29 +/- 1.9 wk (mean +/- SD). Rib cage and abdominal anteroposterior diameters were monitored with magnetometers, and electromyograms of the diaphragm and intercostal muscles were recorded with surface electrodes. Sleep state was monitored using electrooculogram and behavioral criteria. We assessed the decrease in tonic activity of the inspiratory muscles and the fall in end-expiratory lung volume during apnea compared with the period just preceding apnea. A total of 98 apneas were analyzed. In all instances a decrease in diaphragmatic and intercostal tone was associated with a decrease in the anteroposterior diameter of both rib cage and abdomen, indicating a fall in FRC. These changes were more marked during quiet sleep than during rapid-eye-movement sleep (P less than 0.01). Our results suggest that inspiratory muscle tone is a major determinant of FRC in the newborn.

Apnea↗
PubMed1998

Congenital myasthenic syndromes in two kinships with end-plate acetylcholine receptor and utrophin deficiency.

We studied two families with five affected members suffering from ptosis and slowly progressive limb-girdle muscle weakness. All patients had abnormal decremental response on low-frequency nerve stimulation, but there were no repetitive responses to single stimuli. The patients improved on anti-acetylcholinesterase drugs. Intercostal muscle was obtained for special studies from one patient of each family. In vitro microelectrode studies were done in Patient 1. Miniature end-plate potentials were of low amplitude, and the quantal content of the evoked end-plate potentials was normal. Light microscopy revealed a marked type 1 fiber predominance. Acetylcholinesterase reactivity was dispersed over increased length of individual fibers in Patient 2. On morphometry of the end-plate ultrastructure, the number of secondary synaptic clefts per neuromuscular junction and the expansion of the postsynaptic area were markedly reduced. In Patient 1, but not in Patient 2, the envelopment of the nerve terminal by Schwann cell was increased. Acetylcholine-receptor (AChR) density was reduced as judged by the reduced immunoreactivity to antibodies against different receptor subunits. Immunohistochemical analysis of proteins known to be involved in orchestrating the end-plate structure showed deficiency of the AChR-associated protein utrophin. These patients appear to have a defect in the development or maintenance of the postsynaptic clefts; whether this defect results from or causes a reduced expression of utrophin or AChR is unclear.

Adult↗
PubMed1990

Neural respiratory drive and neuromuscular coupling in patients with chronic obstructive pulmonary disease (COPD).

In 15 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) divided into two groups, one with normocapnia (A) and one with chronic hypercapnia (B), we evaluated the maximal voluntary inspiratory muscle strength (MIP), the pattern of breathing, the mouth occlusion pressure (Po.1), the neural respiratory drive (NRD), assessed by surface electromyographic (EMG) activity of the diaphragm (EMGd) and EMG activity of intercostal muscles (EMGint), and the chest wall neuromuscular coupling, assessed in terms of Po.1/EMGd ratio. Compared with an age-matched normal control group, both A and B groups exhibited lower MIP, significantly greater EMGd and EMGint, and lower Po.1/EMGd ratio. However, a similar pattern, along with a rapid and shallow breathing, differentiated group B from group A. In group B we found a significant direct relationship between Po.1/EMGd ratio and MIP, and an inverse relationship between PaCO2 and Po.1/EMGd ratio. These data seem to indicate the following: (1) EMG is a more precise method than Po.1 in assessing the magnitude of the NRD; (2) NRD is increased in these patients; and (3) clinical manifestations probably associated with inspiratory muscle fatigue (marked decrease in muscle strength, rapid and shallow breathing, and alveolar hypoventilation) may be accompanied by a greater NRD and a more marked derangement in chest wall neuromuscular coupling in COPD.

Aged↗
PubMed1994

Electrical myotonia of rabbit skeletal muscles by HMG-CoA reductase inhibitors.

HMG-CoA reductase (HCR) inhibitors are effective cholesterol-lowering agents in the treatment of hypercholesterolemia. Using intracellular microelectrodes, we studied the pathomechanism of myotonia experimentally induced in rabbits by HCR inhibitors, simvastatin, and pravastatin. The external intercostal muscle of rabbits showed some electrophysiologic characteristics of myotonia including repetitive firing after administration of simvastatin (50 mg/kg per day, for 4 weeks). The relative chloride conductance, though reduced in both, was more affected in simvastatin-administered muscles. In normal muscles perfused with a solution containing the inhibitors, both simvastatin and pravastatin produced membrane hyperexcitability with repetitive firing similar to that seen in simvastatin-administered rabbits. The minimum concentrations required to cause repetitive firing was 0.3 mg/L for simvastatin and 30 mg/L for pravastatin. These results indicate that HCR inhibitors induce some characteristics of myotonia by blocking the chloride channel in the muscle membrane.

Action Potentials↗
PubMedDate not supplied

Sarcoplasmic ionic calcium concentration in neuroleptic malignant syndrome.

