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Biomedical subjects

M Aubier

Publications and source records attributed to M Aubier.

At least 199 records · Page 11Linked to original sources
PubMed1983

Effect of caffeine on skeletal muscle function before and after fatigue.

We studied the effect of caffeine on voluntary and electrically stimulated contractions of the adductor pollicis muscle in five adult volunteers. Caffeine (500 mg) was administered orally in a double-blind fashion. Electrical stimulation of the ulnar nerve was performed at 10, 20, 30, 50, and 100 Hz before and after a sustained voluntary contraction held at 50% of the maximal voluntary contraction (MVC). A brief tetanus at 30 Hz was also performed to calculate relaxation rate in the fresh muscle. Contractile properties, relaxation rate, and endurance were then assessed after caffeine and placebo, as well as the response of the fatigued muscle to different frequencies of stimulation. There was no difference in the maximal tension obtained with electrical stimulation (T100) or in the MVC between placebo and caffeine. The tensions developed with electrical stimulation at lower frequencies increased significantly with caffeine ingestion, shifting the frequency-force curve to the left, both before and after fatigue. Mean plasma caffeine concentration associated with these responses was 12.2 +/- 4.9 mg/l. We conclude that caffeine has a direct effect on skeletal muscle contractile properties both before and after fatigue as demonstrated by electrical stimulation.

Adult↗
PubMed1983

Increased ventilation caused by improved diaphragmatic efficiency during aminophylline infusion.

The mechanism underlying the increase in ventilation (VE) observed during aminophylline infusion was investigated in 12 anesthetized spontaneously breathing dogs. Progressive doses of aminophylline were infused every 30 min, leading to plasmatic levels of 10 to 20, 20 to 30, 30 to 50 mg/L. The increase in VE observed while increasing aminophylline plasmatic concentration ranged from 4.2 +/- 6 to 9.5 +/- 1.2 L/min. Concomitantly to VE, we measured an index of the inspiratory neuromuscular output of the diaphragm, the transdiaphragmatic pressure generated at FRC 0.1 s after the onset of a spontaneous inspiration developed against closed airways (Pdi0.1). For each plasmatic level of aminophylline, Pdi0.1 increased as VE (117 +/- 4, 126 +/- 2, 140 +/- 6% of control values for 10 to 20, 20 to 30, 30 to 50 mg/L, respectively). To establish the role played by an improvement in diaphragmatic contractility in the increase in Pdi0.1 with aminophylline, we measured for each plasmatic level of aminophylline the transdiaphragmatic pressure generated at FRC against closed airways during supramaximal stimulation at 10, 20, 50, and 100 Hz of the 2 phrenic nerves (Pdi). Pdi increased while increasing aminophylline plasmatic level for all the frequencies of stimulation. A relationship was found between Pdi and Pdi0.1 at any aminophylline plasmatic level as well as with VE. No change in the mechanical properties of the respiratory system occurred with aminophylline. We conclude that the increase in VE observed after aminophylline administration in our animal model is essentially due to an improvement in diaphragmatic contractility rather than an increase in the central nervous system output.

Aminophylline↗
PubMed1983

Regional blood flow distribution in dog during induced hypotension and low cardiac output. Spontaneous breathing versus artificial ventilation.

Respiratory muscle blood flow and organ blood flow was studied in two groups of dogs with radioactively labeled microspheres to assess the influence of the working respiratory muscles on the regional distribution of blood flow when arterial pressure and cardiac output were lowered by pericardial tamponade. In one group (n = 6), the dogs were paralyzed and mechanically ventilated (Mv), while in the other (n = 6), they were left to breathe spontaneously (Sb). Cardiac output fell to 30% of control values during tamponade in both groups and was maintained constant. None of the dogs was hypoxic. Ventilation in the Sb group peaked after 50 min of hypotension, but remained unchanged in the Mv group. Duplicate measurements of blood flow were made during a control period and after 50 min of tamponade (corresponding to the peak ventilation in Sb). Blood flow to the respiratory muscles increased significantly (P less than 0.001) during tamponade in Sb (diaphragmatic flow increased to 361% of control values), while it decreased in Mv. Although the arterial blood pressure and cardiac output were comparable in the two groups, blood flow distribution during tamponade was different. In Sb, the respiratory muscles received 21% of the cardiac output, compared with only 3% in the Mv group. Thus, by muscle paralysis and Mv, a large fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during low cardiac output state: blood flows to the liver, brain, and quadriceps muscles were significantly higher during tamponade in the Mv group compared with the Sb group. Similarly, blood lactate at all times after the induction of low cardiac output and hypotension was significantly lower in the Mv animals (P less than 0.005).

