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Biomedical subjects

M Decramer

Publications and source records attributed to M Decramer.

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

Physical performance of patients with numerous psychosomatic complaints suggestive of hyperventilation.

In some patients exercise induces numerous complaints which cannot be attributed to an organic disorder, and which are suggestive of hyperventilation. The study was designed to investigate in this type of patient: 1) exercise capacity and muscle force; 2) breathing pattern and symptoms during maximal exercise and recovery; 3) relationships between symptoms and breathing pattern. Twenty-four patients were compared with 20 healthy subjects. They performed a maximal incremental cycle ergometer test and peripheral and respiratory muscle strength were measured. Patients tended to have a decreased exercise capacity and presented with moderately reduced muscle strength. At comparable minute ventilation, breathing frequency was higher (mean: 24 versus 21 per minute) and tidal volume smaller (mean: 1.42 versus 1.67 L). End-tidal partial pressure of carbon dioxide (PET,CO2) was not significantly different. A significant relation was observed between PET,CO2 and respiratory frequency during recovery in patients, suggesting a reduced flexibility of the ventilatory response to exercise. In patients respiratory complaints and paresthesias were weakly correlated to PET,CO2 at moderate exercise. It is suggested that the physical deconditioning observed in those patients is rather a consequence than a cause of the response to exercise. The link between symptoms and breathing pattern might be explained by a psychological conditioning process.

Adult↗
PubMed1998

Biliary cirrhosis induces type IIx/b fiber atrophy in rat diaphragm and skeletal muscle, and decreases IGF-I mRNA in the liver but not in muscle.

BACKGROUND/AIMS: Patients with cirrhosis complain of fatigue, which in part may be due to the progressive muscle atrophy, noted especially when signs of decompensation appear. In addition, weaning from mechanical ventilation may be difficult in some patients following liver transplantation. Since little is known about the peripheral muscles and the diaphragm in cirrhosis, we investigated diaphragm and gastrocnemius histochemical properties, and diaphragm contractile properties in male rats with biliary cirrhosis. In addition, the extent to which insulin-like growth factor I (IGF-I) was involved in the regulation of muscle function was also examined, since IGF-I is known to induce growth and regeneration as well as to exert a protein anabolic action. METHODS: Ten rats underwent a sham operation, while another ten underwent bile duct ligation and excision. After 5 weeks, biliary cirrhosis was confirmed histologically in random liver biopsies. RESULTS: Compared to sham animals, diaphragm mass in cirrhotic rats was decreased by 10% (p<0.05), while masses of other respiratory (e.g. scalenus medius -21%, p<0.001) or peripheral muscles (e.g. gastrocnemius -24%, p<0.0001) decreased more. No changes in diaphragm force nor in its endurance were observed between the two groups. However, a clear decrease in the cross-sectional area of type IIx/b muscle fiber was present in both diaphragm (1360+/-147 vs 1112+/-167 microm2, p<0.02) and gastrocnemius (1954+/-265 vs 2328+/-245 microm2, p<0.02). Finally, hybridization of Northern blot with a rat cDNA IGF-I probe (gift from Dr D. Leroith, Bethesda, USA) labeled with alpha-32P revealed that in cirrhotic rats, the relative expression of IGF-I was markedly reduced by 45% in the liver (p<0.05) but was unchanged in the two muscles studied. CONCLUSIONS: In this model of biliary cirrhosis: (i) muscle wasting was less pronounced in the diaphragm than in other muscles; (ii) type IIx/b fiber atrophy in respiratory (diaphragm) and peripheral muscles (gastrocnemius) developed while diaphragm contractile properties remained unchanged; and (iii) the relative expression of IGF-I was reduced in the liver only, while it remained unchanged in the muscle. The functional significance of these changes, their pathogenesis and presence in other models and in human cirrhosis remain to be elucidated.

Animals↗
PubMed1998

Contractile properties and histochemical characteristics of the rat diaphragm after prolonged triamcinolone treatment and nutritional deprivation.

