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Biomedical subjects

G Manier

Publications and source records attributed to G Manier.

At least 19 recordsLinked to original sources
PubMed1999

Rapid leptin decrease in immediate post-exercise recovery.

OBJECTIVE: Leptin concentrations in humans are known to decrease in response to fasting. The aim of this work was to investigate whether leptin levels might also be modified by exercise-induced negative energy balance. SUBJECTS: Eight male runners reported in the morning from 0800 to 1200 h for (i) one resting session (sitting) and (ii) one exercise-and-rest session (2 h run and 2 h rest). MEASUREMENTS: Plasma leptin, free fatty acids (FFA), glycerol, cortisol and salivary cortisol were assayed in both sessions at 1200 h. RESULTS: After exercise-and-rest the leptin concentrations were lower than after rest (1.7 +/- 0.1 vs 2.5 +/- 0.2 micrograms/l, P < 0.05), i.e. a mean decrease of 30.3 +/- 4.5% (range 9.5-45.8). Plasma FFA, glycerol and cortisol concentrations increased: FFA 0.78 +/- 0.08 vs 0.18 +/- 0.04 mmol/l, glycerol 0.13 +/- 0.01 vs 0.04 +/- 0.01 mmol/l, and cortisol 428 +/- 36 vs 279 +/- 27 nmol/l. A negative correlation was found between plasma FFA and leptin levels (r = -0.5, P < 0.05) and between plasma glycerol and leptin levels (r = -0.05, P < 0.05). No correlation was found between leptin and cortisol levels. CONCLUSIONS: In normal subjects with low body fat, a strenuous exercise-and-rest lowers leptin levels by a mean of 30%. A role of lipolysis possibly via increased plasma free fatty acids and glycerol levels is suggested. Cortisol does not seem to be involved.

Adult↗
PubMed1999

Distribution of lung density after strenuous, prolonged exercise.

The postexercise alteration in pulmonary gas exchange in high-aerobically trained subjects depends on both the intensity and the duration of exercise (G. Manier, J. Moinard, and H. Stoïcheff. J. Appl. Physiol. 75: 2580-2585, 1993; G. Manier, J. Moinard, P. Techoueyres, N. Varène, and H. Guénard. Respir. Physiol. 83: 143-154, 1991). In a recent study that used lung computerized tomography (CT), evidence was found for accumulation of water within the lungs after exercise (C. Caillaud, O. Serre-Cousine, F. Anselme, X. Capdevilla, and C. Prefaut. J. Appl. Physiol. 79: 1226-1232, 1995). On representative slices of the lungs, mean lung density increased by 0.040 +/- 0.007 g/cm(3) (19%, P < 0.001) in athletes after a triathlon. To verify and quantify the mechanism, we determined the change in pulmonary density and mass after strenuous and prolonged exercise using another exercise protocol and methodology for CT scanning. Nine trained runners (age 30-46 yr) volunteered to participate in the study. Each subject ran for 2 h on a treadmill at a rate corresponding to 75% of maximum O(2) consumption. CT measurements were made before and immediately after the exercise test with the subject supine and holding his breath at a point close to functional residual capacity. The lungs were scanned from the apex to the diaphragm and reconstructed in 8-mm-thick slices. Attenuation values of X-rays in each part of the lung were expressed in Hounsfield units (HU), which are related to density (D): D = 1 + HU/1,000. No significant alteration in pulmonary density (0.37 +/- 0.04 vs. 0.35 +/- 0.03, not significant) was observed after the 2-h run test. Although lung volume slightly increased (change of 166 +/- 205 ml, P < 0.05), lung mass remained stable because of a change in density distribution. We failed to detect any changes in postexercise lung mass, suggesting that other mechanisms need to be considered to explain the observed alterations in pulmonary gas exchange after prolonged strenuous exercise.

Adult↗
PubMed1998

Corticotroph axis sensitivity after exercise in endurance-trained athletes.

