PubMed Health⌕ Search

Biomedical subjects

M Decramer

Publications and source records attributed to M Decramer.

At least 55 records · Page 3Linked to original sources

Hyperinflation and respiratory muscle interaction.

Hyperinflation clearly affects respiratory muscle interaction. It commonly increases the rib cage contribution to chest wall motion, whilst it reduces the abdominal contribution. This change is thought to result from the fact that hyperinflation severely reduces the mechanical advantage of the diaphragm, whilst it affects the mechanical advantage of the neck and rib cage muscles to a lesser extent. The mechanical disadvantage in the diaphragm induced by hyperinflation is presumably primarily the result of the length changes undergone by the diaphragm in acute hyperinflation. Changes in diaphragmatic geometry are generally considered to be less important in the reduction of the diaphragm's force-generating capacity. Further factors contributing to the mechanical disadvantage in the diaphragm include a reduction in the appositional component of diaphragmatic action (through reduction in the zone of apposition), and a reduction in the insertional component (through a shift in the alignment of the diaphragmatic fibres from axial to radial). In chronic hyperinflation, the diaphragm adapts to the chronically hyperinflated state. This adaptation to chronic foreshortening is similar to the adaptation occurring in the skeletal muscle. It is caused by a dropout of sarcomeres in series along the muscle fibres. It restores the force-generating capacity of the muscle, in part, but it reduces the capacity of the muscle to undergo length changes. The mechanical advantage of the parasternal intercostals and the scalenes is possibly less affected, because the length changes undergone by these muscles during hyperinflation are smaller. The factors determining the mechanical advantage of the parasternal intercostals are complex. Variables related to the mechanical advantage of the parasternal intercostals include: length changes; changes in angle between the parasternal intercostals and the sternum and between rib and sternum; and changes in mechanical arrangement among different parasternals. At present, it is difficult to develop an integrated view of these factors and of their change with hyperinflation. Finally, hyperinflation commonly results in recruitment of expiratory muscles. The functional significance of this expiratory muscle recruitment in patients is still debated.

Diaphragm↗

Rostrocaudal gradient of electrical activation in the parasternal intercostal muscles of the dog.

1. Because the inspiratory mechanical advantage of the canine parasternal intercostal muscles is greatest in the third interspace and decreases gradually in the caudal direction, the electromyograms of these muscles in interspaces 3, 5 and 7 have been recorded in anaesthetized, spontaneously breathing dogs. Each activity was expressed as a percentage of the activity measured during tetanic, supramaximal stimulation of the internal intercostal nerve (maximal activity). 2. Parasternal inspiratory activity during resting, room air breathing was invariably greater in the third than in the fifth interspace (62.0 +/- 6.0 vs. 41.3 +/- 4.6% of maximal activity; P < 0.001) and smallest in the seventh interspace (22.8 +/- 2.7% of maximal activity; P < 0.001). This distribution of activity persisted during hyperoxic hypercapnia and during breathing against increased inspiratory airflow resistance. 3. This rostrocaudal distribution of activity also persisted after complete paralysis of the diaphragm as well as after deafferentation of the ribcage. 4. Studies of the distribution of the muscle fibre types indicated that the parasternal intercostals in all interspaces had a higher proportion of slow-twitch oxidative (SO; type I) fibres than fast-twitch oxidative-glycolytic (FOG; type II a) fibres. 5. Thus the topographic distribution of parasternal inspiratory activity along the rostrocaudal axis of the ribcage is precisely matched with the topographic distribution of mechanical advantage. This extraordinarily effective pattern of activation probably results from the unequal distribution of central inputs throughout the parasternal motoneurone pool.

Animals↗

Esophageal tuberculosis mimicking malignancy.

A case of pulmonary and esophageal tuberculosis in an 82-year-old female is presented. Esophageal tuberculosis is very rarely seen in Europe and the United States, but the disease is still endemic in India. The major differential diagnosis is esophageal malignancy. Findings that can suggest the diagnosis are tracheo-esophageal fistula formation, enlarged, centrally necrotizing lymph nodes, and a micronodular lung pattern.