The influence of decreased muscle mass and reduced food intake on diaphragm structure and contractility in male Wistar rats was determined after triamcinolone acetate treatment (TR: 0.5 mg per kg per day for 4 weeks) and two degrees of undernutrition (PW: pair-weight, which resulted in a similar (41%) reduction of body weight as TR; PF: pair-fed, which resulted in a moderate (13%) reduction of body weight) and a free-fed control group (FF, with an increase (9%) in body weight). energy intake of TR decreased, but based on daily measurements of food intake and body weight, energy expenditure of the TR rats was increased compared with the other groups. Body (BW) and muscle weights were reduced in proportion to the extent of undernutrition in the nutritionally deprived rates (i.e. BW and diaphragm weight of PF animals were reduced 215 and 16% respectively compared with FF, v. a. 48% and 41% reduction in the PW group). Triamcinolone-induced atrophy was limited to type II fibres (30% of type IIa and 45% of type IIx/b, p < 0.05), while severe chronic undernutrition (PW) induced a generalized fibre type atrophy in the diaphragm (23% type I, 38% type IIa and 49% type IIx/b, p < 0.05), and moderate undernutrition (PF) caused only significant type IIa atrophy (20%, p < 0.05). A leftward shift of the diaphragmatic tension-frequency relationship and a decreased fatiguability of the TR and PW bundles were observed (p < 0.01), while the PF bundles were not significantly different compared with FF. These results suggest that triamcinolone and severe undernutrition cause similar alterations in in vitro contractility of the diaphragm. The effects of triamcinolone treatment on diaphragm structure may be partly explained by the reduced food intake, but the atrophy pattern induced by severe undernutrition (PW) was different.

Age Factors↗
PubMed1998

Low load inspiratory muscle training increases diaphragmatic fiber dimensions in rats.

The effects of 8 wk of inspiratory resistive loading (30 min/d, 3 x/wk) on diaphragm mass, contractile properties, fatigue, and fiber dimensions were studied in 10 male Wistar rats. They were conditioned to breathe through a Hans-Rudolph device. Half of them had to overcome a moderate inspiratory resistance (MR; n = 5), whereas the others only had to overcome the small resistance (SR; n = 5) of the inspiratory valve of the device. Results were compared with control rats (C; n = 5) moving and breathing freely. At the end of training, animals submitted to MR and SR generated mean inspiratory pressures of -2.5 +/- 1.1 and -0.2 +/- 0.05 cm H2O, respectively. TI/Ttot was 0.60 +/- 0.06 and 0.57 +/- 0.05, respectively. Body and diaphragm weight were unaffected by loading. Little or no change in in vitro diaphragmatic twitch kinetics, force generation, and fatigability was found between the three groups. Nevertheless, cross-sectional area of all fiber types increased in the two loaded groups compared with control animals. This increase reached statistical significance for type I fibers in the MR group (846 +/- 74 microm2) compared with the C and SR groups (589 +/- 32 and 683 +/- 96 microm2, respectively, p < 0.05). For IIa fibers both training groups were significantly different from the control group (SR: 768 +/- 99 and MR: 790 +/- 108 versus C: 592 +/- 37 microm2, p < 0.05). A hypertrophy of type IIx/b fibers was seen in MR compared with control animals (C: 1,555 +/- 136, SR: 1,845 +/- 338, MR: 2,053 +/- 326 microm2, p < 0.05). No differences were present in fiber type proportions between the three groups. We conclude that in our training setup, 8 wk of intermittent long-term inspiratory loading stressed the diaphragm already with a small resistance resulting in hypertrophy of predominantly type IIa fibers. A higher resistance resulted in hypertrophy of all fiber types.

Animals↗
PubMed1998

Systolic ventricular dysfunction causes selective diaphragm atrophy in rats.

In order to examine the relative impairment of the diaphragm and other skeletal muscles in systolic ventricular dysfunction (VD), their structure and function were compared between rats with VD induced by left coronary artery ligation (n = 17) and sham-operated rats (Co, n = 10). In addition, in an attempt to unravel the mechanism of the observed impairment, we examined alterations in insulin-like growth factor-I (IGF-I) serum levels and IGF-I expression in the liver, diaphragm, and gastrocnemius. In a second series of rats (VD, n = 5 and Co, n = 5) hemodynamic measurements were performed. All measurements were performed 3 mo after the operation. Infarct size averaged 32 +/- 10 and 44 +/- 20% in the two series, respectively (NS). Hemodynamic measurements revealed a decrease in left ventricular peak systolic pressure of 19% (p < 0. 05). Significant diaphragm atrophy (weight: 622 +/- 52 mg in VD versus 750 +/- 54 mg in Co, p < 0.0005), without alterations in diaphragm contractile properties was present in VD animals. For all animals combined, the reduction in diaphragm weight was related to infarct size (r = -0.74, p < 0.001). No alterations were observed in the other inspiratory and peripheral muscles. ATPase staining of the diaphragm showed atrophy of type I and type IIx/b fibers, their cross-sectional area (CSA) being reduced by 13 and 16%, respectively (p < 0.05). There were no signs of myopathic alterations. IGF-I expression was increased by 55% in the diaphragm of rats with VD (p < 0.05). IGF-I expression in the liver and gastrocnemius and serum IGF-I levels were unaltered. These data suggest the presence of compensatory mechanisms aimed at minimizing diaphragmatic fiber atrophy. We conclude that systolic VD caused: (1) selective diaphragm atrophy, which was related to infarct size; (2) a decrease in diaphragm type I and IIx/b CSA not associated with myopathic changes; (3) an increase in the IGF-I mRNA content of the diaphragm. The selective diaphragm involvement in the present study may be related to the moderate degree of ventricular dysfunction induced.