OBJECTIVE: The present study was conducted in order to describe human hypothalamo-pituitary adrenal (HPA) axis adaptation in a model of repeated physical stress (endurance training) that causes a moderate increase in cortisol levels. SUBJECTS: We performed the same stimulation tests (adrenal stimulation with ACTH or pituitary stimulation with combined CRH/LVP) in a population of 8 endurance-trained athletes in two distinct situations: resting (baseline cortisol values) and 2 h after the end of strenuous exercise (increased cortisol values) to evaluate the HPA axis sensitivity to endogenous sustained increases in cortisol concentrations. MEASUREMENTS: During these tests, saliva and plasma cortisol (Fs and Fp, respectively) were assessed and compared. RESULT: Cortisol values in both plasma and saliva at the end of 2 h of exercise were significantly higher than in rested controls: Fs 11.5 +/- 1.3 vs 6.5 +/- 0.8 nmol.l-1 and Fp 428 +/- 36 vs 279 +/- 27 nmol.l-1 (post exercise vs post rest sessions, respectively, P < 0.001 for both). After either hormone test (CRH/LVP or ACTH), cortisol levels in plasma and saliva increased similarly when rest was compared to post exercise. Saliva variations (delta %) under exogenous hormone stimulation were dramatically greater than plasma variations. For example, under ACTH stimulation, the relative increments in cortisol were on control day: delta Fs 980 +/- 139 vs delta Fp 218 +/- 43% (saliva vs plasma, respectively, P < 0.05) and on exercise day: delta Fs 605 +/- 89 vs delta Fp 102 +/- 14% (saliva vs plasma, respectively, P < 0.05). CONCLUSIONS: In endurance-trained athletes, displaying a moderate but sustained endogenous cortisol increase: (1) ACTH responses following pituitary stimulation are not blunted, (2) cortisol responses following maximal adrenal stimulation are not blunted. Our results favour the hypothesis of a decreased pituitary sensitivity to cortisol negative feedback whereas the hypothesis of a major decreased adrenal sensitivity to ACTH was discarded. The greater ability of saliva assays to detect a cortisol increase strongly supports its use in the study of HPA physiology, whether under basal or dynamic conditions.

Adrenocorticotropic Hormone↗
PubMed1998

Anticholinergic versus beta 2-agonist on gas exchange in COPD: a comparative study in 15 patients.

beta-agonist bronchodilators are known to influence gas exchange and ventilation-perfusion relationships in asthmatic patients, where they induce hypoxaemia via hypoxic vasoconstriction. As this effect could have serious consequences in chronic obstructive pulmonary disease (COPD) patients with chronic hypoxaemia, alternative agents have been sought. It has been shown that inhaled anticholinergic drugs may be of value in this condition. In the present study, we compared the effects of salbutamol (Sb) and ipratropium bromide (IB) inhalation on gas exchange in 15 patients with stable COPD. All patients had a history of COPD (mean arterial oxygen tension (Pa,O2) = 8.2 +/- 1.0 kPa (61.8 +/- 7.3 mmHg) forced expiratory volume in one second (FEV1) = 39 +/- 12%; FEV1/vital capacity (VC) = 42 +/- 6%) and no evidence of acute respiratory failure. Haemodynamic and gas exchange data were recorded after right catheterization by the multiple inert gas elimination technique. Measurements were made under basal conditions, after two puffs of freon propellant (placebo) and after two puffs of either 200 micrograms Sb or 200 micrograms IB in a randomized design. Sb and IB reduced airway resistances to the same extent, but had no significant influence on the haemodynamic and ventilation parameters. There was a slight but significant decrease in arterial carbon dioxide tension (Pa,CO2) = 6.0 +/- 0.8 versus 6.4 +/- 0.8 kPa (45.4 +/- 5.9 versus 47.9 +/- 6.3 mmHg) p < 0.05 with an enhanced perfusion distribution heterogeneity and a slight improvement in ventilation homogeneity shown by a decrease of the decimal logarithm of SD of the ventilation distribution (LogSDV) after inhalation of IB relative to control. Since these alterations did not affect arterial oxygen tension we concluded that inhalation of these doses of salbutamol or ipratropium bromide do not affect gas exchange in patients with stable chronic obstructive pulmonary disease. The normal home treatment: inhalation of two puffs of these bronchodilating drugs thus appears to be safe. The choice of agent will depend on the extent of the bronchodilator effect in a given individual.