Animals↗
PubMed1983

[Physiopathology of acute decompensation in chronic obstructive respiratory insufficiency].

The acute decompensation of chronic obstructive respiratory failure is characterised by a deterioration of the respiratory mechanics which leads to a reduction of maximum ventilatory output, the respiratory muscles are placed at a mechanical disadvantage and in attempting to compensate are vulnerable to muscle fatigue. A large part of ventilation is wasted in ventilatory dead space. Total ventilation is normal but tidal volume is shallow and respiratory rate rapid. This type of breathing is partially responsible for the large dead space effect. Respiratory centre activity is greatly increased. The prescription of bronchodilators is debatable because there is a risk of increasing the dead space effect. The hypoxic and hypercapnic stimuli have a weak and roughly similar effect on ventilatory control, but the effect of pure oxygen on PaCO2 is due to factors other than those relating to respiratory centre activity.

Acute Disease↗
PubMed1982

Changes in EMG power spectrum (high-to-low ratio) with force fatigue in humans.

During and following high-load fatiguing voluntary contractions, the force response of skeletal muscle to electrical stimulation is altered so that the frequency-force curve is moved to the right. Fatiguing contractions also result in a shift to the left of the electromyographic (EMG) power spectrum. In the quadriceps muscle and the diaphragm of normal subjects the change in the force response to electrical stimulation has been correlated with the EMG changes. After repeated submaximal contractions in the quadriceps and diaphragm, the forces produced by electrical stimulation at low frequencies were reduced, indicating low-frequency fatigue. This type of fatigue persisted for several hours but did not result in any change in the EMG high-to-low ratio. Low-frequency fatigue is probably an important aspect of the failure of skeletal muscle to generate adequate force, and the EMG high-to-low ratio may not recognize this type of fatigue.

Diaphragm↗
PubMed1982

Effects of inspiratory loading on respiratory muscle activity during expiration.

We studied respiratory muscle activity during expiration in four normal subjects during inspiratory resistive and elastic loading, with and without positive and expiratory pressure. Net inspiratory muscle activity (Pmus) was measured by relating esophageal pressure to the chest wall relaxation pressure-volume (P-V) curve. Abdominal muscle activity (Pabd) was quantitated by relating gastric pressure to the relaxation P-V curve of the abdomen. The decay rates of Pmus and of transdiaphragmatic pressure (Pdi) were increased during loading, and end-expiratory lung volume decreased. The decay rates of Pmus and Pdi were inversely related to expiratory duration. Inspiratory intercostal/accessory activity during expiration was frequently observed together with Pabd, especially during elastic loading. We conclude that external mechanical loads, acting during inspiration, influence respiratory muscle behavior during expiration. Inspiratory loads diminish expiratory braking by the inspiratory muscles and recruit expiratory muscles. The rate of expiration is enhanced and its duration shortened. Simultaneous persistent action of the inspiratory intercostal and accessory muscles throughout expiration may serve to optimize diaphragmatic length.

Abdominal Muscles↗
PubMed1982

Effects of airway anesthesia on pattern of breathing and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure.

To assess the role played by airway receptors in the genesis of rapid and shallow breathing of patients with chronic obstructive pulmonary disease (COPD), we studied the effects of airway anesthesia in 14 patients with COPD during acute respiratory failure. Airway anesthesia was performed by fiberoptic xylocaine administration from the larynx to the subsegmental bronchi, all patients being intubated or tracheostomized. A small decrease in minute ventilation of 6 +/- 1% of the control values occurred after airway anesthesia. This was due to a decrease (p less than 0.01) in respiratory frequency (f) (14.5 +/- 1%). The latter resulted from an increase (p less than 0.0005) in the expiratory time, whereas the inspiratory time did not change significantly. On the other hand, tidal volume increased (p less than 0.02) by 10.1 +/- 0.6%. In all patients, these modifications were accompanied by arterial blood gas deterioration, mean PaO2 and PaCO2 of 42 +/- 3 mmHg and 62 +/- 3 mmHg, respectively, 15 min after xylocaine administration, as compared with 48 +/- 2 mmHg and 54 +/- 2 mmHg, respectively, during the control period. No correlation was found between the changes in minute ventilation and PaO2 or PaCO2. We conclude that (1) activation of airway receptors are involved in the determination of the rapid and shallow breathing observed in patients with COPD during acute respiratory failure, and (2) airway xylocaine anesthesia that worsens arterial blood gases is contraindicated in these patients.