Aged↗

Diaphragm pacing with a quadripolar phrenic nerve electrode: an international study.

We sought to determine the international experience with the quadripolar diaphragm pacer system and to test two hypotheses: the incidence of pacer complications would be (1) increased among pediatric as compared to adult patients; and (2) highest among active pediatric patients with idiopathic congenital central hypoventilation syndrome (CCHS). Data were collected via a questionnaire coupled with the Atrotech Registry data for a total of 64 patients (35 children and 29 adults) from 14 countries. Thoracic implantation of electrodes and bilateral pacer use each occurred in 94% of all subjects. Tetraplegic (vs pediatric CCHS) patients were more typically paced 24 hours/day (P = 0.001). Pacing duration averaged 2.0 +/- 1.0 years among children and 2.2 +/- 1.1 years among adults. Infections occurred among 2.9% of surgical procedures, all in pediatric CCHS patients (vs pediatric tetraplegic patients, P = 0.01). The incidence of mechanical trauma was 3.8%, without significant differences among patient groups. The incidence of presumed electrode and receiver failure were 3.1% and 5.9%, respectively, with internal component failure greater among pediatric CCHS than pediatric tetraplegic patients (P < 0.01). Intermittent or absent function of 0-4 electrode combinations occurred among 19% of all patients, with increased frequency among pediatric CCHS than pediatric tetraplegic patients (P < 0.03). Complication-free successful pacing occurred in 60% of pediatric and 52% of adult patients. In all, 94% of the pediatric and 86% of the adult patients paced successfully after the necessary intervention. Although pacer complications were not increased among pediatric as compared to adult patients, the incidence of complications was highest among the active pediatric patients with CCHS. Longitudinal study of these patients will provide invaluable information for modification and improvement of the quadripolar system.

Adult↗

Reliability of a commercially available threshold loading device in healthy subjects and in patients with chronic obstructive pulmonary disease.

BACKGROUND: Threshold loading with the Nickerson and Keens' device is frequently applied in the training and assessment of inspiratory muscles. However, this equipment is not easily applied in clinical practice and training. A study was therefore designed to investigate the accuracy and reliability of the Threshold, a commercially available threshold loading device. METHODS: The resolution (accuracy) of the system was determined by measuring variation of pressure and flow during one minute in an experimental setup. The reproducibility and flow independence were then determined during threshold loading at six different inspiratory loads between 25% and 50% maximal inspiratory pressure (PImax) in 10 patients with chronic obstructive pulmonary disease (COPD) and eight healthy subjects. RESULTS: In the first experiment the mean variation of the sustained pressure for all loads was 1.7%. The mean coefficients of variation for pressure and flow measurements were 0.2% and 3%, respectively. In the second experiment the healthy subjects showed mean coefficients of variation for pressure and flow of 0.8% and 20.5%, respectively, and the patients showed mean coefficients of variation of 0.6% and 14.5%, respectively. CONCLUSIONS: During the in vitro experiment as well as during the experiments in patients with COPD and in healthy subjects only small variations in pressure were observed despite large variations in flow. The Threshold is a reliable and reproducible device for loading inspiratory muscles in patients with COPD as well as in healthy subjects.

Aged↗

On the mechanism of the mediolateral gradient of parasternal activation.

Recent studies have shown that in spontaneously breathing dogs the parasternal intercostals are activated according to a mediolateral gradient. To assess the mechanism of this regionalization of activity, we assessed the pattern of activation of these muscles after section of the dorsal roots and examined the topographic distribution of the muscle fiber types from the sternum to the chondrocostal junctions. The pattern of parasternal activity after dorsal rhizotomy was similar in all respects to that previously observed in intact animals. Thus activity in the medial parasternal bundles at the onset of inspiration frequently preceded activity in the middle bundles, and no activity was recorded from the lateral bundles. The amount of medial activity, when expressed as a percentage of the activity recorded during supramaximal tetanic stimulation of the internal intercostal nerve (maximal activity), was also consistently greater than the amount of middle activity (52.6 +/- 4.6 vs. 23.1 +/- 2.6% maximal activity; P < 0.001). Furthermore, the medial, middle, and lateral parasternal bundles had a higher proportion of slow-twitch oxidative fibers than of fast-twitch oxidative-glycolytic fibers; no topographic difference in fiber type distribution was observed. We conclude, therefore, that the mediolateral gradient of parasternal activity is probably due to the unequal distribution of central inputs throughout the pool of alpha-motoneurons.