Administration, Inhalation↗
PubMed1997

Trained versus untrained men: different immediate post-exercise responses of pituitary adrenal axis. A preliminary study.

The hypothalamo-pituitary-adrenal axis is involved throughout the exercise-recovery cycle. Nevertheless, differences in hormone responses during early recovery between sedentary and endurance trained subjects are not well known. The aim of this preliminary study was to monitor plasma cortisol and adrenocorticotropic hormone (ACTH) concentrations both during and after the end of running exercise performed by four endurance trained adults (marathon men) compared to four sedentary subjects. Two parameters, i.e. intensity and duration, were changed on 4 consecutive days. The 1st day (D0) was spent in the laboratory: all blood samples were obtained at rest to determine diurnal variations of each hormone. On the following days (D1-D4) the subjects exercised: D1 and D2 brief (20 min), light (50% maximal heart rate HRmax, D1) or strenuous (80% HRmax, D2), D3 and D4 prolonged (120 min), light (D3) or strenuous (D4). In both groups, neither brief (D1, D2) nor prolonged light exercise (D3) induced any significant variation in plasma ACTH or cortisol concentrations. Plasma ACTH and cortisol concentrations increased only if the exercise was intense and prolonged (D4). The training factor did not modify the intensity or duration thresholds for the activation of the pituitary-adrenocortical response to exercise in the conditions of our experiment. However, during immediate recovery from the four exercise regimens, the plasma ACTH concentrations of the marathon men were constantly above the values of the sedentary subjects, although plasma cortisol concentration remained similar in both groups. As an indirect means of evaluating the relationships between ACTH and cortisol we compared the areas under the cortisol and ACTH curves (AUC) from 0.5 to 3.5 h during recovery from D1 to D4 compared to D0 at the same time. Cortisol AUC were similar in the sedentary subjects and marathon men although the ACTH AUC were different in the sedentary subjects and marathon men, suggesting a change in the pituitary-adrenal relationship at some yet indeterminate level. During the immediate recovery from exercise whatever its intensity, the magnitude of the ACTH response was increased in the trained subjects but with a reduced effect upon its target, the adrenal glands. This phenomenon has not been described in the literature. Two non-exclusive phenomena may be involved, i.e. a decreased adrenal sensitivity to ACTH stimulation, and/or a decreased hypothalamo-pituitary axis sensitivity to cortisol negative feedback.

Adrenal Glands↗
PubMed1996

Does functional alteration of the gonadotropic axis occur in endurance trained athletes during and after exercise? A preliminary study.

