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Biomedical subjects

H Guénard

Publications and source records attributed to H Guénard.

At least 19 recordsLinked to original sources
PubMed1997

The inhibitory effect of fluoride on carbachol-induced bovine bronchial contraction.

The effect of sodium fluoride (NaF) on the responsiveness of airway smooth muscle was investigated in bovine bronchial segments. NaF (0.5-10 mM) induced a delayed concentration-dependent active pressure (AP) and reduced the lactate concentration in the solution. Pyruvate (10 mM) increased the NaF-induced contraction. There was a 50 +/- 7% decrease in carbachol (10 microM)-induced AP when bronchi were pretreated with NaF (5 mM) and a 37 +/- 9% decrease when NaF (5 mM) was added during the maintained carbachol-induced contraction. These inhibitory effects were enhanced by KCN and hypoxia. When bronchi were pre-incubated with 10 microM verapamil, a calcium channel inhibitor, the contractile effect of 5 mM NaF was reduced to 8 +/- 3% of the control. PKC activity in bronchial smooth muscle was significantly increased by NaF (5 mM). Staurosporine (30 nM) abolished the contractile effect of NaF. These results suggest that: (1) NaF either contracts or relaxes bronchial smooth muscle depending on the experimental conditions; (2) the relaxing effect is related to the inhibitory action of NaF on glycolysis; (3) the contractile effect of NaF is possibly mediated by modulation of a calcium channel via a PKC-dependent pathway; (4) carbachol-induced contraction is glycolysis pathway dependent in the absence of NaF but switches to oxidative dependent in its presence.

Animals↗
PubMed1996

Effects of nitric oxide inhalation on pulmonary serial vascular resistances in ARDS.

The pulmonary vasculature site of action of nitric oxide (NO) in patients with acute respiratory distress syndrome (ARDS) is still unknown. Seven patients were studied during the early stage of ARDS. The bedside pulmonary artery single-occlusion technique, which allows estimation of the pulmonary capillary pressure (Pcap) and segmental pulmonary vascular resistance, was used without NO or with increasing inhaled NO concentrations (15 and 25 parts per million [ppm]). Systemic circulatory parameters remained unaltered during 15 ppm NO inhalation, whereas 25 ppm NO inhalation slightly decreased mean systemic arterial pressure from 76.7 +/- 5.1 (mean +/- SEM) to 69 +/- 5.2 mm Hg (p < 0.01). Mean pulmonary arterial pressure (Ppam) and mean pulmonary capillary pressure (Pcapm) fell during 25 ppm NO inhalation from 27.4 +/- 3.5 to 21 +/- 2.2 mm Hg (p < 0.001) and from 14.8 +/- 1.5 to 10.7 +/- 1.4 mm Hg (p < 0.001) respectively, the total pulmonary resistance decreased by 28% (p < 0.01). The resistance of the capillary-venous compartment fell during 25 ppm NO inhalation from 100 +/- 16 to 47 +/- 16 dyn x s x m(2) x cm(-5) (p < 0.01), whereas the pulmonary arterial resistance was unchanged. In these patients NO inhalation during the early stage of ARDS reduces selectively Ppam and Pcapm by decreasing the pulmonary capillary-venous resistance. This latter effect may reduce the filtration through the capillary bed and hence alveolar edema during ARDS.

Administration, Inhalation↗
PubMed1996

Pulmonary gas exchange in elderly subjects.

Although important alterations in structure and function develop with age, the hypothesis that the lungs are capable of maintaining adequate gas exchange for the maximum human life span is generally accepted. This hypothesis was examined by measuring arterial oxygen and carbon dioxide tension (Pa,O2 and Pa,CO2) alveolo-arterial differences in oxygen and carbon dioxide tension (PA-a,O2 and Pa-A,CO2), steady state transfer capacity of the lung for carbon monoxide (TL,CO,ss) as well as the gas exchange ratio (R) in a series of 74 healthy subjects aged more than 68 yrs (69-104 yrs). In addition, Pa,O2 and Pa,CO2 were measured in a series of 55 young healthy subjects, who acted as controls. In the elderly subjects, except for TL,CO,ss, there was no significant correlation between any of the other variables and age. However, for a given Pa,CO2, Pa,O2 was always lower in the group of elderly subjects than in the group of young control subjects. TL,CO,ss, as well as TL,CO,ss/minute ventilation (V'k) ratio, was correlated with age, according to the following regression equations: TL,CO,ss (mL.min-1.kPa-1) = 126-0.90 x age (yrs), and TL,CO,ss/V'k (kPa-1 x 10(3)) = 13.5-0.085 x age, respectively. These results show that arterial oxygen tension did not decrease with age in this series of elderly subjects. However, the decrease in steady-state transfer capacity of the lungs for carbon monoxide with age indicates that oxygen transport could be diffusion-limited in elderly subjects, at least when oxygen consumption is increased.

Adult↗
PubMed1995

Respiratory mechanics before and after late artificial surfactant rescue.

