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Biomedical subjects

B Nemery

Publications and source records attributed to B Nemery.

At least 127 records · Page 7Linked to original sources
PubMed1987

Putrescine and 5-hydroxytryptamine accumulation in rat lung slices: cellular localization and responses to cell-specific lung injury.

The cellular localization of putrescine (1,4-diaminobutane) and 5-hydroxytryptamine (5HT) following the accumulation of tritium-labeled putrescine (2.5 microM) or 5HT (0.5 microM) into rat lung slices was determined by autoradiography at the light microscope level. Putrescine labeling was found to occur in type II alveolar epithelial cells and in branchiolar nonciliated (Clara) cells, and possibly also in type I alveolar epithelial cells. The pattern of 5HT labeling was clearly different from that with putrescine, since the parenchyma was diffusely labeled with no preferential location in type II cells, but with strong labeling of the endothelium of large vessels and also the pleural mesothelium. The apparent kinetic parameters for the tissue uptake of [3H]putrescine (2.5 to 80 microM) and [14C]5HT (0.5 to 16 microM; both being simultaneously present in a 5 to 1 molar ratio) were studied in lung slices from normal rats and rats pretreated with O,S,S-trimethyl phosphorodithioate (OSSMe, 11 to 95 mg/kg, po), with paraquat (20 mg/kg, ip), or with alpha-naphthylthiourea (ANTU, 5 or 10 mg/kg, ip). OSSMe and paraquat were used as models for pulmonary epithelium-damaging agents, and ANTU was taken as a model for a pulmonary endothelium-damaging agent. The Vmax for the uptake of 5HT was significantly increased (without change in Km) following treatment with OSSMe and paraquat. Following ANTU treatment the Vmax for the uptake of 5HT was unchanged (5 mg/kg) or increased (10 mg/kg, Km also increased). These results indicate that in lung slices the response to lung injury may be associated with an increased accumulation of 5HT. The Vmax for the uptake of putrescine was significantly decreased (without change in Km) following treatment with OSSMe and paraquat. Following ANTU treatment the Vmax for the uptake of putrescine was unchanged (5 mg/kg) or decreased (10 mg/kg, no change in Km). These results suggest that a decreased putrescine uptake is a sensitive index of pulmonary epithelial damage.

Animals↗
PubMed1987

Metabolic alkalosis following administration of an organophosphorus compound, O,S,S-trimethyl phosphorodithioate.

The oral administration of a single dose of O,S,S-trimethyl phosphorodithioate (OSSMe) to rats was found to result, 24 hours after treatment, in a dose-related metabolic alkalosis. Non-invasive indices of kidney damage revealed that during the first 4 hours after OSSMe administration there was a fourfold increase in urine flow with increases in albumin, beta 2-microglobulin and N-acetyl-glucosaminidase excretion. These results suggest that OSSMe-induced metabolic alkalosis may result from early renal functional disturbances.

Acetylcholinesterase↗
PubMed1986

Hysteresis of the alveolar capillary membrane in normal subjects.

Weibel and associates (Respir. Physiol. 18: 285-308, 1973), using morphometric techniques, demonstrated in the rat that changes in lung volume related to inflation and deflation caused a hysteretic variation in alveolar capillary membrane which is locally pleated at low pulmonary volume, unfolds during inflation but does not immediately refold during deflation, possibly enhancing the CO diffusion throughout the membrane. The present study was conducted to verify the existence of this hysteresis in human lungs in vivo. Single-breath diffusing capacity for CO (DLCO) was measured in five healthy seated subjects before and 0, 0.5, 1, 3, and 7 min after an inflation-deflation maneuver (IDM) in 6 separate days. The value of mean DLCO was 36.4 +/- 3 (SD) before and 42.1 +/- 2.9, 41.6 +/- 3.3, 40.3 +/- 3.3, 39.2 +/- 3.2, and 38.1 +/- 2.7 ml X min-1 X Torr-1 after the IDM. Two mechanisms can explain our findings: an active filling of the capillary bed, or an unfolding of the alveolar capillary membrane. The first mechanism should be accompanied by changes in pulmonary circulation. Therefore, right-heart catheterization was performed in two normal subjects and in four patients examined for a chest pain syndrome. At the end of the IDM, the values for the pulmonary artery pressure and capillary wedge pressure had returned to control levels. This suggests that the capillary bed is not directly involved in the DLCO increase observed from 0.5 to 7 min after the IDM. The unfolding of the alveolar capillary membrane appears to better explain our findings.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Volume↗
PubMed1985

Some aspects of the toxicology of trimethyl and triethyl phosphorothioates.

