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Biomedical subjects

M Aubier

Publications and source records attributed to M Aubier.

At least 181 records · Page 10Linked to original sources
PubMed1986

Effects of digoxin on diaphragmatic strength generation.

Contrary to hindlimb muscle, extracellular calcium plays an important role in diaphragmatic strength generation (J. Appl. Physiol. 58: 2054-61, 1985). Since the inotropic effect of digitalis appears to be related to cell membrane transport of calcium, we studied the effect of digoxin on diaphragmatic contractility in 20 anesthetized dogs. The diaphragm was electrically stimulated with intramuscular electrodes. The transdiaphragmatic pressure (Pdi) during supramaximal (50 V) 2-s stimulations applied over a frequency range of 10-100 Hz was measured with balloon catheters at functional residual capacity. Cardiac output was measured with a Swan-Ganz catheter and diaphragmatic blood flow (Qdi) by timed volume collections of left inferior venous effluent. The force generated by the sartorius muscle during electrical stimulations was studied concomitantly to Pdi. In 10 dogs (group A) 0.04 mg/kg of digoxin was infused in 10 min. In 10 other dogs (group B) 0.2 mg/kg was administered. All measurements were performed during control and 30, 60, 90, and 120 min after digoxin administration. In group A, digoxin plasmatic level at 60 min reached a therapeutic range in all dogs (1.8 +/- 0.3 ng/ml), whereas in group B, digoxin plasmatic level was higher (8 +/- 1.3 ng/ml). No significant change in cardiac output and Qdi was noted after administration of digoxin, either in the dogs of group A or those of group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Diaphragmatic contractility after upper abdominal surgery.

Postoperative dysfunction of the diaphragm has been reported after upper abdominal surgery. This study was designed to determine whether an impairment in diaphragmatic contractility was involved in the genesis of the diaphragmatic dysfunction observed after upper abdominal surgery. Five patients undergoing upper abdominal surgery were studied. The following measurements were performed before and 4 h after surgery: vital capacity (VC), functional residual capacity (FRC), and forced expiratory volume in 1 s. Diaphragmatic function was also assessed using the ratio of changes in gastric pressure (delta Pga) over changes in transdiaphragmatic pressure (delta Pdi). Finally contractility of the diaphragm was determined by measuring the change in delta Pdi generated during bilateral electrical stimulation of the phrenic nerves (Pdi stim). Diaphragmatic dysfunction occurred in all the patients after upper abdominal surgery as assessed by a marked decrease in delta Pga/delta Pdi from 0.480 +/- 0.040 to -0.097 +/- 0.152 (P less than 0.01) 4 h after surgery compared with preoperative values. VC also markedly decreased after upper abdominal surgery from 3,900 +/- 630 to 2,060 +/- 520 ml (P less than 0.01) 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after upper abdominal surgery compared with the preoperative values. We conclude that contractility of the diaphragm is not altered after upper abdominal surgery, and diaphragmatic dysfunction is secondary to other mechanisms such as possible reflexes arising from the periphery (chest wall and/or peritoneum), which could inhibit the phrenic nerve output.

Abdomen↗
PubMed1986

Effects of theophylline on isolated diaphragmatic fibers. A model for pharmacologic studies on diaphragmatic contractility.

An in vitro model of isolated diaphragmatic muscle fibers was developed to study the effects of theophylline on diaphragmatic contractility. The effects of theophylline on this model were compared for each dose with the effects of the drugs on a "classic" hemidiaphragmatic muscle preparation. Diaphragmatic strips obtained from 20 rats were placed into an open topped channel of a plexiglass tissue chamber and perfused with continuously flowing Krebs solution heated to 37 degrees and bubbled with a 95% O2 and 5% CO2 gas mixture so as to maintain pH, PO2, PCO2 constant (7.4, 100, and 35 mmHg, respectively). Isometric force generated in response to 1 Hz supramaximal electrical stimulation was measured with a highly sensitive photoelectric transducer. Graded doses of aminophylline (15 to 75 mg/L) were administered and their effect assessed on diaphragmatic peak twitch tension. On the single diaphragmatic muscle fibers preparation, theophylline produced a dose dependent increase in peak twitch tension, which, at a concentration of theophylline of 15 mg/L, a therapeutic dose, amounted to 111 +/- 1.5% of control (p less than 0.05). At a concentration of 60 mg/L the increase in peak twitch tension averaged 35 +/- 2.5% of control, (p less than 0.001). On the other hand, theophylline had no effect on the hemidiaphragm preparation until a dose of 250 mg/L. These findings suggest that the effects of theophylline on diaphragmatic contractility are due to a direct action of the drug on the contractile properties of the diaphragmatic fibers and also validate the presented in vitro model as a promising one for future pharmacologic studies on diaphragmatic contractility.