Aged↗
PubMed1982

Respiratory muscle contribution to lactic acidosis in low cardiac output.

The role of the respiratory muscles in the evolution of experimental low cardiac output and lactic acidosis was studied in 2 groups of dogs. One group (6 dogs) was paralyzed and artificially ventilated, and the other (6 dogs) was breathing spontaneously. Shock was induced by cardiac tamponade; cardiac output during shock amounted to 25 to 35% of control values in both groups. All the spontaneously breathing dogs died from ventilatory failure (mean time, 2 h), whereas the artificially ventilated dogs were still alive 3 h after the onset of cardiogenic shock. At any given time after the onset of shock, arterial pH was significantly lower in the spontaneously breathing dogs than in the artificially ventilated ones. This was due to a greater increase in arterial blood lactate in the spontaneously breathing dogs than in the artificially ventilated ones (9.47 +/- 2.7 versus 4.74 +/- 56 mmoles/L at 2 h, respectively). Greater glycogen depletion associated with higher muscle lactate concentrations were found in the respiratory muscles of the spontaneously breathing dogs when compared with that in the artificially ventilated ones. It is concluded that artificial ventilation in cardiogenic shock decreases substantially the severity of lactic acidosis and prolongs survival.

Abdominal Muscles↗
PubMed1982

Comparison of esophageal, tracheal, and mouth occlusion pressure in patients with chronic obstructive pulmonary disease during acute respiratory failure.

In 14 acutely ill patients with chronic obstructive pulmonary disease who were either intubated or breathed via a tracheostomy, we measured the pressures generated in the esophagus and trachea during the first 0.1 s of spontaneous inspiratory efforts against closed airway (P0.1). No significant difference was found between P0.1 in the trachea and esophagus, where it was measured at 2 balloon levels (distance from balloon tip to nares: 35 and 45 cm). In 4 of the patients we also compared esophageal and mouth occlusion pressures during mouth breathing, the orifice of tracheostomy being temporarily obstructed. Mouth P0.1 in the 4 patients averaged approximately 47% of the esophageal occlusion pressure (4.4 +/- 1.7 versus 8.9 +/- 3.1 cm H2O, respectively). Because in patients with COPD with upper airways bypassed (tracheostomized or intubated) the changes in esophageal and tracheal pressure during occluded respiratory efforts were similar, it is concluded that the difference between esophageal and mouth occlusion pressure is due to the tissue compliance of the oropharynx.

Aged↗
PubMed1982

[Effect of sleep on respiration].

Physiologists as well as chest physicians are both interested in respiratory control and disturbances during sleep. Many studies have demonstrated episodic falls in oxygen saturation in lung disease during sleep related to episodic alveolar hypoventilation and/or apneas. A better understanding of these sleep-induced disorders has been possible since the use of electroencephalo-and oculogram (EEG-EOG) to separate the two stages of sleep i.e rapid eye movement sleep (REM sleep) and slow wave sleep (non-REM sleep), and of non invasive methods in assessment of respiratory parameters. Several mechanisms may explain respiratory disturbances during sleep: --a failure of respiratory control systems which differ between the two stages of sleep (central apnea); --a decrease in activity of all upper airway muscles, mainly during REM sleep (occlusive apnea); --a worsening in ventilation-perfusion inhomogeneities which may occur independently of the apnea periods. The detection of such falls in oxygen saturation in pulmonary patients, especially in hypoxemic ones appear to be very important to avoid the adverse effects of hypoxemia on pulmonary circulation. This could be realized by: --an evaluation of respiratory disorders during sleep; --a better assessment of the respiratory control systems in cold patients; --suppression of predisposing factors of occlusive apnea. These different investigations would lead us to a more logical management of respiratory disturbances during sleep, especially in patients suffering from chronic respiratory insufficiency.

Animals↗
PubMed1981

Aminophylline improves diaphragmatic contractility.

