Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In eight extrinsic asthmatic subjects (age range 16-38 years) there was a significant reduction (p less than 0.01) in the severity of bronchoconstriction after a treadmill exercise test performed 30 minutes after nifedipine 20 mg sublingually. The maximum fall in peak expiratory flow after exercise was 36.0 +/- SEM 5.3% compared with a maximum fall of 56.5 +/- 4.1% after matched placebo capsules when given in double-blind randomised manner on separate days. There was no significant resting bronchodilation or change in blood pressure or heart rate after nifedipine. there was a significant rise in venous plasma histamine during exercise with placebo (6.1 +/- 0.8 to 13.5 +/- 3.5 nmol/l, p less than 0.01) but no significant increase with nifedipine (4.6 +/- 0.6 to 4.7 +/- 0.6 nmol/l) suggesting that nifedipine inhibits the release of mast cell mediators. The dose of inhaled histamine which provoked a 20% fall in peak expiratory flow was also significantly higher (p less than 0.05) with nifedipine (1.5 +/- 0.31 mg/ml) compared with placebo (2.7 +/- 0.63 mg/ml), indicating that there is a small inhibitory effect on bronchial smooth muscle contractility. Nifedipine is a potent antagonist of calcium ion influx in smooth muscle and secretory cells, and these studies suggest that it may inhibit release of mast cell mediators and reduce bronchial smooth muscle contractility in asthma.
Thorax 1981 Oct
PMID:A calcium antagonist, nifedipine, modifies exercise-induced asthma. 703

Ten patients with severe dyspnoea and chronic airflow obstruction entered a randomised double-blind crossover trial comparing the effect of carbimazole 80 mg daily for two months with that of placebo. Assessment of thyroid function, lung function, and exercise tolerance was performed monthly. The mean free thyroxine index after two months of carbimazole was significantly lower at 64.1 (+/- 10.5, SEM) than the 89.1 (+/- 3.8) while on placebo. Serum tri-iodothyronine was reduced and thyroid stimulating hormone raised while on the active drug. There was no significant difference in the 12-minute walking distance (TMD), the rating of perceived exertion during the TMD, the oxygen cost score, the dyspnoea grade, the resting arterialised capillary blood gas tensions or the resting minute ventilation. During a progressive exercise test to exhaustion on a cycle ergometer, there was no significant difference in the minute ventilation, heart rate, blood gas tensions at exhaustion, or the total work done. There were no symptoms or signs of hypothyroidism. Lung function (FEV1, FVC, TLC, KCO) was unchanged. Thus a 28% reduction in the free thyroxine index produced no symptomatic or objective benefit in exercise tolerance in patients with severe airflow obstruction. These results provide no support for the use of carbimazole in chronic airflow obstruction.
Thorax 1982 Jan
PMID:Carbimazole and exercise tolerance in chronic airflow obstruction. 704 24

Peak plasma concentrations of lignocaine were recorded in 41 patients receiving topically applied lignocaine for fiberoptic bronchoscopy. Adequate anaesthesia was achieved in all patients with an average dose per unit weight of 9.3 +/- 0.5 mg/kg (SEM) giving a mean peak plasma concentration of 2.9 +/- 0.5 mg/l-1 (SEM) (+/- SEM 0.5). The plasma concentration exceeded toxic levels of 5.0 mg/l-1 in only two patients, and no complications were observed. Peak concentrations were influenced only by dose per unit weight administered and not by factors considered likely to influence mucosal absorption from the bronchial tree, such as sputum production, airflow obstruction, or cigarette smoking. A major proportion of the total dose of lignocaine was required to anaesthetise the nose, pharynx, and larynx, only a small proportion being needed for the bronchial tree. Lignocaine gel (2% w/v) was preferred by patients, and in a study of 10 volunteers, produced lower plasma concentrations when used as a topical anaesthetic than did lignocaine aerosol (10% w/v) or lignocaine solution (4% w/v).
Thorax 1982 Jan
PMID:Plasma concentrations of lignocaine during fibreoptic bronchoscopy. 707 96