Animals↗
PubMed1985

Effect of hypophosphatemia on diaphragmatic contractility in patients with acute respiratory failure.

We studied the effects of hypophosphatemia on diaphragmatic function in eight patients with acute respiratory failure who were artificially ventilated. Their mean serum phosphorus level was 0.55 +/- 0.18 mmol per liter (normal value, 1.20 +/- 0.10). The contractile properties of the diaphragm were assessed by measuring the transdiaphragmatic pressure generated at functional residual capacity during bilateral supramaximal electrical stimulation of the phrenic nerves. Diaphragmatic function was evaluated in each patient before and after correction of hypophosphatemia, which was achieved by administration of 10 mmol of phosphorus (as KH2PO4) as a continuous infusion for four hours. After phosphate infusion, the mean serum phosphorus level increased significantly (1.33 +/- 0.21 mmol per liter, P less than 0.0001). The increase in serum phosphorus was accompanied by a marked increase in the transdiaphragmatic pressure after phrenic stimulation (17.25 +/- 6.5 cm H2O as compared with 9.75 +/- 3.8 before phosphate infusion, P less than 0.001). Changes in the serum phosphorus level and transdiaphragmatic pressure were well correlated (r = 0.73). These results strongly suggest that hypophosphatemia impairs the contractile properties of the diaphragm during acute respiratory failure, and they emphasize the importance of maintaining normal serum inorganic phosphate levels in such patients.

Acute Disease↗
PubMed1985

[Hypophosphoremia during mechanical ventilation for chronic obstructive bronchopathies].

Hypophosphoremia may interfere with respiratory function in chronic obstructive pulmonary diseases (COPD) through different mechanisms: muscular exhaustion and weakness. Accordingly, the frequency and magnitude of hypophosphoremia was studied in 36 consecutive patients with acute respiratory failure and mechanical ventilation. Initial phosphoremia was normal (1,32 +/- 0,12 mmol/l) but often and rapidly decreased in all patients after mechanical ventilation had been started (0,54 +/- 0,14 mmol/l after 24 h). After this, phosphoremia remained low, slowly increasing with continued enteral nutrition (2000 Kcal, 276 g of glucides, 33 mmol/l of phosphorus). Four patients had severe hypophosphoremia after 24 h of mechanical ventilation (less than 0,30 mmol/l). Phosphoremia returned to a normal level 36 h after extubation. Hypophosphoremia was closely linked to pH improvement (r = + 0,67, P less than 0,001) and was paralleled by a drop in phosphaturia, suggesting intra-cellular penetration of phosphorus.

Acidosis↗
PubMed1985

[Function of the respiratory muscles in acute cardiac decompensation].

In anesthetized dogs the performance of the respiratory muscles during cardiogenic shock and their influence on its outcome was studied. Shock was induced by cardiac tamponade. Cardiac output during shock amounted to 25-35% of control and was kept constant. Minute ventilation (VE) initially increased and then progressively decreased until respiratory arrest. The latter was due to impairment of respiratory muscle contractility, the pressure generated by the diaphragm (Pdi) decreasing despite a marked increase in the diaphragmatic electromyogram and of the phrenogram. Mechanical ventilation during shock prolonged survival for the same decrease in cardiac output, and also decreased substantially the severity of lactic acidosis. Furthermore, blood flow to the respiratory muscles during shock was different in the animals breathing spontaneously (SB) from that in mechanically ventilated animals (MV). The fraction of cardiac output distributed to the respiratory muscles during control amounted to 1.85% in MV and 2.79% in SB. With shock this decreased to 1.55% in MV while in SB it decreased by 21%, which suggests that mechanical ventilation during shock preserves a large portion of cardiac output used by the respiratory muscles during spontaneous breathing, thus making it available to other organs.

Animals↗
PubMed1985

Bilateral phrenic stimulation: a simple technique to assess diaphragmatic fatigue in humans.