In an attempt to explain the clinical efficacy of aminophylline, we studied its effect on diaphragmatic function in eight normal subjects. The relation between the electrical activity of the diaphragm and the pressure generated by the diaphragm was assessed during voluntary contractions before and after aminophylline infusion. Aminophylline shifted the electrical activity/pressure curve to the left; the pressure at a given electrical activity increased an average of 15 per cent (P less than 0.001). In four subjects, pressure was also measured during stimulation of the phrenic nerve at various frequencies before and after diaphragmatic fatigue was produced by resistive breathing, with and without aminophylline infusion. Pressure increased after fatigue at all stimulation frequencies with aminophylline, as compared with the pressure after identical fatigue runs at the same stimulation frequencies without aminophylline. The mean plasma aminophylline concentration associated with these responses was 13 +/- 0.9 mg per liter. We conclude that aminophylline improves the diaphragm's contractility and renders it less susceptible to fatigue.

Adult↗
PubMed1981

Neural drive and electromechanical alterations in the fatiguing diaphragm.

It is suggested that respiratory failure in the compromised circulation might occur as a result of respiratory muscle fatigue in the presence of adequate neural drive and muscle excitation. As the cardiac output decreases acidosis develops and ventilation increases, resulting in an increase in the work of breathing, which requires the delivery of large supplies of energy. As these demands cannot be met by the energy supply, because of low cardiac output, the diaphragm fails as a force generator and respiratory failure ensues. Diaphragmatic fatigue may occur in normal subjects if the pressure developed with each breath is greater than 40% of the maximum transdiaphragmatic pressure and hypoxia predisposes the diaphragm to fatigue. Diaphragmatic fatigue, as in other skeletal muscles, might be located either at the neuromuscular junction or distal to it and can be detected either by phrenic stimulation or by frequency analysis of the myoelectric signal. Phrenic stimulation shows that after fatigue the diaphragm develops less force at any frequency of stimulation, but the loss of force at low frequencies persists for a longer period than at high frequencies. Frequency analysis of the electromyogram reveals that the power spectrum shifts to lower frequencies. This shift occurs long before the diaphragm fails as a force generator.

Animals↗
PubMed1981

Detection of diaphragmatic fatigue in man by phrenic stimulation.

Transdiaphragmatic pressure (Pdi) was measured at functional residual capacity (FRC) in four normal seated subjects during supramaximal, supraclavicular transcutaneous stimulation of one phrenic nerve (10, 20, 50, and 100 Hz--0.1 ms duration) before and after diaphragmatic fatigue, produced by breathing through a high alinear inspiratory resistance. Constancy of chest wall configuration was achieved by placing a cast around the abdomen and the lower one-fourth of the rib cage. Pdi increased with frequency of stimulation, so that at 10, 20, and 50 Hz, the Pdi generated was 32 +/- 4 (SE), 70 +/- 3, and 98 +/- 2% of Pdi at 100 Hz, respectively. After diaphragmatic fatigue, Pdi was less than control at all frequencies of stimulation. Recovery for high stimulation frequencies was complete at 10 min, but at low stimulation frequencies recovery was slow: after 30 min of recovery, Pdi at 20 Hz was 31 +/- 7% of the control value. It is concluded that diaphragmatic fatigue can be detected in man by transcutaneous stimulation of the phrenic nerve and that diaphragmatic strength after fatigue recovers faster at high than at low frequencies of stimulation. Furthermore, it is suggested that this long-lasting element of fatigue might occur in patients with chronic obstructive lung disease, predisposing them to respiratory failure.

Adult↗
PubMed1981

Respiratory muscle fatigue during cardiogenic shock.

The effect of cardiogenic shock (tamponade) on respiratory muscles performance was studied in 13 dogs breathing spontaneously. These 13 dogs were compared with 7 dogs artificially ventilated and paralyzed. Cardiac output amounted in both groups to 25-35% of the control value and was maintained constant. None of the dogs were hypoxic. All the spontaneously breathing dogs died on the average 140 +/- 15 min after the onset of cardiogenic shock, whereas the seven dogs artificially ventilated were all alive after 3 h and then killed. Death in the spontaneously breathing dogs was secondary to respiratory failure. Transdiaphragmatic pressure increased during the 1st h by 152 +/- 25% of control and then decreased by 286 +/- 18% in relation to the peak value before the death of the animals. No major changes in the mechanical properties of the respiratory system occurred. The decrease in transdiaphragmatic pressure occurred despite a marked increase per breath in the amplitude of the integrated electrical activity of the diaphragm and of the phrenic nerve. It is concluded that the ventilatory failure of cardiogenic shock is due to an impairment of the contractile process of the respiratory muscles. Artificial ventilation avoids respiratory failure and prolongs survival, which may bear important therapeutic implications.