Pulmonary fat embolism occurs frequently after trauma but its functional significance is often unclear. To obtain direct evidence of lung damage caused by fat embolism we have measured changes in permeability of the alveolar-capillary interface. A permeability index was derived from the half time clearance from lung to blood (T1/2LB) of 99mTcDTPA introduced into the lung in a 1 ml bolus. Three groups of rabbits were studied. Baseline T1/2LB. did not differ significantly between groups. After intravenous injection of saline placebo in one group and of 300 mg/kg triolein in another group there was no change in permeability index. After intravenous injection of 100 mg/kg oleic acid in the third group there was an immediate change in T1/2LB from a monoexponential baseline 280 +/- 20 min (SEM) to a multiexponential curve which was resolved into two components, one with a T1/2LB of 3.2 +/- 0.6 min (SEM) and the other 39.5 +/- 7.6 min (SEM). Statistically significant changes in alveolar-arterial PO2 difference, dynamic compliance, chest radiography, and postmortem lung water accompanied the changes in T1/2LB in this group. There were no significant changes in these variables in the placebo or triolein group. Histological studies of the lung tissue of these animals using the osmic acid stain for fat showed no fat in the placebo group, extensive fat embolisation which was densely stained in the triolein group and much less densely stained fat in the oleic acid group. Measurement of the permeability of the alveolar-capillary interface provides direct evidence of lung damage after oleic acid embolisation. There were no functional changes in animals with extensive embolisation with triolein.
Thorax 1982 Mar
PMID:Pulmonary epithelial permeability is immediately increased after embolisation with oleic acid but not with neutral fat. 710 Dec 21

The diffusing capacity of the lung, or transfer factor, for carbon monoxide (TLCO) was measured in 12 patients with polycythaemia rubra vera. This was significantly raised (mean 152% predicted, SEM +/- 14%) and remained so even after correction to a standard haemoglobin concentration of 14 . 6 g/dl (mean 139% predicted, SEM +/- 13%). Serial measurements of TLCO on two patients after treatment of polycythaemia rubra vera showed a greater fall in relation to haemoglobin concentration than would have been predicted on theoretical grounds if the increases in TLCO had been due entirely to the increased haemoglobin concentration. The pulmonary capillary blood volume (estimated from TLCO) also fell in these two patients after treatment. There was a strong correlation between TLCO and the technetium-99m-labelled red cell volume for the seven men (r = 0 . 92; p less than 0 . 01) and five women (r = 0 . 99; p less than 0 . 001) when studies were performed on the same day. In patients with polycythaemia rubra vera who have no evidence of coexistent pulmonary disease the pulmonary capillary bed appears to share in the expansion of the body blood volume. The single-breath TLCO test may act as a convenient and simple monitor for the response of the disease to treatment.
Thorax 1982 Jul
PMID:Carbon monoxide diffusing capacity in polycythaemia rubra vera. 713 94

To determine whether anaesthesia of the intrathoracic airways would attenuate the development of exercise-induced asthma, we studied eight symptomless asthmatic patients by cycle ergometry after saline or lignocaine pretreatment while they were breathing air at 24 degrees C with 9.1 mg of H2O/l. Pulmonary mechanics were measured before and after the administration of each agent, and again five minutes after cessation of exercise. Sufficient lignocaine was administered to abolish the gag reflex and the cough response to aerosols of citric acid. Before exercise there were no significant differences for any lung function variable between the saline and lignocaine results. Equally, there were no significant differences between these agents for minute ventilation (VE) during exercise (VE lignocaine = 71.0 +/- 7.4 (SEM) l/min; VE saline 67.2 +/- 8.1 l/min;), or in the severity of the subsequent bronchospastic response (for example, the FEV1 with saline was 22.6 +/- 2.9% decrease, and with lignocaine 23.6 +/- 8.5%). Thus these results do not support the idea that there are thermally sensitive neural receptors in intrathoracic airways that play a role in the pathogenesis of exercise-induced asthma.
Thorax 1982 Oct
PMID:Controlled-analysis of the effects of inhaled lignocaine in exercise-induced asthma. 715 12