Adenosine Triphosphatases↗
PubMed1998

[The effect of corticotherapy on respiratory muscles].

Skeletal muscle myopathy is one of the main side-effects of systemically administered corticosteroids, and involves respiratory as well as peripheral muscles. After prolonged treatment with moderate doses of either fluorinated or non-fluorinated corticosteroids, chronic myopathy may occur. In patients, such myopathy is characterized by the gradual onset of proximal limb muscle weakness and a sudden increase in creatine excretion in 24h urine. This myopathy is associated with a generalized fiber atrophy of the quadriceps in which myopathic changes are present. Since these changes were also observed in animal models, it was concluded that steroid treatment was responsible for them. After cessation of treatment, recovery of muscle force occurs but may be protracted. The severity of corticosteroid-induced myopathy appears to depend upon the type of steroid used, the treatment duration, the dose and the treatment regimen where repetitive burst treatment effects are worse than those obtained with continuous treatment with the same dose. During short-term treatment with massive doses of corticosteroids as frequently used to treat status asthmaticus, acute myopathy may develop and is characterized by generalized fiber necrosis and rhabdomyolysis. Because such necrosis was not observed in animal studies, it was suggested that the necrosis may result from the combined effect of corticosteroids with other agents such as aminoglycoside antibiotics and/or muscle relaxants.

Adrenal Cortex Hormones↗
PubMed1998

Peripheral skeletal muscles and exercise performance in patients with chronic obstructive pulmonary disease.

Impaired exercise capacity is a common finding in chronic obstructive pulmonary disease (COPD) patients. This reduction is not a simple consequence of airflow limitation. Peripheral muscle weakness, deconditioning and impaired gas exchange, were recognized as important contributors to exercise intolerance. In this overview, the contribution of peripheral muscle function and muscle training to exercise performance is discussed by means of three questions: 1) Is peripheral muscle dysfunction contributing to exercise limitation in COPD? 2) How do we measure peripheral muscle function? 3) Are peripheral muscle training modalities effective? At present, there is substantial evidence for peripheral muscle dysfunction. Both reduced force generating capacity as well as impaired muscle metabolism were observed and these findings contributed substantially to the reduced exercise capacity in COPD. Peripheral muscle strength measurements are feasible with mechanical or electronic devices and revealed muscle weakness in COPD patients. However, this weakness is not uniform for all muscle groups. Upper arm and leg muscles were more affected than hand muscles. This may, at least in part, be related to differences in the levels of inactivity between leg and hand muscles. In addition, muscle weakness is associated with impaired exercise capacity and symptoms of increased exertion during exercise. Endurance exercise training, i.e. cycling and treadmill walking, improved exercise capacity and was associated with alterations in muscle metabolism. Strength training of peripheral muscles showed increases in submaximal exercise performance and quality of life measures. These improvements were observed independently of the degree of airflow obstruction. The optimal training regimen (strength or endurance), and the muscle groups to be trained, remain to be determined.

Exercise↗
PubMed1997

Montelukast causes prolonged, potent leukotriene D4-receptor antagonism in the airways of patients with asthma.

Montelukast, a new specific oral cysteinyl LT3-receptor antagonist was evaluated for its activity in attenuating inhaled leukotriene D4 (LTD4) bronchoconstriction in patients with asthma. In two double-blind, placebo-controlled, randomized crossover studies, patients with mild asthma (forced expiratory volume in 1 second [FEV1] > or = 70%) were studied. In trial A, LTD4 challenge began 4 hours (peak plasma concentration) after a single dose of placebo or 5, 20, 100, and 250 mg montelukast. In trial B, and LTD4 challenge was started 20 hours after administration of placebo, 40 mg montelukast, or 200 mg montelukast. During each challenge, twofold increasing concentrations of LTD4 were inhaled until specific airways conductance (sGaw) decreased by at least 50% (PC50) or the highest concentration of LTD4 was inhaled. In trial A with all doses and in trial B with the 200 mg dose, bronchoconstriction was attenuated (50% fall in sGaw was not observed) up to the highest dose of LTD4 administered. In trial B, during the 40 mg period, only two of six patients exhibited a 50% fall in sGaw; PC50 ratios (montelukast 40 mg/placebo) were 18 and 45 in these two patients. These results indicate that montelukast is a highly potent and long-lasting antagonist of LTD4-induced bronchoconstriction in patients with asthma.

