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Biomedical subjects

S Delpierre

Publications and source records attributed to S Delpierre.

At least 55 records · Page 3Linked to original sources

Interaction between vagal and chemoreceptors afferents in ventilatory response to transient hypercapnia (awake rabbits).

The ventilatory response to a transient hypercapnia was studied in four awake rabbits maintained in a volume displacement plethysmograph : the increase in inspiratory volume (VI) was associated or not with an increase in inspiratory and expiratory durations (TI and TE). These ventilatory variations were consistent with the activation of the peripheral chemoreceptors by carbon dioxide (short latency of the initial response). After vagal blockade by local anaesthesia, relative ventilatory variations were not significantly different from those previously measured. Central activity seems an important factor reducing inhibitory vagal input and favouring peripheral chemoreceptor afferents.

Afferent Pathways↗

Interaction between vagal and chemoreceptors afferents in ventilatory response to transient hypercapnia (anaesthetized rabbit).

In rabbits anaesthetized with ethyl-carbamate, stimulation of chemoreceptors afferents was allowed by transient hypercapnia, before and after vagal blockade by DC current. In these relatively fast breathing animals, the transient hypercapnia produced light changes of inspiratory tidal volume (VI), inspiratory (TI) and expiratory durations (TE). Despite the identity of transient hypercapnia, it ensued that: (1) the higher the spontaneous VI and the lower the respiratory frequency (fR), the greater their respective changes (deltaVI and deltafR) during the ventilatory response; (2) after vagal blockade, greater changes in VI, TI, TE and mean inspiratory flow rate (VI/TI) occurred than in control state, while the relation between deltafR and fR was more significant than in control state. Respective roles played by vagal and chemoreceptors afferents in the ventilatory response to transient hypercapnia are discussed.

Animals↗

[Periodic oscillating respiration outside of comatous stages].

A periodic oscillating breathing was observed in 11 subjects during study of their pulmonary function. All these patients were male and more than 50 years old. A cardiovascular disease was clinically evident in eight of them. Arterial hypoxemia was found in five subjects and a light hypocapnia in three. Analysis of oscillating rhythms first, revealed unexistence of ventilatory pauses between periods of deep breaths in some subjects and secondly, showed existence of permanent or discontinuous periodic rhythms. Breath by breath changes in ventilation were essentially induced by oscillations in tidal volume. Discontinuous oscillating breathing appeared after forced maximal inspiration and this periodic rhythm was frequently associated with sights. This periodic breathing began or persisted under progressive hypoxia but disappeared under normobaric hyperoxia. These data are discussed in terms of changes in the ventilatory control system and in central regulation of breathing patterns.

Aged↗

Relationships between eupnoeic pattern of breathing and ventilatory control in man: I. Response to airways occlusion during active lung inflation.

The apnoeic response following interruption of the air flow at different levels of the inspiratory capacity (deltaVL) was studied in conscious children and adults. Changes in mouth pressure were used to measured the duration of the apnoe. The total duration of the interrupted breath (T1) was compared to mean value of the ventilatory period of the five preceding breaths (T0). A monoexponential regression could be fitted to the relationship between T1/T0 ratio and change in lung volume (deltaVL) measured at the onset of interruption: T1/T0=k-exp (S-deltaVL), S begin the sensitivity of the response to lung inflation. When T1/T0=1, the intrathoracic lung volume was called threshold volume (VTh.L.). The parameters S and VTh.L. were used for characterization of the individual importance of the Breuer-Hering inspiratory-inhibitory reflex (B.H. reflex). The high reproducibility of the T1/T0 vs. deltaVL relationship in many subjects showed the light influence of voluntary control on apnoea's duration. In each subject, S and VTh.L. were compared with ventilatory variables measured during eupnoea. A fast pattern of breathing (i.e. small inspired volume and short inspiratory duration) was associated with high value of S and low VTh.L. Moreover VTh.L. was near the tidal volume range in subjects where the B.H. reflex was the more potent. Thus, vagal afferents relating to this reflex could modulate the eupnoeic pattern of some subjects.

Adolescent↗

[The role of afferent barosensory neurons in respiratory and bronchomotor control].