The pharmacokinetics (disposal curves) of trimethyl and triethyl phosphorothioates have been determined. The concentrations to which the lung has been exposed at the LD50 dose of different chemical structures have been compared with the dose administered to the animal; the variation of LD50 of different chemical structures is little reduced. The in vitro kinetics of the reaction of O,S,S-trimethyl phosphorodithioate or O,O,S-triethyl phosphorothioate with plasma cholinesterase and carboxylesterase and brain acetylcholinesterase have been determined. The relation between inhibition and circulating concentrations in vivo have been examined. Changes in Clara cells reported by others seem to be physiological rather than pathological. O,S,S-Trimethyl phosphorodithioate is metabolised by rat lung and liver slices and microsomes. From these studies and the effect of various pretreatments of the rats on toxicity to the lung, it is probable that the proximal toxin is produced in the lung by oxidative attack on the alkylthio moeity of the compounds.

Animals↗
PubMed1985

Effects of methyl isocyanate on the respiratory tract of rats.

Static exposure of rats to methyl isocyanate, for one hour, led to respiratory impairment during and after exposure. The resultant changes in breathing pattern suggest that this compound is both a sensory and a pulmonary irritant. Low concentrations resulted in extensive necrosis and loss of epithelial cells in the proximal airways but widespread alveolar damage was found only after exposure to high, lethal concentrations. At high concentrations methyl isocyanate probably caused peracute death through reflex inhibition of breathing. Animals surviving the exposure exhibited signs of airway narrowing and development of (haemorrhagic) pulmonary oedema. The epithelial lesions were repaired rapidly, but residual peribronchial fibrosis and signs of renewed injury/inflammation were apparent.

Animals↗
PubMed1985

Lung function measurements over 21 days shiftwork in steelworkers from a strandcasting department.

On the assumption that short term changes in lung function may reflect the potential for a long term decline the evolution of lung function indices in 25 steelworkers from a strandcasting department and in 11 comparable steelworkers not exposed to dust was investigated over an almost uninterrupted 21 day working period and over three different workshifts. The mean total dust level in the strandcasting department, assessed by personal sampling, was 11.8 mg/m3. All subjects were examined at the beginning, in the middle, and at the end of their first (day 1) morning shift (0600 to 1400), their last (day 14) afternoon shift (1400 to 2200), and their last (day 21) night shift (2200 to 0600). Indices measured were vital capacity (VC), forced expiratory volume in one second (FEV1) and in three seconds (FEV3), forced expiratory flow over the middle half of the forced vital capacity (FEF25-75), peak expiratory flow rate (PEFR), the slope of the N2 plateau (delta N2) and the closing volume (CV) of the single breath oxygen test. Differences in indices between initial values (0600 on day 1) and final values (0500 on day 21) were not significant in the control group (except delta N2 which became lower); in the casting group there were significant (p less than 0.05) decreases in FEF25-75 and FEV3, but these decreases were not significantly greater than in the control group. Lung function changes were not significant in either group over the morning shift. During the afternoon there were significant decreases in spirometric indices in the casting group, with no significant decreases in the control group, but the interactions between exposure and time were generally not significant. During the night shift, however, the decreases in FEV1 and FEF25-75 observed in the strandcasting group were significantly more pronounced than in the control group. The single breath test, which many subjects failed to perform correctly on each occasion, showed no significant changes in closing volumes, and an "improvement" of delta N2 over the morning and the night shift in the control but not the exposed subjects needs to be interpreted with caution. The more pronounced decrease in spirometric indices, suggestive of slight airways obstruction, found over the night shift in the strandcasting workers is attributed to their working environment.

Belgium↗
PubMed1983

Smoking, lung function, and body weight.