Acetates↗
PubMed1997

Effects of nandrolone decanoate on respiratory and peripheral muscles in male and female rats.

Thirty male and 18 female adult rats received weekly an intramuscular injection of either saline (control; C), 1.5 mg/kg (low-dose; LD) nandrolone decanoate or 7.5 mg/kg (high-dose; HD) nandrolone decanoate during 5 wk. Compared with respective C, growth rate was stunted in male HD rats from 2 wk of treatment on, whereas it was enhanced in female LD and HD rats after 1 wk. Mass of all muscles studied varied proportionally to body weight, except for the gastrocnemius (males: 0.49 +/- 0.04 vs. C: 0.52 +/- 0.03%, not significant; females: 0.17 +/- 0.01 vs. C: 0.15 +/- 0.01%, P < 0.05). In vitro contractile and fatigue properties of the diaphragm remained unchanged, except for a decrease in twitch kinetics (time to peak tension: C, 21 +/- 2; LD, 19 +/- 1; HD, 19 +/- 2 ms, P < 0.05; half-relaxation time: C, 26 +/- 5, LD, 25 +/- 5, HD, 23 +/- 3 ms, P < 0.01). Histochemistry of the diaphragm and the gastrocnemius revealed a significant increase in type IIx/b dimensions. In the gastrocnemius, type I fiber dimensions also increased. A pair-fed study, including another 24 female rats, showed that the changes in oral food intake only partly accounted for the observed anabolic effects.

Anabolic Agents↗
PubMed1997

Broxaterol increases force output of fatigued canine diaphragm more than salbutamol.

We previously demonstrated that broxaterol enhanced recovery of fatigued canine diaphragm. The aim of this study was to compare the inotropic effects of salbutamol and broxaterol on fatigued canine diaphragm. Low-frequency fatigue was induced in 14 mongrel dogs by electrophrenic stimulation, which was continued until transdiaphragmatic pressure (Pdi) at 20 Hz was reduced by 50% or for 1 h. After stabilization of fatigue, the animals received a bolus (18.5 microg/kg) of either broxaterol or salbutamol, followed by a continuous infusion (0.43 microg/kg/min). A second bolus of 74.0 microg/kg, followed by a continuous infusion of 1.72 microg/kg/min, was given after 90 min. Both drugs significantly increased twitch Pdi. Twitch Pdi measured 90 min after the first and second doses of broxaterol increased by 28 +/- 23% and 42 +/- 34%, respectively, whereas the salbutamol-induced increase was clearly smaller (9 +/- 10% and 17 +/- 15%, respectively). Broxaterol increased Pdi at 20 Hz by 25 +/- 28% with the first dose and by 29 +/- 21% with the second dose. In contrast, salbutamol did not alter Pdi at 20 Hz. Neither drug affected Pdi at 100 Hz. We conclude that broxaterol promoted recovery of low-frequency fatigue of the canine diaphragm in vivo in a dose-dependent manner, whereas salbutamol only minimally improved force production by the fatigued diaphragm.

Adrenergic beta-Agonists↗
PubMed1997

Intermittent inspiratory muscle training induces fiber hypertrophy in rat diaphragm.

The effects of 8 wk of moderate load intermittent inspiratory resistive loading on diaphragm contractility, and histochemistry of the diaphragm, scalenes, and gastrocnemius were studied in rats. A resistance was placed in the inspiratory port of a Hans-Rudolph valve, through which each animal breathed during 30 min/d, 5 times/wk (loaded group, n = 10). These rats were compared with animals breathing through the same device without inspiratory resistance (control group, n = 10). During loading, animals generated mean inspiratory pressures of -3.2 +/- 1.7 cm H2O with a TI/Ttot of 0.69 +/- 0.06, resulting in a tension-time index of 0.050. At the end of training, the diaphragm mass increased in loaded animals (0.17 +/- 0.01% body mass) compared with control animals (0.15 +/- 0.01%, p < 0.01), while scalene and gastrocnemius mass remained unchanged. Diaphragmatic force as well as fatigue resistance were similar in both groups, whereas time to peak tension was significantly (p < 0.01) shorter in loaded rats (18.8 +/- 1.7 ms) compared with control rats (21.2 +/- 1.8 ms), half-relaxation time remaining unchanged. Finally, hypertrophy of diaphragmatic type IIa (+19%, p < 0.01) and IIx/b (+12%, p < 0.05) was present in the loaded group. Histochemistry of the scalenes remained unchanged, whereas type IIx/b hypertrophy (+12%, p < 0.001) was observed in the gastrocnemius internus. We speculate that the latter was due to multiple escape maneuvers. We conclude that intermittent inspiratory muscle training: (1) caused fast twitch fiber hypertrophy in the diaphragm; (2) did not produce any effect in the scalenes.