Ventilatory and bronchomotor responses to baroreceptor afferent stimulation were studied in anaesthetized rabbits breathing spontaneously. The stimuli used were either the increase in carotid sinus pressure or the electrical stimulation of the cut central end of the aortic nerve. Respiratory effects of aortic barodenervation were also studied. Normoxic, normocapnic steady state was verified by repeated measurement of PO2, PCO2 and pH in arterial blood. Stimulation of both aortic and carotid baroreceptors provoked an early decrease of tidal volume and total pulmonary resistances without change in respiratory frequency. Aortic nerve stimulation induced an important and slowly adapting ventilatory and bronchomotor effect, whereas changes in carotid sinus pressure produced slight variation in respiratory parameters. Aortic nerve section resulted in an early and prolonged increase of total pulmonary resistances. Surgical or chemical (atropine) vagotomy did not change the bronchodilation observed under stimulation of the carotid sinus; however this effect was suppressed by intravenous injection of propranolol. This observation shows the importance of the sympathetic outflow in the genesis of bronchomotor responses following baroreceptor stimulation. In conclusion the baroreceptor stimulation provokes simultaneous decrease of both ventilation and total pulmonary resistances; aortic nerves seemed to exert permanent control on bronchomotor tone.

Animals↗

Long-term exposure of adults to outdoor air pollution is associated with increased airway obstruction and higher prevalence of bronchial hyperresponsiveness.

The authors studied the association between long-term exposure (i.e., > 10 y) to outdoor air pollution and the severity of obstructive pulmonary disease and prevalence of bronchial hyperreactivity to beta2 agonists in two groups of adult patients who were of similar ages and who had similar smoking habits. The subjects lived in downtown districts or in the outer suburbs of Marseilles, the neighborhood that contained air samplers. The regions were similar with respect to sulfur dioxide levels, but levels of nitric oxides and particulate matter (10 millimeters or less) were higher in the downtown area than the suburbs. The authors assessed airway obstruction, as determined by a decrease in forced expiratory volume in 1 s, mean forced expiratory flow measured between 25% and 75% of vital capacity, and an elevated value of central airway resistance. The authors tested the changes in these variables induced by inhalation of a beta2 agonist. Baseline lung function was altered more significantly in both male and female patients who lived in downtown Marseilles than in those who resided in the suburbs, and the differences persisted regardless of the season during which the study occurred. Prevalence of bronchial hyperreactivity and symptoms of asthma (but not of rhinitis) were higher in the downtown than suburban male subjects. The results of this study suggest that an association exists between actual environmental exposure to outdoor air pollution (i.e., nitrogen oxides and/or particulate matter of 10 millimeters or less) and respiratory effects in sensitive adults represented by patients with chronic obstructive pulmonary disease or asthma.

Adult↗

[The hyperammonemia of exercise; value of automatic measurement].

Ammonia blood level (NH3) was measured during maximum exercise performed on cycloergometer, in 11 patients. NH3 measurements through an automatic chemical method (whole blood) were compared to those of the enzymatic reference method (plasma). Automatic analysis made it possible to quickly obtain [NH3] values, that were highly correlated with those of the enzymatic method (P < 0.001). Plasma [NH3] may be calculated from the following equation, where it is expressed versus [NH3] obtained with the automatic method (c anal): [NH3] mumol.l-1 = 0.795. [c] anal.microgram.dl-1 + 5.446.

Ammonia↗

Changes in blood ammonia induced by a maximum effort in trained and untrained subjects.

Twelve healthy male volunteers, either trained or untrained, performed a maximal exercise on a cycloergometer. Venous blood samples were taken for analysis during the effort and the following recovery. Blood concentrations of lactate and ammonia, and plasmatic concentrations of alanine, glutamate and glutamine were measured. At the beginning on the effort, ammonia decreased by 32% (P < 0.01) in comparison with its mean level at rest; at 77% and 78% of maximum load there was a steeper ascent of blood ammonia and lactate vs load curve. There was a high correlation (P < 0.001) between ammonia and lactate during exercise. At the end of the effort, these two variables had significantly increased in comparison with their values at rest (P < 0.01 for ammonia and P < 0.001 for lactate), but they did not correlate with VO2max. The negative correlation existing between ammonia and VO2max at the beginning of the recovery period may imply that muscle NH3 release is inversely proportional to the subject's sports training level, this relation being less evident when blood lactate vs VO2max correlation was considered. Increase in blood glutamate level was greater in trained subjects (P < 0.05). This finding suggests that ammonia elimination is favoured by physical training. In conclusion, ammonia measurements during exercise provide a valuable information about muscle cell oxidative capacity.

Ammonia↗

[Relationship between the initial dimensions of bronchial ring and its contraction after acetylcholine (author's transl)].

Contractions produced by comulative doses of acetylcholine were studied in isolated canine bronchical rings from 2 to 10 mm internal diameter. The maximal active tension achieved was directly related to the initial caliber of the ring and to the amount of smooth muscle. The maximal decrease in caliber was relatively greater (--39%) in the smaller than in the larger bronchi (--17%). However the corresponding increase in airway resistance may be predicted to be more important in the larger resistive bronchi.