Animals↗

Recovery of corticosteroid-induced changes in contractile properties and morphology of rat diaphragm.

Treatment with the fluorinated steroid triamcinolone (TR) induced type IIb fiber atrophy and the contractile profile of a slow muscle in rat diaphragm. In contrast, the nonfluorinated steroid prednisolone (PR) caused myogenic changes without fiber atrophy, and increased fatigability. The aim of the present study was to investigate the extent to which these changes were reversed 2 mo after discontinuation of treatment. Adult rats were randomly assigned to receive saline, PR 1.25 or 5 mg/kg, or TR 0.25, 0.5, or 1 mg/kg, intramuscularly daily during 4 wk. Administration of TR resulted in severe loss of body weight and dose-dependent mortality. During recovery, body weight in the TR groups increased gradually, still remaining reduced compared with the other groups. Two months after discontinuation of treatment, diaphragm weight was increased in proportion to body weight. Twitch characteristics, maximal tetanic force, force-frequency curve, and fatigue resistance of isolated diaphragm bundles were similar in all groups. Histologic examination of the diaphragm revealed no gross abnormalities in the PR and TR groups. Mild but significant type IIb fiber atrophy was still present in the diaphragm and gastrocnemius muscle of all TR-treated animals. In conclusion, recovery of alterations in morphology of respiratory and peripheral skeletal muscles induced by administration of TR is prolonged.

Animals↗

Peripheral muscle weakness contributes to exercise limitation in COPD.

Recently, it was suggested that fatigue of peripheral muscles could contribute to exercise limitation in patients with chronic obstructive pulmonary disease (COPD). In order to quantify the role of peripheral muscle force, we restudied potential determinants of exercise capacity (6-min walking distance [6 MWD] and maximal oxygen consumption [V02max]) in 41 consecutive COPD patients (FEV1, 43 +/- 19% of predicted, TLCO, 56 +/- 25% of predicted) admitted to our pulmonary rehabilitation program. VO2max (incremental cycle ergometer test), 6 MWD (best of three), lung function (FEV1, FVC, TLC, FRC), diffusing capacity (TLCO), isometric quadriceps force (QF), hand grip force (HF), and maximal inspiratory (PImax) and expiratory (PEmax) pressures were measured. Patients had a poor 6 MWD (372 +/- 136 m) and VO2max (1.35 +/- 0.60 L, 71%), reduced respiratory (PImax 65 +/- 27%) and peripheral muscle force (QF 74 +/- 27%, HF 82 +/- 23%). In single regression analysis, significant correlations (r) were found for VO2max and TLCO (0.68), FEV1 (0.64), QF (0.55), HF (0.53), and body weight (0.49). Walking distance was significantly correlated with QF (0.63), HF (0.61), PImax (0.49), and TLCO (0.38). In stepwise multiple regression analysis, the variables significantly contributing to 6 MWD were QF and Plmax. For VO2max, variables significantly contributing were TLCO, QF, and FEV1. We conclude that lung function and peripheral muscle force are important determinants of exercise capacity in COPD.

Body Weight↗

Effects of acute steroid administration on ventilatory and peripheral muscles in rats.

