PubMed HealthSearch

Biomedical subjects

G Manier

Publications and source records attributed to G Manier.

At least 19 recordsLinked to original sources

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

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

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

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

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

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

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

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

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

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

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

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

Determinants of hypoxemia during the acute phase of pulmonary embolism in humans.

The determinants of hypoxemia were studied in 10 patients with acute pulmonary embolism demonstrated by pulmonary angiography. Two patients were mechanically ventilated, and in the 8 who breathed room air spontaneously, the mean arterial PO2 was 61.5 mmHg. Measurements of the distributions of ventilation (VA) and perfusion (Q) against VA/Q ratios by the multiple inert gas infusion technique demonstrated an increase in VA/Q inequality. The major part of pulmonary blood flow was distributed in a mode near to, or slightly above, a VA/Q ratio of 1. The cumulative fraction of blood in true shunt and low VA/Q mode (VA/Q less than 0.01) was 9.1%. For a small part of the AaDO2 (13%), an oxygen diffusional component was found. The remaining hypoxemia was due to the fall in the mixed venous PO2 (PVO2), irrespective of its cause: low cardiac output, low hemoglobin concentration, high oxygen consumption, low P50. The fall in PVO2 led to a fall in end-capillary blood PO2 in both shunt or ventilated and perfused units. We conclude that the major determinant of hypoxemia in these patients suffering from acute pulmonary embolism is the fall in PVO2. This is enhanced by a moderate increase in the fraction of blood flowing through low VA/Q units. Diffusion impairment plays only a minor role.

Acute Disease

Gas exchange alterations in patients with chronic obstructive lung disease.

In a series of 23 patients with COPD, Wagner et al showed three distinct patterns of VA/Q distributions and a correlation between Burrows' clinical classification and the observed distribution patterns. Using the inert gas method, we studied 51 patients suffering from severe but stable COPD (FEV1 = 0.84 +/- 0.38 L; PaO2 = 58.5 +/- 10.5 mm Hg; PaCo2 = 48 +/- 6 mmHg; Ppa = 22 +/- 8 mmHg) breathing room air in a steady state. The H pattern (high mode of VA in high VA/Q) was found in 24 cases. There was an L pattern (Q mode in low VA/Q units) in nine cases and an HL (high-low) pattern in 16 cases (two patients were assigned another group). The analysis of the distribution data confirmed that VA/Q heterogeneity was the main factor underlying gas exchange disturbances in COPD. The PaO2 of the H subjects was higher than that of both HL (p less than 0.02) and L subjects. The true shunt value in the L group was significantly lower than in the H and HL groups. However, the relationship between clinical or functional aspects and distribution was not direct. The fraction of patients of H, HL, or (H + HL) types was nearly identical in the three clinical groups. The H pattern was found to be predominant in cases of COPD.

Aged

[The inert gas method in respiratory physiopathology].

The main results obtained, in healthy or unhealthy man, with the inert gas method are gathered together. The major factor at the source of hypoxemia is the uneven distribution of VA/Q ratios. The fall in the partial pressure of oxygen in mixed venous blood amplifies this effect. Only hypoxemia, during muscular exercise, in patients with interstitial lung diseases could be explained, in part, by a decrease in membrane diffusion and a reduction in the transit time of blood in pulmonary capillaries. The differences between the methods used to analyse pulmonary gas exchange are discussed.

Adult

[Outcome of patients with chronic respiratory insufficiency treated at home with tracheotomy and assisted ventilation].

60 patients were studied with severe chronic respiratory failure (IRC) and a permanent tracheostomy treated with domiciliary ventilation (VADT). The study commenced from the time of the tracheostomy and included length of survival (by the actuarial method) quality of life, subjectively and objectively (progress of blood gases in a stable clinical state and cumulative length of periods in hospital). Factors influencing the decision for tracheostomy and VADT were examined. Restrictive cases benefitted from the technique as much from the improved quality of life as from the duration of survival (77% at 5 years). Patients with an obstructive or mixed pattern had a 5 years survival of 73% after the first episode of acute or chronic respiratory failure which was 73% better than comparable patients given neither a tracheostomy nor oxygen therapy. The five years survival of 42% on VADT in our series compares favourably with the main series published. In our opinion the improved survival in these patients (which tends to rejoin that of the general population) and the improved quality of life justifies the use of this treatment in severe obstructive IRC, despite a greater demand and cost of this treatment than those with a restrictive defect.

Actuarial Analysis

[Influence of almitrine dimesylate on gas exchange. Preliminary results in patients with chronic obstructive bronchopneumopathies under artificial ventilation].

From a study conducted in 1981 in patients with chronic obstructive pulmonary disease breathing spontaneously, it was concluded that almitrine ensured a more even distribution of ventilation-perfusion ratios in the lung. Another study has recently been undertaken to suppress the effects of stimulated ventilation observed and to measure more accurately the pulmonary vascular effect of this new drug. This was a randomized double-blind drug versus placebo trial using the same doses of almitrine (1.5 mg/kg orally) in patients of the same type under stable artificial respiration controlled by repeated measurements of ventilation during the weaning period at the end of an episode of acute respiratory failure. The preliminary results obtained in one-half of the patients (4 under almitrine, 4 under placebo) are reported. There was little difference in haemodynamic values between the two groups. Improvement in PaO2 was maximum 90 min after almitrine was administered and varied from 0.7 to 1.4 kPa; there was no modification in the control group. In the absence of any change in ventilation and respiratory rate, perfusion was reduced in lung areas with low ventilation-perfusion ratio. These partial results seem to confirm that almitrine exerts a moderate, though real, effect on pulmonary vessels.

Almitrine