Acetylcholine↗

[Role of the acid-base status on the changes of haemoglobin oxygen affinity in arterial hypoxemia (author's transl)].

Fifty-seven patients, all with chronic respiratory insufficiency and hypoxemia, have been classified in five groups according to their acid-base status, determined by the intra-erythrocytic pH (pHi) : A. normal acid-base balance ; B. chronic alkalosis ; C. acute alkalosis ; D. acute acidosis ; E. chronic acidosis. We have measured in the arterial blood : Po2, PCO2, plasmatic pH (pHp1), pHi, P50(7,40) and 2,3-DPG. From these values. the base-excess (B.E.) and the P50 to real pH [P50 I.V.] have been computed. There is a good correlation between 2,3-DPG and P50 (r = 0.707), none between P50 and Pao2. For a normal acid-base balance, P50 and 2.3-DPG also are normal. Increased in chronic alkalosis, the amount of DPG is decreased in chronic acidosis. The DPG-pHi correlation is very good (r = 0.691 ; pless 0.001) and the changes of the acid-base balance seem to be the main factors for controlling the DPG synthesis : it increases it in chronic alkalosis and reduces it in chronic acidosis. Thus the P50(I.V.) returns to the normal range on account of the Bohr effect adjustement. On the contrary, in acute acidosis and alkalosis, the amount of DPG is normal and the P50(I.V.) is increased or reduced. Therefore the duration of the acid-base lack of balance also interfers.

Acid-Base Equilibrium↗

Effects of buprenorphine on respiratory and cardiovascular functions during hypoxia in anaesthetized rabbits.

Respiratory and cardiovascular variables were studied in 10 anaesthetized rabbits, before and after buprenorphine i.v. injections (cumulative doses of 5 to 100 micrograms/kg). In normoxic conditions, buprenorphine induced hypoventilation, due to a decrease in respiratory rate, and bradycardia: mean maximum modifications in ventilation (-17%) and heart rate (-7%) were obtained with buprenorphine 10 and 100 micrograms/kg, respectively. Isocapnic hypoxia, produced by the inhalation of a gas mixture containing 10% O2 in nitrogen for 5 min, provoked a mean 44% increase in base line ventilation and a mean 15% decrease in heart rate. The ventilatory response to hypoxia was not significantly modified by buprenorphine on an average; large decreases in hypoxic drive could still be observed in 3 out of 10 animals with buprenorphine 5 and 10 micrograms/kg. Buprenorphine enhanced hypoxia-induced bradycardia: a mean maximum decrease in heart rate (-29%) was reached with 10 micrograms/kg of this opioid.

Anesthesia↗

Increased ventilatory chemosensitivity induced by domperidone, a dopamine antagonist, in healthy humans.

Respiratory and cardiovascular effects of domperidone (0.1 mg X kg-1 i.v.) and placebo given on separate test days to eleven healthy volunteers were assessed in a double-blind study. Domperidone caused no significant change in ventilation, heart rate and blood pressure while they were resting and breathing room air. However, it produced an increase in the slope of the hypoxia-induced ventilatory response, from 2.35 +/- 1.10 to 3.71 +/- 2.91 1 X min-1 per 1% decrease in SaO2 (mean +/- SD; p less than 0.05). We conclude that domperidone augments hypoxic responsiveness in humans, presumably by blocking the dopaminergic receptors that modulate the activity of carotid body chemoreceptors, as it does not readily cross the blood-brain barrier.

Adult↗

Lung reflexes in anaesthetized rabbits with elastase-induced emphysema.

The effects of elastase-induced emphysema on vagal pulmonary reflexes were studied in seven rabbits, given 600 IU of porcine pancreatic elastase intratracheally (E group), and eight untreated rabbits (U group) under pentobarbital anaesthesia. The presence of emphysema was confirmed by histological and pathological criteria and by documented changes in lung mechanics seven months after treatment. The strength of the Hering-Breuer inflation reflex (HBIR), indicative of pulmonary stretch receptor excitability, was unchanged in the U group, but was significantly increased in the E group at inflation volumes greater than the tidal volume (VT) range, as she slope of the curve relating HBIR to inflation volume was significantly steeper (0.40 vs 0.22 ml-1; p less than 0.05). The early ventilatory response (first 3 breaths) to right atrial injections of phenyldiguanide (20 and 30 micrograms X kg-1 i.v.) was used as an indication of the excitability of lung receptors with non-myelinated vagal afferents. This response, characterized by a significant decrease in expiratory duration (TE) without effect on VT or inspiratory time (TI), was not significantly different between the E and U groups. The overall pattern of breathing in the E group showed a significant decrease in VT associated with an increase in TI.

Animals↗