Occasional case reports have shown that acute myopathy may occur in patients treated with massive doses of corticosteroids. The mechanism of this myopathy is poorly understood. Therefore, 60 male rats were randomly assigned to receive daily injection of saline (C), methylprednisolone (M), or triamcinolone (T) 80 mg/kg/d for 5 d. Nutritional intake, measured daily in 15 animals, showed a significant reduction of food intake in the steroid-treated groups (-50 and -79% in M and T, respectively). This was associated with a similar loss in body weight. In the 45 remaining animals, diaphragm contractility and histopathologic features of several muscles were studied. Weights of respiratory and peripheral muscles were similarly decreased after steroid treatment. Maximal twitches of the diaphragm were lower in the C group (653 +/- 174 g/cm(2)) than in the M group (837 +/- 171 g/cm(2); p < 0.05) and the T group (765 +/- 145 g/cm(2), NS). Half-relaxation time was prolonged in both steroid groups, and time to peak tension was longer with M, whereas tetanic tensions were similar. Steroid treatment also induced a leftward shift of the force-frequency curve at 25 and 50 Hz when compared with saline treatment (p < 0.05). ATPase staining of the diaphragm, scalenus medius, and gastrocnemius showed type IIb fiber atrophy in the steroid groups and also diaphragmatic type IIa atrophy with T, whereas histologic examinations revealed a normal muscular pattern with absence of necrosis. Finally, a pair-fed (PF) study, performed in 18 rats (C, T, and PF), showed that muscle atrophy was considerably less pronounced in PF animals than in T-treated animals. We conclude that (1) short-term treatment with massive doses of steroids induced severe respiratory and limb muscle wasting; (2) both types of steroids induced predominantly type IIb atrophy, resulting in the expected alterations in diaphragm contractile properties; (3) neither steroid caused muscle necrosis; (4) type IIb atrophy was not caused by acute nutritional deprivation alone.

Adrenal Glands↗

Functional and histologic picture of steroid-induced myopathy in chronic obstructive pulmonary disease.

The functional and histologic picture of steroid-induced myopathy was systematically examined in eight patients with chronic obstructive pulmonary disease (COPD) and compared with control patients with COPD matched for age, sex, and degree of airflow obstruction. Steroid-induced myopathy was associated with severe peripheral muscle weakness, quadriceps force being 23 +/- 14 versus 71 +/- 23% in control patients with COPD (p < 0.001). In addition, clear ventilatory muscle weakness was present. PImax was 37 +/- 15 versus 67 +/- 24% in control patients (p < 0.001 ), and PEmax averaged 34 +/- 10 versus 74 +/- 23% (p < 0.001). Vital capacity tended to be slightly reduced compared with that in control patients (69 +/- 21 versus 80 +/- 16%, p = 0.11). The only biochemical abnormalities associated to steroid-induced myopathy were a moderately increased lactic dehydrogenase level (697 +/- 301 versus 421 +/- 128 IU/L, p < 0.001) and an increased creatine excretion in 24-h urine (990 +/- 609 versus 159 +/- 219 mg/24 h, p< 0.001). On quadriceps biopsy steroid-induced myopathy was characterized by increased variation in diameter of fibers, with several angular atrophic fibers and diffuse necrotic and basophilic fibers. In addition, increased amount of connective tissue in between fibers and increased number of subsarcolemmal and central nuclei were present. On ATPase stain diffuse fiber atrophy predominantly affecting fast fibers was present, but there was no indication that atrophy was confined to type IIb fibers in contrast to conventional thinking. On follow-up, survival of patients with steroid-induced myopathy was reduced in comparison with control patients with COPD with similar degree of airflow obstruction (p < 0.025).

Aged↗

Peripheral and respiratory muscles in chronic heart failure.

It is well-established that in patients with congestive heart failure (CHF), exercise is limited by fatigue and shortness of breath. The poor correlation between the fatigue and indices of central haemodynamic function might indicate that peripheral muscle alterations contribute to impaired exercise capacity. Intrinsic abnormalities of the skeletal muscles have been suggested as a possible explanation. Since the shortness of breath correlates poorly with changes in lung function, changes in the respiratory muscles have been investigated. Studies have demonstrated diaphragmatic myopathy and atrophy similar, in part, to the changes in peripheral skeletal muscles. In CHF, type I (slow twitch) fibre atrophy is seen in respiratory as well as in peripheral muscles. The mechanism of these alterations remains to be elucidated. Studies into the mechanism of muscle dysfunction in congestive heart failure are relevant to the prospect of treatment of the changes in peripheral and respiratory muscles.