In men, the hypothalamic-pituitary-testicular axis controls the secretion of testosterone which, in this sex, is a major anabolic hormone. Physical exercise modulates testosterone concentration, affecting the whole axis by poorly understood mechanisms. We have reported in this preliminary study the short and long-term effects of exercise on the function of the gonadotropic axis in trained compared to untrained subjects. Environmental factors known to interfere with pituitary function were minimized. Four marathon and four sedentary men, were studied during 5 days successively using different combinations of two factors: duration and intensity of running tests. Day 0 (D0) was a rest day, and the exercises were: D1 and D2 brief (20 min), light (50% maximal heart rate, HRmax, D1) or intense (80% HRmax, D2), D3 and D4 prolonged (120 min) and light (50% HRmax, D3) or intense (80% HRmax, D4). Testosterone (free and total) and luteinizing hormone (LH) concentrations were measured before, during and after exercise. The baseline concentrations of plasma testosterone were lower in the long distance runners than in the sedentary group [41.8 (SEM 5.5) vs 64.5 (SEM 7.9) pmol.l-1, respectively; P < 0.05]. This phenomenon was centrally mediated as LH concentration was apparently inappropriately low [3.4 (SEM 0.4) vs 4.3 (SEM 1.0) UI.l-1; P > 0.05]. Light to moderate exercise did not modify testosterone and LH concentrations. Conversely, intense and prolonged exercise increased testosterone concentration [73.2 (SEM 9.0) vs 92 (SEM 11.0) pmol.l-1 in the long distance runners and sedentary group, respectively; P < 0.05] and lowered LH concentrations [2.1 (SEM 0.3) vs 3.4 (SEM 0.3) UI.l-1 in the long distance runners and sedentary group, respectively; P < 0.05 compared to D0, at the same time]. In our conditions of exercise, negative feedback of testosterone upon LH persisted, as positive feedback of low testosterone concentrations was apparently lacking (inappropriately low LH concentration with regard to low basal testosterone concentration).

Adult↗
PubMed1994

Effect of inhaled nitric oxide on hemodynamics and VA/Q inequalities in patients with chronic obstructive pulmonary disease.

Nitric oxide (NO) has been reported to be an endothelium-derived relaxing factor, and hypoxic pulmonary vasoconstriction seems to be enhanced by inhibitors of endothelially dependent vascular relaxation. We examined the circulatory effects of inhalation of 15 ppm NO in air in 14 hypoxic patients suffering from chronic obstructive pulmonary disease (COPD). Of these patients 4 breathed 100% O2 before NO. The effects of NO inhalation on pulmonary gas exchange were also studied in 12 of these patients using the multiple inert gas elimination technique, 3 of whom breathed air, 100% O2, and 15 ppm NO in air in succession. Under baseline conditions, both mean +/- SD pulmonary artery pressure and pulmonary vascular resistance were increased (Ppa = 24.3 +/- 10.4 mm Hg and PVR = 3.3 +/- 1.1 mm Hg/L/min, respectively). Although the pulmonary circulatory effects were not immediate, with no detectable changes after 1 min NO inhalation, Ppa and PVR fell significantly (-19.1 +/- 10.5%, p < 0.02 and -29.3 +/- 15.1%, p < 0.02, respectively) after 10 min NO inhalation. Moreover, the extent of the NO-induced reduction in Ppa was found to depend on the level of baseline pulmonary arterial hypertension. No systemic circulatory effects were observed. The mean VA/Q ratio and the dispersion of ventilation and blood flow distributions were not altered by NO inhalation, although there was a significantly higher percentage of ventilation (7.3 +/- 7.3%, p < 0.05) in poorly and unperfused areas (VA/Q > 10).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1993

Pulmonary diffusing capacity after maximal exercise.

To determine the effect of maximal exercise on alveolocapillary membrane diffusing capacity (Dm), 12 professional handball players aged 23.4 +/- 3.3 (SD) yr were studied before and during early recovery from a progressive maximal exercise [immediately (t0), 15 min, and 30 min (t30) after exercise]. Lung capillary blood volume and Dm were determined in a one-step maneuver by simultaneous measurement of CO and NO lung transfer (DLCO and DLNO, respectively) with use of the single-breath breath-hold method. At t0, DLCO was elevated (13.1 +/- 12.0%; P < 0.01) but both DLNO and Dm for CO remained unchanged. Between t0 and t30, both DLCO and DLNO decreased significantly. At t30, DLCO was not different from the control resting value. DLNO (and consequently Dm for CO) was significantly lower than the control value at t30 (-8.9 +/- 8.1%; P < 0.01). Lung capillary blood volume was elevated at t0 (18.0 +/- 19.0%; P < 0.01) but progressively decreased to near control resting values at t30. Differences in the postexercise kinetics of both DLCO and DLNO point to a role of the transient increase in pulmonary vascular recruitment during the recovery period. We concluded that Dm was somewhat decreased in the 30 min after maximal exercise of short duration, but the exact pulmonary mechanisms involved remain to be elucidated.