In a cross-sectional study of steelworkers aged 45-55 years, smokers (n = 105; mean weight 76.1 kg) were found to weigh significantly less than non-smokers (n = 54; 81.6 kg) and ex-smokers (n = 51; 82.6 kg). The lower weight of smokers was attributable to a group with airflow obstruction (n = 37; forced expiratory volume in one second/vital capacity (FEV1/VC) less than 66%), who weighed less (4.8 kg; p less than 0.05) than smokers with normal FEV1/VC (n = 68). In smokers, but not in ex-smokers or non-smokers, body mass index and FEV1/VC ratio were closely related (r = 0.34; p less than 0.001). This association was apparently not due to an effect of body weight on lung function. Weight loss in smokers may be the consequence of impaired lung function or reflect the effect of cigarette smoking on both the respiratory tract and metabolism in susceptible subjects.

Body Weight↗
PubMed1983

Effects of gas density on pulmonary gas exchange of normal man at rest and during exercise.

Changes in the physical properties of inspired gas might be expected to influence the distribution of ventilation in the lungs as well as the diffusive and convective (cardiogenic) mixing of inspired gas with lung residual gas, thus possibly affecting pulmonary gas exchange for O2 and CO2. The purpose of our work was to assess to what extent this occurs in practise in human subjects, who could compensate for the changes directly brought about by altering the physical characteristics of the inhaled gas by changing their breathing pattern. Six healthy, non-smoking men breathed, at rest and during moderate exercise, gas mixtures containing 21% oxygen completed either by 79% nitrogen (air), helium (O2-He) or sulphur hexafluoride (O2-SF6). We observed that the inhalation of these three different gas mixtures whilst at rest did not affect arterial partial pressures of O2 or CO2, the physiological dead space to tidal volume ratio, or the alveolo-aADCO2). During exercise, AaDO2 was slightly (2-3 mm Hg) but significantly higher with both O2-He and O2-SF6 than with air. Although minute ventilation did not change, breathing frequency was slightly but significantly affected by the type of gas mixture breathed, being lower with O2-SF6 and higher with O2-He. We conclude that, within the range studied, the physical properties of the inhaled gas do not affect pulmonary gas exchange in healthy man, either because the changes affected are minimal or because they compensate for each other.

Adult↗
PubMed1983

Pulmonary vascular tone is a determinant of basal lung perfusion in normal seated subjects.

In the human upright lung the downward increase in lung perfusion reverses in the lower third, thus giving rise to a zone of reduced basal perfusion (zone 4). The flow in zone 4 is regulated by the extra-alveolar vessels, the diameter of which is determined by lung volume, perivascular interstitial pressure, and vasomotor tone. To estimate the role of pulmonary vascular tone in the formation of zone 4, we infused nitroprusside (NTP), a potent pulmonary vasodilator, in six normal seated subjects. We measured their regional perfusion distribution using 133Xe in control conditions and at two dose levels of NTP (20.8 and 52.1 micrograms/min). Regional perfusion distribution was measured similarly and according to the same protocol in six subjects receiving only a placebo solution. In four of the six subjects receiving NTP, right-heart catheterization allowed simultaneous estimations of cardiac output and pulmonary arterial pressure to be made. NTP slightly decreased the perfusion of the nondependent parts of the lungs and markedly increased the perfusion of the lung bases, thus reducing the extent of zone 4. No changes were observed in the placebo experiments. Cardiac output and indices of ventilation and gas exchange did not change significantly. Peripheral and pulmonary arterial pressure fell slightly but significantly during NTP infusion. We attribute the observed changes in basal perfusion to the vasodilatory effects of NTP on the extra-alveolar vessels. Our findings thus support the hypothesis that in normal subjects zone 4 is partly created by the pulmonary vascular tone.

Adult↗
PubMed1982

Effect of age on the regional perfusion and washouts of injected xenon in normal men.

The aim of this work was to localize the alveoli with low ventilation-perfusion ratio which are responsible for the age related increase of the ideal alveolar-arterial O2 partial pressure difference. For this purpose, we measured: (1) the washouts of perfused 133 Xenon (Xe) in the whole lung and in 6 horizontal slices of the right lung, and (2) the topographical distribution of perfusion (Qi) in 27 healthy, non-smoking seated men, between 18 and 65 years. The distribution of Qi is unaffected by age. The global and regional washouts slowed with age, the trends being the same in the 6 investigated regions. This data was interpreted as indicating that in our subjects the low VA/Q units are not situated predominantly at the base, but are scattered throughout the lung.