Atrophy↗

Corticosteroid treatment and nutritional deprivation cause a different pattern of atrophy in rat diaphragm.

Triamcinolone (TR) causes type IIb fiber atrophy in the rat diaphragm, which is associated with changes in contractile properties. We investigated whether this is a direct effect of TR or the result of an accompanying loss of body and diaphragm weights. For 6 wk, adult rats received saline intramuscularly, TR (0.5 mg/kg im), or nutritional depletion (ND) that resulted in a similar (approximately 40%) reduction in body weight as TR. In these animals, the half-relaxation time of the diaphragm bundles increased, the force-frequency relationship shifted leftward, and the resistance to fatigue was increased. No histological changes were found in the ND diaphragm, in contrast to severe myogenic alterations in the TR diaphragm. Type IIb fiber cross-sectional area (CSA) in the TR diaphragm was reduced by 51%, whereas type I and IIa CSAs were unaffected. In the ND animals, the CSAs of type I, IIa, and IIb fibers were reduced by 31, 33, and 52%, respectively. Similar changes occurred in the deep part of the m. gastrocnemius. In conclusion, myogenic changes and selective type IIb fiber atrophy were caused by TR, whereas ND induced generalized fiber type atrophy without histological changes.

Adrenal Cortex Hormones↗

Theophylline increases oxygen consumption during inspiratory resistive loading.

The effect of theophylline on diaphragmatic blood flow (Qdi) and oxygen consumption (VO2di) was studied in eight lightly anesthetized dogs during quiet breathing and inspiratory resistive loading. Qdi was determined with the radioactive microsphere tracer technique, and VO2di was calculated as the product of Qdi and the diaphragmatic arterio-venous oxygen difference. During quiet breathing, theophylline increased minute ventilation (9.3 +/- 1.7 versus 5.1 +/- 0.4 L/min), mean inspiratory flow (547 +/- 60 versus 378 +/- 56 ml/s), and duty cycle (0.270 +/- 0.042 versus 0.192 +/- 0.024) but did not significantly alter Qdi or VO2di. Conversely, Qdi increased significantly during loaded breathing compared with quiet breathing (37 +/- 4 versus 27 +/- 3 ml/100 g/min) and was further increased by theophylline (45 +/- 7 ml/100 g/min). Theophylline did not alter the tension-time index of the diaphragm (TTdi) during inspiratory resistive loading (0.054 +/- 0.006 versus 0.056 +/- 0.004, p NS) but resulted in a disproportionate and significant increase in VO2di (2.66 +/- 0.53 versus 1.78 +/- 0.26 ml/100 g/min). Similarly, total-body oxygen consumption (VO2TB) during inspiratory loading increased significantly after theophylline (24%), but the tension-time index of the inspiratory muscles (TTi), a measure of the total respiratory load, was unchanged. We conclude that theophylline significantly increases VO2di and VO2TB at the same TTdi and TTi during resistive loading. This enhanced energy expenditure needs consideration in the clinical management of pulmonary disorders that increase the work of breathing.

Animals↗

Mechanism of theophylline-induced inotropic effects on foreshortened canine diaphragm.