OBJECTIVE: To assess the effect of late administration of synthetic surfactant (Exosurf) on the ventilatory function of premature infants with hyaline membrane disease (HMD). METHODOLOGY: Prospective non-randomized study in the Neonatal Intensive Care Unit (NICU) of a major referral hospital. The patients included two groups of premature infants with a birthweight between 750 and 2000 g who developed HMD. In group 1 with moderate to severe HMD, 2 x 5 mL/kg doses of Exosurf were given 12 h apart (first dose given at a mean age of 18.7 +/- 3.4 h [mean +/- s.e.m.]). In group 2 with milder HMD, no surfactant was given. RESULTS: Significant reductions (P < 0.05) in the fraction of inspired oxygen (FIO2) occurred 6 h after surfactant administration (24 h of life) and by 48 h (64 h of life) in group 2. These improvements in gas exchange preceded improvements in passive respiratory compliance which occurred 24 h after surfactant (42 h of life) and by 72 h (88 h of life) in group 2 (P < 0.01). In both groups pulmonary resistance increased and was significant (P < 0.05) by 48 h (66 h of life) in group 1. CONCLUSIONS: Synthetic surfactant given as late as a mean age 18.7 +/- 3.4 h still improves gas exchange but these early improvements cannot be completely explained by modifications of respiratory compliance.

Age Factors↗
PubMed1994

Bronchial smooth muscle energetics: effect of iodoacetate and hypoxia.

The active pressure (AP) and the oxygen consumption (VO2) of segments of bovine bronchi were measured during a 10 microM carbachol stimulation. VO2 did not increase during the carbachol-induced contraction whereas there was a twofold increase in the lactate production. Addition of the glycolytic blocker, iodoacetate (83 microM), decreased the AP to 68.9 +/- 6.4% of control value (n = 10, P < 0.05) whereas VO2 remained constant. The lactate concentration in the physiological solution decreased significantly (P < 0.05). When the solution was supplemented with pyruvate (10 mM), the effect of iodoacetate was antagonized. Under hypoxic condition, i.e. when the solution was bubbled with 5% CO2 in N2, VO2 decreased sharply to 7.7 +/- 3.1% of control (n = 8, P < 0.05) whereas AP did not change. The combined effect of iodoacetate and hypoxia led to a fall in both AP (12.4 +/- 3.0% of control, n = 7, P < 0.05) and VO2 (21.2 +/- 5.1%, P < 0.05). These results suggest that the energy required by bronchial smooth muscle to generate contraction could be supplied by either the aerobic or the anaerobic pathway.

Animals↗
PubMed1992

Responsiveness to histamine in human sensitized airway smooth muscle.

Passive sensitization of human isolated airway smooth muscle increases contractile responses to histamine. We looked to see whether this increase was due to an alteration in the relative role of histamine H1 and H2 receptors. Human bronchial spiral strips obtained at thoracotomy were passively sensitized by incubation in serum from atopic asthmatic patients to Dermatophagoïdes pteronyssinus and control strips were incubated in serum from healthy non-allergic non-atopic subjects. We also studied spiral strips dissected from two spontaneously sensitized human lung specimens. Cumulative concentration-response curves (CCRC) to Ca2+ (10(-5) -3 x 10(-2) M) were constructed either in the presence of 10(-5) M histamine alone or in that of the combination histamine and the H2 antagonist cimetidine (10(-5) M). Unlike in the absence of histamine, Ca2+ CCRC in the presence of histamine alone were significantly shifted to the left in the passively sensitized tissues (mean EC50: 5.7 x 10(-4) M) compared to control ones (mean EC50: 9.3 x 10(-4) M, n = 6, P < 0.05). Addition of cimetidine to histamine did not alter the Ca2+ CCRC either in the control or in passively or spontaneously sensitized airway smooth muscle. These results suggest that (i) passive sensitization increases contractile response to Ca2+ of human bronchial smooth muscle in the presence of histamine; (ii) this increase is not due to a difference in the H1- vs H2-mediated response; and (iii) H2-mediated effects do not play a significant role in spontaneously sensitized human lung as both in the non-sensitized and passively sensitized lung.

Aged↗
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↗
PubMed1987

Effect of breathing dry warm air on respiratory water loss at rest and during exercise.