The neuroleptic malignant syndrome (NMS) is an uncommon but serious adverse effect of antipsychotic medication. Similarities in the clinical picture, and muscle alterations, between NMS and susceptibility to malignant hyperthermia (MH) suggest common mechanisms underlying both disorders. Sarcoplasmic ionic calcium concentration ([Ca2+]i) was measured by means of Ca2+ selective microelectrodes in intact intercostal muscle fibers isolated from NMS patients and from subjects with no evidence of neuromuscular disease, who served as controls. The mean resting membrane potential and [Ca2+]i were -84 +/- 0.4 mV and 0.11 +/- 0.01 microM (mean +/- SEM) in the control subjects, while they were -84 +/- 0.6 mV and 0.51 +/- 0.02 microM in NMS muscle fibers. Only the difference in [Ca2+]i is significant (P less than 0.001). The incubation of control and NMS muscle bundles in dantrolene (10(-6) M) induced a reduction of [Ca2+]i to 0.06 +/- 0.01 microM and 0.20 +/- 0.04 microM respectively. These results show an alteration in sarcoplasmic ionic [Ca2+] in NMS muscle fibers, suggesting that a dysfunction in skeletal muscle plays some role in the pathogenesis of NMS.

Adult↗
PubMed1986

Muscle stiffness and electrical activity in paramyotonia congenita.

To investigate the pathomechanism of paramyotonic stiffness, the mechanogram of isometric finger force and the electromyogram of the flexor digitorum muscle were simultaneously recorded in five unrelated paramyotonia congenita patients. Cooling of the forearm provoked "spontaneous" electrical activity, but the accompanying force was less than 5% of the maximal voluntary isometric contraction amplitude. The relaxation of maximal voluntary contractions executed in the cold had a normal first phase and a very slow second phase. The force amplitude at the beginning of the slow phase was up to 80% of the maximal contraction amplitude; the duration of the slow phase was up to several minutes. It was concluded that the slowed muscle relaxation is more important as a factor contributing to paramyotonic stiffness than spontaneous force generation. Involuntary electrical activity recorded during the slow relaxation phase was too low to account for the force. Intercostal muscle biopsies obtained from four patients showed similar phases of slow relaxation when stimulated to give isometric twitches or tetani in the cold. Extracellular recording with electrodes designed to pick up all activity from the small bundles clearly showed that the slow relaxation phase was not caused by spontaneous action potentials. One possible explanation for the slowed relaxation is a long-lasting depolarization-induced contracture of the muscle fibers following activation in the cold.

Adult↗
PubMed1999

In vitro contractile responses and contracture testing of skeletal muscle from Quarter Horses with exertional rhabdomyolysis.

OBJECTIVE: To determine whether increased sensitivity to pharmacologic agents was a general property of equine exertional myopathies, including polysaccharide storage myopathy (PSSM) in Quarter Horses. ANIMALS: 5 adult Quarter Horses with exertional rhabdomyolysis and abnormal polysaccharide accumulation in skeletal muscle and 4 clinically normal adult Quarter or Quarter-type horses. PROCEDURES: Twitch time course measurements and contracture responses to various concentrations of caffeine and halothane for small bundles of intact external intercostal muscle fibers were measured in all horses. RESULTS: Caffeine contracture threshold of muscles from Quarter Horses with PSSM was not different from that of clinically normal horses (5 mM in both groups). Muscles from horses with PSSM and from clinically normal horses did not have contracture in response to up to 2% halothane. CONCLUSIONS AND CLINICAL RELEVANCE: Results were in contrast to the increased sensitivity to caffeine and halothane for muscles from Thoroughbreds with recurrent exertional rhabdomyolysis (RER). Although clinical signs of muscular stiffness after exercise are similar between Quarter Horses with PSSM and Thoroughbreds with RER, these breeds appear to have 2 distinct myopathies with different pathophysiologic bases. Unlike RER in Thoroughbreds, PSSM in Quarter Horses does not appear to be accompanied by a defect in regulation of muscle contraction.

Animals↗
PubMed2001

Age-related skeletal muscle atrophy in humans: an immunohistochemical and morphometric study.

The aim of this study was to determine age-related changes in three human muscles with different function and location in the body. The cross sectional area and the percentage of fibers type I, type IIA and type IIX were studied in vastus lateralis, deltoideus and external intercostal muscle. Muscle samples were obtained from 30 male subjects, aged 20-80 years. Fiber types were defined immunohistochemically, using monoclonal antibodies specific for type I, type IIA and type IIX fibers. Cross sectional area of muscle fibers was analyzed morphometrically by computerized image analysis. All muscle fiber types (I, IIA, IIX) showed the reduction in the fiber size in all three examined muscles. In all muscles the proportion of type I and type IIA was changed, but not in type IIX. With increasing age results showed the increase in proportion of type I, while proportion of type IIA fibers decreased, with vastus lateralis muscle being the most affected. These results suggest that age-related muscle atrophy is not a general phenomenon, and does not affect all muscles equally.