The mechanisms of theophylline-induced inotropic effects at shorter diaphragm length have not yet been explored. We wondered whether the greater inotropic effects of the drug at shorter diaphragm length might result from an effect on intracellular calcium level. Forty pairs of diaphragm bundles were stimulated at 70% of optimal length in the presence of either verapamil (10(-5)M), calcium-free Krebs solution (buffered or not with 2 mM ethylene glycol tetra-acetic acid (EGTA)) or ryanodine (10(-6) M). Theophylline (1 mM) was subsequently added to one muscle bundle and, after 15 min, twitches were repeated. The twitch potentiation induced by theophylline (37 +/- 21%) was unaffected by verapamil (43 +/- 26%), or zero calcium (39 +/- 18%) and virtually unchanged when the latter was buffered with EGTA. By contrast, theophylline failed to increase twitch tension after pretreatment with ryanodine, a blocker of the calcium release by the sarcoplasmic reticulum. This decreased twitch tension in control (-5 +/- 11%) and experimental (-14 +/- 12%) bundles and prolonged half-relaxation time as a result of impaired sarcoplasmic reticulum calcium reuptake. We conclude that the inotropic effects of theophylline on twitch tension in foreshortened canine diaphragm bundles were not related to sarcoplasmic reticulum. This is consistent with an action of theophylline on the sarcoplasmic reticulum.

Analysis of Variance↗

Rat diaphragm contractility and histopathology are affected differently by low dose treatment with methylprednisolone and deflazacort.

The extent to which treatment with low doses of the nonfluorinated steroid methylprednisolone affects diaphragm contractility and morphology is unknown. In the present study, we compared the effects of equipotent doses of methylprednisolone and deflazacort, an oxazoline derivate of prednisolone with less systemic side-effects on bone structure and carbohydrate metabolism. Twenty six male adult rats were randomized to receive daily saline (control), methylprednisolone 0.4 mg.kg-1 or deflazacort 0.5 mg.kg-1 i.m. Contractile properties and histopathology were measured after a 6 week treatment period. During treatment, body weight increased in control and methylprednisolone-treated animals, but decreased by 4.2 +/- 1.1% (mean +/- SD) in the deflazacort group. Similarly, diaphragm mass in the deflazacort group was decreased compared to control and methylprednisolone groups. Twitch tension and twitch characteristics of isolated diaphragm bundles were similar in the three groups. Maximal tetanic tension was decreased in the deflazacort group. The force-frequency curve of the deflazacort bundles shifted downwards compared to control. Fatigue occurring during this protocol was greatest in the methylprednisolone- and deflazacort-treated animals. Microscopic examination revealed no gross abnormalities in the three groups. Histochemical analysis after staining for myosin adenosine triphosphatase (ATP-ase) showed that in the deflazacort group cross-sectional area of type I, IIa and IIb fibres were decreased. We conclude that low doses of methylprednisolone caused subtle and negligible changes in rat diaphragm contractile properties without affecting fibre dimensions, while deflazacort at an equipotent dose induced generalized fibre atrophy and changes in diaphragm contractility.

Animals↗

Contribution of the parasternal intercostals to inspiratory rib elevation in dogs.

To estimate the contribution of the parasternal intercostals to rib elevation during quiet breathing, parasternal intramuscular pressure, Pim, in the fourth interspace and displacement of the rib just below were measured in eight supine anesthetized dogs during: (1) bilateral stimulation of the parasternals, (2) quiet breathing before, after phrenicotomy, and subsequent vagotomy. During quiet breathing, the parasternal contribution averaged 66 +/- 12% of the rib elevation caused by inspiratory rib cage muscles. This contribution decreased in relative terms after phrenicotomy (37 +/- 14%) and subsequent vagotomy (26 +/- 14%) while it tended to increase in absolute terms (from 1.9 +/- 2.4 to 2.1 +/- 2.5 NS, and 2.4 +/- 2.4 mm P < 0.01, respectively). Rib elevation caused by inspiratory rib cage muscles increased after phrenicotomy (116 +/- 63%, P < 0.001) and subsequent vagotomy (279 +/- 60%, P < 0.001) as did Pim (19 +/- 10% NS and 41 +/- 36% P < 0.01, respectively). Moreover, the mechanical interaction of the parasternals among different interspaces measured in three other dogs, was likely to be limited during quiet breathing. We conclude that after diaphragm paralysis, the parasternals played a progressively smaller role while other rib cage muscles were increasingly recruited.

Animals↗