Transdiaphragmatic pressure (Pdi) and the rate of relaxation of the diaphragm (tau) were measured at functional residual capacity (FRC) in six normal seated subjects during single-twitch stimulation of both phrenic nerves. The latter were stimulated supramaximally with needle electrodes with square-wave impulses of 0.1-ms duration at 1 Hz before and after diaphragmatic fatigue produced by resistive loaded breathing. Constancy of chest wall configuration was achieved by monitoring the diameter of the abdomen and the rib cage with a respiratory inductive plethysmograph system. During control the peak Pdi generated during the phrenic stimulation amounted to 34.4 +/- 4.2 (SE) cmH2O and represented in each subject a fixed fraction (17%) of its maximal transdiaphragmatic pressure. After diaphragmatic fatigue the peak Pdi decreased by an average of 45%, amounting to 18.1 +/- 2.7 cmH2O 5 min after the fatigue run, and tau increased from 55.2 +/- 9 ms during control to 77 +/- 8 ms 5 min after the fatigue run. The decrease in peak Pdi and the increase in tau observed after the fatigue run persisted throughout the 30 min of the recovery period studied, the peak Pdi amounting to 18.4 +/- 2.8 and 18.9 +/- 3.3 cmH2O and tau to 81.3 +/- 5.7 and 88.7 +/- 10 ms at 15 and 30 min after the end of the fatigue run, respectively. It is concluded that diaphragmatic fatigue can be detected in man by bilateral phrenic stimulation with needle electrodes without any discomfort for the subject and that the decrease in diaphragmatic strength after fatigue is long lasting.

Action Potentials↗
PubMed1985

Effects of hypocalcemia on diaphragmatic strength generation.

We studied the effects of hypocalcemia on diaphragmatic force and diaphragm blood flow (Qdi) in 12 anesthetized dogs. The diaphragm was electrically stimulated with intramuscular electrodes surgically implanted in the ventral surface of each hemidiaphragm. The transdiaphragmatic pressure (Pdi) during supramaximal (50 V) 2-s stimulations applied over a frequency range of 10-100 Hz was measured with balloon catheters during tracheal occlusion at functional residual capacity. A catheter was placed via the femoral vein into the left inferior phrenic vein, and Qdi was measured by timed volume collections of left inferior venous effluent. A catheter was introduced in a femoral artery to monitor blood pressure (BP). In five additional dogs, the force generated by the sartorius muscle during electrical stimulation was also studied concomitantly to diaphragmatic force. The animals were mechanically ventilated throughout the experiment, and the arterial blood gases and pH were maintained constant. Hypocalcemia was induced by a continuous infusion of EGTA (70 mg X kg-1 X h-1), which led to a progressive decrease (P less than 0.0001) of ionized calcium plasmatic level from 2.21 +/- 0.4 meq/1 during control to 1.69 +/- 0.06, 1.25 +/- 0.5, and 1.07 +/- 0.5 meq/1 after 30, 60, and 120 min, respectively. Hypocalcemia decreased progressively Pdi, which amounted to 84 +/- 3 (P less than 0.001) and 98 +/- 2% of control values for the low frequencies (10 and 20 Hz) and the high frequencies (50 and 100 Hz), respectively, after 30 min of EGTA infusion and to 74 +/- 5 and 79 +/- 6% for the low and high frequencies, respectively, after 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Work of breathing in patients with chronic obstructive pulmonary disease in acute respiratory failure.

In 11 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) in acute ventilatory failure, we measured the total inspiratory (WItot) and total resistive (WI + Eres) work rate of breathing, together with lung mechanics (dynamic pulmonary elastance and inspiratory and expiratory pulmonary flow resistance). All variables were markedly increased compared with those in normal subjects. No significant correlation was found between WItot and WI + Eres with lung mechanics data. However, when WItot and WI + Eres were expressed per liter of ventilation, a significant positive correlation was found with all lung mechanics data. These results indicate that although in patients acutely ill with COPD, work rate and work per liter of ventilation are increased, only the latter is related to the severity of pulmonary mechanical impairment, and it could be used as one of the criteria for extubation. In addition, our results indicate that at end-expiration the alveolar pressure was positive (range, 6 to 13 cm H2O) in all patients (intrinsic PEEP), a fact that must necessarily affect hemodynamics; furthermore, it imposes an extra burden on the inspiratory muscles.

Acute Disease↗
PubMed1985

Effect of theophylline on respiratory muscle function.