Adult↗
PubMed1992

Influence of cardiac output on oxygen exchange in acute pulmonary embolism.

We investigated interactions between cardiac output, VA/Q distribution pattern, pulmonary gas exchange, O2 transport, and tissue oxygenation in 16 patients during the acute phase of pulmonary embolism (PE). The effects of breathing room air, O2 therapy (FIO2 = 0.40) (11 patients), and dobutamine (four patients) were studied after right catheterization using the multiple inert gas elimination technique. The pattern of VA/Q ratio distributions was found to depend essentially on cardiac output level. The individual blood flow perfusing ventilated areas was found to be inversely related to the mean VA/Q ratio of blood flow distribution. PVO2 was directly related to cardiac index (p less than 0.02), and negatively related to the mean VA/Q of blood flow distribution. In view of the influence of low VA/Q ratios and PVO2 on arterial hypoxemia, our results showed that the heart's response to PE conditioned the strategy of pulmonary gas exchange and O2 transport. Oxygen breathing led to a slight but consistent fall in cardiac output (-0.6 +/- 0.5 L/min, p less than 0.01). However, although PaO2 remained normal and PVO2 was slightly improved, we found no evidence for a role of hypoxic pulmonary vasoconstriction in the pulmonary hypertension observed during the acute phase of PE. Administration of dobutamine improved O2 transport and tissue oxygenation, although PaO2 remained constant or even fell in some cases because of increased VA/Q mismatch.

Acute Disease↗
PubMed1991

Pulmonary diffusion limitation after prolonged strenuous exercise.

To determine the effect of strenuous prolonged exercise on alveolo-capillary membrane diffusing capacity, 11 marathon runners aged 37 +/- 7 years (mean +/- SD) were studied before and during early recovery (28 +/- 14 min) from a marathon race. Lung capillary blood volume (Vc) and the alveolo-capillary diffusing capacity (Dm) were determined in a one-step maneuver by simultaneous measurements of CO and NO lung transfer (DLCO and DLNO, respectively) using the single breath, breath-holding method. After the race, both DLCO and DLNO were significantly decreased in all subjects (-10.9 +/- 4.8%, P less than 10(-4) and -29.0 +/- 11.1%, P less than 10(-4), respectively). The mean value of the derived DmCO decreased by -29.3 +/- 11.1%, whereas Vc had not entirely returned to control resting value. Although these results do not indicate the detailed mechanism involved, interstitial lung fluid was suspected to accumulate, particularly in alveoli, during the race. We concluded that the high overall work load and the extended duration of the exercise both contributed to a transient change in the structure of the alveolo-capillary membrane thereby affecting the diffusing capacity of the alveolo-capillary membrane.

Adult↗
PubMed1991

Echocardiographic assessment of myocardial performance after prolonged strenuous exercise.

To determine the effect of strenuous prolonged exercise on systolic and diastolic left ventricular function, 11 non-elite marathon runners aged 37 +/- 7 years (mean +/- SD) were studied before and during early recovery from a marathon race. Cavity dimensions, wall thickness, and fractional shortening were computed from two-dimensionally guided M-mode echocardiograms. Doppler left ventricular inflow tract recordings were analysed for peak early and late velocities and their ratio. In seven subjects, heart frequency was recorded throughout the race. These subjects ran the marathon at 87 +/- 4% of their maximal heart rate. Left ventricular diastolic dimension was slightly reduced at the end of the race (49.4 +/- 4.2 mm to 47.3 +/- 5.1 mm; P less than 0.05). Fractional shortening remained unchanged, although blood pressure (P less than 0.001) and systolic wall stress (P less than 0.01) were decreased. The left ventricular filling pattern was unchanged, and the ratio of early to late velocities remained constant. These results suggest that the fractional shortening was a result of the opposing effects of changes in preload and afterload. However, the absence of a change in the end systolic dimension, despite a marked reduction in afterload and the occurrence of septal akinesia in one subject after the race could only suggest that strenuous prolonged exercise may alter myocardial performance.