Adult↗
PubMed1979

[Familial cardiomyopathy: a study of two families with myocardial and skeletal muscle biopsies].

Cardiomyopathy was diagnosed in several members of two families. This familial cardiomyopathy showed symmetrical or asymmetrical hypertrophy of the ventricular walls with or without obstruction to the left ventricular outflow tract. Certain forms were asymptomatic and were revealed by the family history and echocardiography. Myocardial and intercostal muscle biopsy was performed for a biochemical and ultrastructural analysis. Different myocardial features were observed in the two families: a large increase in the glycogen deposits in the one, without clinical signs of a glycogen storage disease, and intracellular deposits of a filamentous protein substance in the other.

Cardiomyopathies↗
PubMed2006

Dysfunction of the canine respiratory muscle pump in ascites.

Ascites, a complicating feature of many diseases of the liver and peritoneum, commonly causes dyspnea. The mechanism of this symptom, however, is uncertain. In the present study, progressively increasing ascites was induced in anesthetized dogs, and the hypothesis was initially tested that ascites increases the impedance on the diaphragm and, so, adversely affects the lung-expanding action of the muscle. Ascites produced a gradual increase in abdominal elastance and an expansion of the lower rib cage. Concomitantly, the caudal displacement of the diaphragm and the fall in airway opening pressure during isolated stimulation of the phrenic nerves decreased markedly; transdiaphragmatic pressure during phrenic stimulation also decreased. To assess the adaptation to ascites of the respiratory system overall, we subsequently measured the changes in lung volume, the arterial blood gases, and the electromyogram of the parasternal intercostal muscles during spontaneous breathing. Tidal volume and minute ventilation decreased progressively as ascites increased, leading to an increase in arterial PCO2 and parasternal intercostal inspiratory activity. It is concluded that 1) ascites, acting through an increase in abdominal elastance and an expansion of the lower rib cage, impairs the lung-expanding action of the diaphragm; 2) this impairment elicits a compensatory increase in neural drive to the inspiratory muscles, but the compensation is not sufficient to maintain ventilation; and 3) dyspnea in this setting results in part from the dissociation between increased neural drive and decreased ventilation.

Animals↗
PubMed2006

[Glycogenesis Type II (M. Pompe). Selective failure of the respiratory musculature--a rare first symptom].

Late-onset Pompe's disease, a generalized lysosomal glycogen storage disease caused by acid maltase deficiency, usually presents as a slowly progressive muscular weakness of proximal muscles in lower limbs, followed by involvement of respiratory muscles. In the case presented here, however, respiratory failure was the first and selective symptom which caused the uncommon appearance of a patient entering our outpatient clinic on foot carrying his own artificial respirator. Intercostal muscle biopsy eventually led to the diagnosis.

Adult↗
PubMed1992

Intermediate syndrome due to prolonged parathion poisoning.

A parathion-poisoned patient with prolonged cholinesterase inhibition due to impaired hepatic metabolism and urinary excretion is reported. An intermediate syndrome characterized by respiratory paresis, weakness in the territory of several motor cranial nerves and of proximal limb and neck flexor muscles, persisted for 3 weeks. During this whole period, cholinesterase remained markedly reduced. Serial EMGs with repetitive nerve stimulation pointed to a combined pre- and postsynaptic disorder of neuromuscular transmission. Electron microscopy of an intercostal muscle biopsy showed focal degeneration at the poorly branched postsynaptic folds, and was considered to be nonspecific.

Acetylcholinesterase↗
PubMed1985

Airway resistance and respiratory muscle function in snorers during NREM sleep.

The effect of non-rapid-eye-movement (NREM) sleep on total pulmonary resistance (RL) and respiratory muscle function was determined in four snorers and four nonsnorers. RL at peak flow increased progressively from wakefulness through the stages of NREM sleep in all snorers (3.7 +/- 0.4 vs. 13.0 +/- 4.0 cmH2O X 0.1(-1) X s) and nonsnorers (4.8 +/- 0.4 vs. 7.5 +/- 1.1 cmH2O X 1(-1) X s). Snorers developed inspiratory flow limitation and progressive increase in RL within a breath. The increased RL placed an increased resistive load on the inspiratory muscles, increasing the pressure-time product for the diaphragm between wakefulness and NREM sleep. Tidal volume and minute ventilation decreased in all subjects. The three snorers who showed the greatest increase in within-breath RL demonstrated an increase in the contribution of the lateral rib cage to tidal volume, a contraction of the abdominal muscles during a substantial part of expiration, and an abrupt relaxation of abdominal muscles at the onset of inspiration. We concluded that the magnitude of increase in RL leads to dynamic compression of the upper airway during inspiration, marked distortion of the rib cage, recruitment of the intercostal muscles, and an increased contribution of expiratory muscles to inspiration. This increased RL acts as an internal resistive load that probably contributes to hypoventilation and CO2 retention in NREM sleep.

Abdomen↗