To investigate the role of endorphins in central respiratory control, the effect of naloxone, a specific opiate antagonist, on resting ventilation and ventilatory control was investigated in a randomised double-blind, placebo-controlled study of normal subjects and patients with chronic airways obstruction and mild hypercapnia due to longstanding chronic bronchitis. In 13 normal subjects the ventilatory response to hypercapnia increased after an intravenous injection of naloxone (0.1 mg/kg), ventilation (VE) at a PCO2 of 8.5 kPa increasing from 55.6 +/- SEM 6.2 to 75.9 +/- 8.21 min-1 (p less than 0.001) and the delta VE/delta PCO2 slope increasing from 28.6 +/- 4.4 to 34.2 +/- 4.21 min-1 kPa-1 (p less than 0.05). There was no significant change after placebo (saline) injection. Naloxone had no effect on resting ventilation or on the ventilatory response to hypoxia in normal subjects. In all six patients naloxone significantly (p less than 0.02) increased mouth occlusion pressure (P 0.1) responses to hypercapnia. Although there was no change in resting respiratory frequency or tidal volume patients showed a significant (p less than 0.01) decrease in inspiratory timing (Ti/Ttot) and increase in mean inspiratory flow (VT/Ti) after naloxone. These results indicate that endorphins have a modulatory role in the central respiratory response to hypercapnia in both normal subjects and patients with airways obstruction. In addition, they have an inhibitory effect on the control of tidal breathing in patients with chronic bronchitis.
Thorax 1982 Nov
PMID:Endogenous opiates and the control of breathing in normal subjects and patients with chronic airflow obstruction. 716 1

Respiratory volumes and timing have been measured in 19 healthy adults during wakefulness and sleep. Minute ventilation was significantly less (p less than 0.05) in all stages of sleep than when the subject was awake (7.66 +/- 0.34(SEM) 1/min), the level in rapid-eye-movement (REM) sleep (6.46 +/- 0.29 1/min) being significantly lower than in non-REM sleep (7.18 +/- 0.39 1/min). The breathing pattern during all stages of sleep was significantly more rapid and shallow than during wakefulness, tidal volume in REM sleep being reduced to 73% of the level during wakefulness. Mean inspiratory flow rate (VT/Ti), an index of inspiratory drive, was significantly lower in REM sleep than during wakefulness or non-REM sleep. Thus ventilation falls during sleep, the greatest reduction occurring during REM sleep, when there is a parallel reduction in inspiratory drive. Similar changes in ventilation may contribute to the REM-associated hypoxaemia observed in normal subjects and in patients with chronic obstructive pulmonary disease.
Thorax 1982 Nov
PMID:Respiration during sleep in normal man. 716 2

Children with cerebral palsy (CP) have been shown to have altered trunk movements during gait resulting in increased loads at the lower lumbar spine. Detailed assessment is possible using 3D gait analysis. However, reliability and quantification of measurement error have not been established. The aim of this study was to evaluate test-retest reliability of thorax and lumbar segment kinematics and L5/S1 kinetics during gait in children with CP. Eight children with CP participated in this study with repeat assessments conducted within 1 week. Reliability was assessed using the one-way random ICC, standard error of measurement and an examination of extrinsic-to-intrinsic variability. Thorax kinematics demonstrated mixed level of reliability with SEM values ranging from 5.94o to 1.15o. Lumbar kinematics demonstrated poor-to-good reliability with the largest SEM values for peak lumbar flexion at 4.14o. L5/S1 moment values demonstrated only poor to good test-retest reliability while L5/S1 reactive forces demonstrated poor to excellent test-retest reliability.This study provides estimates of reliability and change needed to exceed measurement error. While reliability was mixed and some measures for thorax movement were above 5o, stated as a measure of acceptable error, the results of this study support the use of these measures in children with CP.
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PMID:Reliability and measurement error of multi-segment trunk kinematics and kinetics during cerebral palsy gait. 3173 93


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