Adult↗
PubMed1989

Hemodynamic disturbances and VA/Q matching in hypoxemic cirrhotic patients.

Arterial oxygen desaturation is commonly found in patients with cirrhosis of the liver, but severe hypoxemia is unusual. To investigate the mechanism of the impairment in gas exchange, six severely hypoxemic (mean PaO2, 55.9 +/- 5.9 mm Hg) cirrhotic patients (five confirmed by biopsy), without pulmonary or cardiovascular disease and in the absence of acute hepatic disease, were submitted to right heart catheterization. Inequalities of VA/Q were estimated in the respiratory steady state using the multiple inert gas technique. The mean pulmonary arterial pressure was low (7.2 +/- 2.3 mm Hg) and the cardiac output high (Q = 11.0 +/- 2.06 L/min), indicating a low PVR. The VA/Q mismatching of the ventilated and perfused units ranged from mild to moderate, but a large percentage of Q flowed through unventilated areas. Furthermore, there was a significant difference between predicted and measured PaO2 (9.27 +/- 5.9 mm Hg; p less than 0.01), which was attributed to either an unmeasured postpulmonary shunt (between portal and pulmonary vein) or a diffusion defect. The impairment in gas exchange in these patients is thus due primarily to an intrapulmonary, and possibly extrapulmonary, shunt. This was thought to be due mainly to an impaired regulatory mechanism of the microcirculation by the hepatic dysfunction.

Adult↗
PubMed1988

Pulmonary gas exchange in Andean natives with excessive polycythemia--effect of hemodilution.

Pulmonary gas exchange in Andean natives (n = 8) with excessive high-altitude (3,600-4,200 m) polycythemia (hematocrit 65.1 +/- 6.6%) and hypoxemia (arterial PO2 45.6 +/- 5.6 Torr) in the absence of pulmonary or cardiovascular disease was investigated both before and after isovolemic hemodilution by use of the inert gas elimination technique. The investigations were carried out in La Paz, Bolivia (3,650 m, 500 mmHg barometric pressure). Before hemodilution, a low ventilation-perfusion (VA/Q) mode (VA/Q less than 0.1) without true shunt accounted for 11.6 +/- 5.5% of the total blood flow and was mainly responsible for the hypoxemia. The hypoventilation with a low mixed venous PO2 value may have contributed to the observed hypoxemia in the absence of an impairment in alveolar capillary diffusion. After hemodilution, cardiac output and ventilation increased from 5.5 +/- 1.2 to 6.9 +/- 1.2 l/min and from 8.5 +/- 1.4 to 9.6 +/- 1.3 l/min, respectively, although arterial and venous PO2 remained constant. VA/Q mismatching fell slightly but significantly. The hypoxemia observed in subjects suffering from high-altitude excessive polycythemia was attributed to an increased in blood flow perfusing poorly ventilated areas, but without true intra- or extrapulmonary shunt. Hypoventilation as well as a low mixed venous PO2 value may also have contributed to the observed hypoxemia.

Adult↗
PubMed1986

Heat and water respiratory exchanges: comparison between mouth and nose breathing in humans.