Adult↗
PubMed1982

Effect of nitroglycerin on pulmonary perfusion distribution and gas exchange of normal subjects.

In eight healthy subjects we assessed the effects of 3 mg sublingual nitroglycerin on lung distribution of ventilation and perfusion using 133Xe (sitting, supine and lateral decubitus) and on alveolo-arterial O2 and CO2 partial pressure differences [(PAO2-PaO2), (PaCO2-PACO2)] and physiological dead space to tidal volume ratio (VD/VT) (sitting). In all studied positions, nitroglycerin induced a significant decrease in uppermost perfusion indices, and a significant increase in dependent perfusion indices, without changing the distribution of ventilation. Significant increases in (PaCO2-PACO2) and VD/VT were observed up to 60 min after nitroglycerin. No changes in (PAO2-PaO2) occurred, except for a transient decrease due to transient hyperventilation following nitroglycerin. The redistribution of pulmonary perfusion after nitroglycerin may be attributed to the passive effects of lowered pulmonary vascular pressures, and to possible action on extra-alveolar vessels. The evolution of the indices of pulmonary gas exchange is compatible with the observed redistribution of ventilation/perfusion relationships.

Adult↗
PubMed1982

Effect of nitroglycerin on DL of normal subjects at rest and during exercise.

By use of the single-breath diffusing capacity for carbon monoxide (DL) as an index of the pulmonary capillary filling, the effects of 3 mg sublingual nitroglycerin (NTG) were studied in eight healthy subjects at rest and during exercise. At rest, NTG induced a significant and persistent decrease of DL when subjects were sitting or supine (60 min of observation) and also when they were in the lateral decubitus or supine with legs up position (30 min of observation). Subjects in the supine positions showed more pronounced percentage decreases in DL than when sitting. In the sitting position 1 mg NTG also induces a decrease of DL. During a moderate upright cycloergometer exercise, NTG also induces a significant decrease of DL; the decrease is smaller and of shorter duration (less than 15 min) than at rest, but it reappears as soon as the exercise is stopped. The decrease of DL may be attributed to an outward shift of blood from the thorax to the periphery or to a redistribution of lung perfusion consequent to changes in pulmonary vascular pressures.

Adult↗
PubMed1982

Changes in lung function after smoking cessation: an assessment from a cross-sectional survey.

Cross-sectional lung function data of 51 ex-smokers (mean, 8 +/- 7 yr since smoking cessation) were compared with those of 54 nonsmokers and 105 current smokers. All subjects were steel workers 45 to 55 yr of age. In order to assess whether lung function indexes improve after smoking cessation, "expected" values were calculated for the ex-smokers, taking into account both duration of smoking and time since cessation. Observed values of forced expiratory volume in one second, vital capacity, residual volume, peak expiratory flow rate, slope of the N2 single-breath washout, and bolus closing volume were significantly different from "expected" ones. This suggested that smoking cessation not only stopped the smoking-induced fast decline in lung function, but even led to some reversal toward nonsmoking values. This was already apparent in 22 subjects who had quit smoking less than 5 yr previously.

Cross-Sectional Studies↗
PubMed1981

Pattern of breathing and ventilatory response to CO2 in subjects practicing hatha-yoga.

WE studied eight Belgian subjects well advanced in the practice of hatha-yoga and compared them with eight sex-, age-, and height-matched control subjects. Practice of yoga (range 4-12 yr) involves control of posture and manipulation of breathing, including slow near-vital capacity maneuvers accompanied by apnea at end inspiration and end expiration. Average values for the yoga and the control group (in parentheses) are as follows: ventilation (VE) 5.53 1 X min-1 (7.07); tidal volume (VT), 1.03 liters (0.56); rate of breathing, 5.5 min-1 (13.4); end-tidal PCO2, 39.0 Torr (35.3). All differences are significant (P less than 0.05). Ventilatory response to CO2 (rebreathing technique) was significantly lower in the yoga group (P less than 0.01). The regression relating VE to VT during rebreathing of CO2 was VE = 8.1 (VT - 0.23) for the yoga group and VE = 15.8 (VT - 0.16) for the control group (P less than 0.005). We attribute these changes to chronic manipulation of respiration.

Adult↗