The changes in respiratory water loss with time, expressed as the mass of water vapour lost per liter BTPS of ventilation (MH2O), and expired temperature (TE), used to calculate the relative humidity (ERH), were investigated in ten normal subjects while breathing warm dry air by mouth (PIH2O = 0 kPa; TI = 30 degrees C): at rest for a period of 35 min; during 15 min light muscular exercise (50 W); at increasing work load from 50 to 100 W between the 5th and 10th min of the exercise. The data collected were compared to those obtained in room air conditions (PIH2O = 0.68-1.3 kPa) and under conditions with slightly heated inspired air (TI = 28-30 degrees C). At rest, when breathing dry warm air MH2O and ERH fell during the first 15 min, while they recovered their initial values during the last 20 min. In contrast no differences in MH2O or ERH were observed when breathing ambient warm air. At constant and moderate work load for 15 min, the respiratory water loss fell significantly (compared to the 5th min) at the 10th and the 15th min when breathing warm dry air. The added hyperpnea which was obtained by increasing work load from 50 to 100 W between the 5th and 10th min of exercise did not further reduce MH2O and ERH. The transient fall in MH2O and ERH, which lasted at least 15 min either at rest or during muscular exercise, suggested that the mechanism underlying humidification of expired gas is overwhelmed by thermal stress. Since the upper airways mucosa is unable to saturate expired gas, this also suggested that the mucosa is dehydrated and probably hyperosmotic. The progressive recovery in MH2O and ERH after 15 min of warm dry air breathing at rest, suggest operation of a slow adaptive mechanism.

Female↗
PubMedDate not supplied

A sampling method for mean alveolar gas in normal subjects and patients with respiratory disease.

The paper describes an alveolar gas sampling method based on the criterion of equality of mean alveolar (RA) and expired (RE) respiratory quotients. Expired gas is sampled at an expired volume equal to VT/2 + VD by means of a mechanical sampler controlled by an analog computer. Eleven normal subjects and 50 patients with cardiopulmonary disease have been tested. When the difference between mean alveolar and expired respiratory quotients did not exceed 0.05, the result was considered to be satisfactory. Such results have been obtained in 40 patients and all of the normal subjects. For the remaining 10 patients, either experimental error and/or particular non-homogeneities in ventilation seemed to be the cause of the unsatisfactory results. Arterial to alveolar PCO2 differences have been calculated. The mean difference in normal subjects was never negative (1.86 +/- 1.58 torr).

Analysis of Variance↗
PubMedDate not supplied

[Double-blind study on the action of almitrine in patients with polycythemia of high altitude].

Chronic polycythaemia in people living at high altitude is associated with hypoxaemia due to a marked reduction in hypoxic and hypercapnic drives. The effect of almitrine, a chemoreceptor stimulant, was evaluated in 40 patients, with haematocrit values over 57%, living in La Pa2 (3,600-4,000 m). Two studies were carried out. The aim of the first was to assess the ventilatory response, and the increase in PaO2 due to almitrine in a double blind, placebo controlled protocol including 40 patients (mean haematocrit 66.8%). Almitrine was given orally at a dose of 3 mg X kg-1. Variance analysis showed that three hours later there was a significant increase in PaO2 (+0.46 kPa), pH and respiratory frequency, with a significant reduction in PaCO2 (-0.4 kPa). The increase in ventilation (+17%) was not significant. The aim of the second study was to assess the effect of almitrine on the polycythaemia. It was given orally at a dose of 1.5 mg X kg-1 X day-1 to twelve patients over a four week period. Blood gases, ventilation (VE), oxygen consumption (VO2), carbon dioxide, production (VCO2) and haematocrit were measured every week. There was a slight but significant reduction in haematocrit (-3.5%). PaO2 and all the other measured parameters (VE, PaCO2, pH, VO2 VCO2) remained constant. The reduction in haematocrit was not therefore due to an increase in diurnal PaO2 but is perhaps due to the improvement in pulmonary ventilation during sleep.

Adult↗
PubMedDate not supplied

Effect of 26% oxygen breathing on ventilation and perfusion distribution in patients with cold.

Fourteen patients suffering from severe but stable chronic airway obstruction were studied while breathing room air and mildly hyperoxic mixture (26%). The data were collected at the end of each 30 min randomized breathing period. The multiple inert gas elimination technique was used to detect alterations in ventilation-perfusion (VA/Q) mismatching. Ventilatory, arterial and mixed venous blood gases, and hemodynamic measurements were made simultaneously. To show a possible effect of O2 on hypoxic pulmonary vasoconstriction (HPV), the fractional part of cardiac output perfusing low VA/Q areas was separated using as upper limit of VA/Q the compartments with PAO2 70, 60 and 50 mmHg while breathing oxygen, compared to the percentage of blood flow in the same areas limited by the same VA/Q unit in air breathing conditions. Only a few changes due to O2 are statistically significant: 1) a rise in PaO2 (+20.2 +/- 8.3 mmHg) and PvO2 (+4.2 +/- 2.18 mmHg) without any change in ventilation, respiratory frequency, pH, PaCO2, haemodynamics and overall criterion of distribution; 2) a moderate increase in inert gas dead space; 3) an increase in the percentage of blood flow under the limit when chosen at 50 mmHg (+3 +/- 2.8%). This change could be related to an inhibition of HPV response while breathing O2 in compartments previously placed above the limit in air. Consequently, their VA/Q decrease and their perfusions are summed with those under the limit in O2. These data suggest that mild hyperoxia has a slight but real deleterious effect on pulmonary gas exchange.

Aged↗