Adaptation, Physiological↗
PubMed1997

Muscle weakness is related to utilization of health care resources in COPD patients.

The factors determining utilization of health care resources in patients with chronic obstructive pulmonary disease (COPD) are poorly understood. In order to obtain insight into these factors, we studied the utilization of health care resources in 57 stable COPD patients with a forced expiratory volume in one second (FEV1) of 36 +/- 9% predicted. Patients were divided into two groups: admitted at least twice in the last year (high medical consumption; n = 23) or not admitted in the last year (low medical consumption; n = 34). Other variables related to utilization of health care resources studied were; the number of hospital days; the number of out-patient visits to a pulmonary department in the last year; and the average daily dose (ADD) of corticosteroids taken in the last 6 months. The actual cost of utilization of health care resources, however, was not studied. In addition, pulmonary function, serum electrolytes, blood gas values, 6 min walking distance, respiratory and peripheral muscle force, and appraisal of self-care agency (ASA score) were studied. Pulmonary function, serum electrolytes, blood gas values, ASA score and walking distance were not different between the two groups (e.g. FEV1 36 +/- 8 vs 36 +/- 10% pred). Respiratory muscle forces tended to be lower in the high medical consumption group, this tendency almost reaching statistical significance for maximal expiratory pressure (PE,max) (p = 0.08). Peripheral muscle force, however, was clearly reduced in the high medical consumption group (quadriceps force 63 +/- 20 vs 82 +/- 26% pred; p < 0.05). The number of admissions, the number of hospital days, the number of out-patient visits, and ADD were interrelated and also related to ventilatory and peripheral muscle force (r -0.18 to -0.38). This relationship was statistically significant for PE,max, whilst a similar tendency was present for maximal inspiratory pressure (PI,max). In stepwise multiple regression analysis, only quadriceps force was a significant determinant of utilization of health care services. We conclude that utilization of health care services in patients with chronic obstructive pulmonary disease is related to ventilatory and peripheral muscle force. Whether or not reduced muscle force is simply an expression of disease severity remains to be determined.

Activities of Daily Living↗
PubMed1997

Exercise training in COPD patients: the basic questions.

Pulmonary rehabilitation programmes aim at improving exercise capacity, activities of daily living, quality of life and perhaps survival in patients with chronic obstructive pulmonary disease (COPD). Recently, well-designed studies investigated and confirmed the efficacy of comprehensive pulmonary rehabilitation programmes, including exercise training, breathing exercises, optimal medical treatment, psychosocial support and health education. In the present overview, the contribution of exercise training in clinical practice to the demonstrated effects of pulmonary rehabilitation is discussed by means of six basic questions. These include: 1) the significance of exercise training; 2) the optimal intensity for exercise training; 3) prescribing training modalities; 4) the effects of exercise training combined with medication, nutrition or oxygen; 5) how training effects should be maintained; and 6) where the rehabilitation programme should be performed: in-patient, out-patient or homecare? First, exercise training has been proven to be an essential component of pulmonary rehabilitation. Training intensity is of key importance. High-intensity training (>70% maximal workload) is feasible even in patients with more advanced COPD. In addition, the effects on peripheral muscle function and ventilatory adaptations are superior to low-intensity training. There is, however, no consensus on the optimal training modalities. Both walking and cycling improved exercise performance. Since peripheral muscle function has been recognized as an important contributor to exercise performance, specific peripheral muscle training recently gained interest. Improved submaximal exercise performance and increased quality of life were found after muscle training. The optimal training regimen (strength or endurance) and the muscle groups to be trained, remain to be determined. Training of respiratory muscles is recommended in patients with ventilatory limitation during exercise. The additional effects of anabolic-androgenic drugs, oxygen and nutrition are not well-established in COPD patients and need further research. In order to maintain training effects, close attention of the rehabilitation team is required. The continuous training frequency necessary to maintain training effects remains to be defined. At this point in time, out-patient-based programmes show the best results and guarantee the best supervision and a multidisciplinary approach. Future research should focus on the role of homecare programmes to maintain improvements.

Exercise↗
PubMed1997

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↗
PubMed1996

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↗
PubMed1996

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↗