Animals↗
PubMed1981

[The place of respiratory analeptics in chronic respiratory failure (author's transl)].

The recent renewed interest in respiratory analeptic action in chronic respiratory failure raises the problem of the site of action and nature of these drugs. They lead to a direct or reflex increase in central nervous activity, which in consequence increases respiratory muscle activity. Indeed, patients with respiratory failure develop pressures two or three times greater than normal subjects to achieve adequate ventilation. During acute exacerbations the pressures generated are five or six times as large. This increase in pressure may risk precipitating fatigue. In general the anomalies of blood gases seem much more related to changes in ventilation-perfusion relationships than to global hypoventilation. Finally, a large increase in the force of muscular contraction may only have a minor effect on ventilation, given the alinear nature of the dynamic compliance curve. An increase of central respiratory activity may thus be ineffective and possibly even dangerous. In the overall assessment of drug considered as an analeptic one always ought to consider the possible non-analeptic actions on the bronchial calibre, the force of the respiratory muscles and the ventilation-perfusion relationships. Thus, it is possible that the therapeutic effects of certain analeptic drugs may be due to actions other than those of respiratory stimulation.

Central Nervous System↗
PubMed1980

Central respiratory drive in acute respiratory failure of patients with chronic obstructive pulmonary disease.

Control of breathing was studied in patients with chronic obstructive pulmonary disease, both in the chronic state and during acute respiratory failure. The results were compared to those in a group of age-matched normal subjects. In patients breathing air, minute ventilation was not different during acute and chronic states, and was similar to that in normal subjects. The pattern of breathing, however, was different: acutely ill patients took shorter and smaller breaths, with a breathing frequency higher than that of normal subjects. The pattern of the chronic group was intermediate between that of acutely ill patients and that of normal subjects. Mouth occlusion pressure, an index of neuromuscular respiratory drive, was 5 times greater in acutely ill patients than in normal subjects. Administration of O2 at a flow of 5 L/min caused a small (14%), bus significant, decrease in minute ventilation due to decreased respiratory frequency. The tidal volume did not change, so the decrease in minute ventilation was the result of decreased inspiratory flow. This was associated with a decreased mouth occlusion pressure that was still 3 times greater than that of normal subjects. The increase in arterial PCO2, observed after administration of O2 was not correlated with the decrease in ventilation, indicating that other factors must be responsible for the increase in arterial PCO2. We concluded that (1) despite the poor mechanical advantage of the respiratory muscles in acute respiratory failure, the increased drive to breathe results in high mouth occlusion pressure and inspiratory flow, and (2) the increase in arterial PCO2, observed during administration of O2 is not related solely to changes in respiratory drive.

Aged↗
PubMed1980

Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure.

The effects of the administration of 100% oxygen on minute ventilation (VE) and arterial blood gases were studied in patients with chronic obstructive pulmonary disease during acute respiratory failure. The administration of O2 resulted in an early decrease in VE, which averaged 18% +/- 2 SE of the control VE, and was due to a decrease in both tidal volume (VT) and respiratory frequency (f). This was followed by a slow increase in VE, such that after 15 min of breathing O2, VE rose to 93 +/- 6% of the control room air value, with both VT and f similar to control values. Despite the small difference between VE while breathing room air and that at the fifteenth minute of O2 inhalation, PaCO2 increased by 23 +/- 5 mmHg, and no significant correlation was found between the changes in VE and PaCO2. By the fifteenth minute of O2 inhalation the PaO2 averaged 225 +/- 23 mmHg, and it was concluded that despite the removal of the hypoxic stimulus of O2 inhalation, the activity of the respiratory muscles remained great enough to maintain VE at nearly the same degree as that while breathing room air. Consequently, the changes in PaCO2 after the administration of O2 were mainly due to increased inhomogeneity of VA/Q distribution within the lungs.

Aged↗