The temperatures (TI, TE) of inspired and expired gas and the mass of expired water (MEH2O) have been measured in four subjects at rest during mouth and nose breathing of dry air at room temperature. TI and TE were measured by copper-constantan thermocouples, MEH2O by freezing and ventilatory parameters by total body plethysmography. During mouth breathing, temperatures are significantly higher (TI = 28.1 degrees C, TE = 31.5 degrees C) and the amount of expired water larger (MEH2O = 27.8 mg dm-3 BTPS) than during nose breathing (TI = 24.8 degrees C; TE = 29.6 degrees C; MEH2O = 26.6 mg dm-3 BTPS). From these experimental data the appropriate computations show clearly that in humans, while either nose or mouth breathing, the expired air is not water saturated; the latent heat exchanges represent the larger part of the respiratory heat exchanges; the counter current expiratory heat recovery is imperfect; in terms of heat and water respiratory exchanges, no large difference exists between the oral and nasal routes. This last point is confirmed by the calculation of a difference less than 10% in the total respiratory heat losses between mouth and nose breathing.

Body Temperature Regulation↗
PubMed1986

Improvement in ventilation-perfusion relationships by almitrine in patients with chronic obstructive pulmonary disease during mechanical ventilation.

Although the respiratory stimulant effects of almitrine bismesylate (AB) via an action on the peripheral chemoreceptors have been demonstrated, the mechanism of its intrapulmonary action has not yet been elucidated. In order to abolish the stimulation of ventilation, observed in studies on spontaneously breathing patients, an investigation of patients suffering from severe COPD under constant mechanical ventilation, with FIO2 = 0.21, during the weaning period was carried out. Eighteen patients were randomly divided into 2 groups (9 receiving 1.5 mg/kg AB and 9 receiving placebo). The ventilatory and hemodynamic variables, blood and alveolar gases, and the VA/Q ratio distributions using the multiple inert gas technique were collected before treatment with drug or placebo, as well as 90 and 180 min afterwards. The PaO2 was found to be raised 90 min after AB administration (+57 +/- 3.9 mm Hg, p less than 0.01) and remained above the baseline value at 180 min (+5.4 +/- 4.6 mm Hg, p less than 0.01). Compared with those in the placebo group, these increases were significant (p less than 0.01). A slight decrease in PaCO2 but similar in the 2 groups was observed despite constant ventilation. The hemodynamic data were the same for the 2 groups. The changes in overall criteria of the distributions (mean VA/Q and SD) were small. The main finding was a decrease in the percentage of the perfusion flowing through the true shunt and the underventilated areas after AB treatment. In the control group, the blood flow percentage in the true shunt and low VA/Q units was either stable or increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Almitrine↗
PubMed1985

Series dead space for inert gases in healthy subjects.

In ten normal subjects, series dead space was determined for six intravenously infused inert gases (SF6, ethane, cyclopropane, fluothane, ether, acetone) from their expired and alveolar concentrations. The method for sampling alveolar gas was based on the criterion of identity of mean alveolar and expired gas exchange ratios. Inert gases were analysed chromatographically. Acetone, the most soluble gas, yielded the lowest dead space, the difference to the other gases being about 4.5%. This is probably due to the non-infinite value of the series dead space ventilation-perfusion ratio (VA/Q) which was estimated at about 2,000. The diffusivity, inversely related to the molecular weight, also played a role, the heaviest gas (fluothane) having a greater dead space than the lightest (ethane). The underestimation of the dead space from acetone is expected to be greater in subjects with low tidal volume and high bronchial blood flow, i. e. in some patients with respiratory disease.

Humans↗
PubMed1985

Acute inflammatory demyelinating polyneuropathy in a diabetic patient: predominance of vesicular disruption in myelin sheaths.

A diabetic woman underwent an incision of the right big toe for an abscess and developed a typical Guillain-Barré syndrome 48 h later. A biopsy of a peripheral nerve, performed 10 days later, showed modifications usually seen in diabetic patients, as well as the characteristic ultrastructural modifications of the Guillain-Barré syndrome (GBS). Moreover, 22% of myelinated fibers exhibited vesicular disruption of the myelin sheaths. This lesion is rarely encountered on the biopsies of peripheral nerve in GBS and concerns only a few myelinated fibers. Such a prominence of myelinic vesicular disruption and its occurrence in a diabetic patient are discussed.

Acute Disease↗