Theophylline improves diaphragmatic contractility of the respiratory muscles both in isolated muscle preparations, as well as in animals and normal human beings. Furthermore, theophylline restores diaphragmatic fatigue and prevents fatigue of the diaphragm when given prophylactically. Finally, it was recently shown that theophylline improves diaphragmatic function in COPD patients, all of whom were CO2 retainers (PaCO2 53 +/- 3 mm Hg) and hypoxemic (PaO2 57 +/- 8 mm Hg). Patients improved transdiaphragmatic pressure and were less susceptible to fatigue. Presently the mechanisms of action of theophylline regarding its effects on diaphragmatic function are not fully elucidated. Experimental evidence, however, suggests that theophylline may have an effect on transmembrane calcium movements by blocking adenosine receptors.

Aminophylline↗
PubMed1984

[Fatigue of the respiratory muscles].

When respiratory muscle demands for energy exceed supplies, the energy stored within the muscles is depleted and the force of contraction diminishes. This state is called inspiratory muscle fatigue. When it occurs alveolar ventilation decreases, arterial carbon dioxide tension (Pa CO2), increases and hypercapnic respiratory failure ensues. It has also been suggested that such a dysfunction of the respiratory muscles contributes to the pathogenesis of dyspnoea. The purpose of this article is to review: those factors that predispose to respiratory muscle fatigue and determine energy demand and supply, and the principal means of investigation available, including the study of pressures created by muscular contraction, and electromyography.

Abdominal Muscles↗
PubMed1984

Effects of theophylline on diaphragmatic strength and fatigue in patients with chronic obstructive pulmonary disease.

We studied the effects of theophylline on diaphragmatic strength and fatigue in 15 patients with severe chronic obstructive pulmonary disease. Diaphragmatic strength was assessed by measurement of the transdiaphragmatic pressure generated at functional residual capacity during a maximal inspiratory effort against closed airways. Diaphragmatic fatigue was induced by resistive loaded breathing. The electrical activity of the diaphragm was recorded with an esophageal electrode during the fatigue runs, and the high-low ratio of the electrical signal was analyzed to assess diaphragmatic fatigue. Studies were performed before and after 7 and 30 days of theophylline administration (mean plasma level, 13 +/- 2 mg per liter). A control group received a placebo instead of theophylline. Theophylline increased maximal transdiaphragmatic pressure by 16 per cent after 7 days of administration (P less than 0.01), and this increase persisted after 30 days. No significant change in maximal transdiaphragmatic pressure was observed in the group given the placebo. Theophylline also suppressed diaphragmatic fatigue in all patients who received it. We conclude that theophylline has a potent and long-lasting effect on diaphragmatic strength and fatigue in patients with fixed airway obstruction.

Diaphragm↗
PubMed1984

Effects and mechanism of action of terbutaline on diaphragmatic contractility and fatigue.

We studied the effects of intravenously administered terbutaline on diaphragmatic force and fatigue during electrical stimulation of the diaphragm in 17 anesthetized dogs. The diaphragm was stimulated indirectly through the phrenic nerves with electrodes placed around the fifth roots and directly with electrodes surgically implanted in the abdominal side of each hemidiaphragm. Transdiaphragmatic pressure (Pdi) during direct or indirect supramaximal 2-s stimulation applied over a frequency range of 10-100 Hz was measured with balloon catheters during tracheal occlusion at functional residual capacity. In seven dogs the administration of terbutaline (0.5 mg) had no effect on Pdi at any stimulation frequency applied directly or indirectly. The effect of terbutaline (0.5 mg) on diaphragmatic fatigue was then tested in 10 other dogs. Diaphragmatic fatigue was produced by continuous 20-Hz electrical supramaxial stimulation of the phrenic nerves during 30 min. At the end of the fatigue procedure Pdi decreased by 50 +/- 5 and 30 +/- 8% of control values at 10 and 100 Hz, respectively, for either direct or indirect stimulation. The decrease in Pdi for low frequencies of stimulation (10 and 20 Hz) lasted 100 +/- 18 min, whereas it lasted only 40 +/- 10 min for the high frequencies (50 and 100 Hz). When terbutaline (0.5 mg) was administered after the fatiguing procedure, Pdi increased within 15 min by 20 +/- 4% at 10 Hz and by 12 +/- 3% at 100 Hz for either direct or indirect stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effects of aminophylline on diaphragmatic fatigue during acute respiratory failure.

The effects of aminophylline on diaphragmatic fatigue and recovery in the face of hypoxemia and hypercapnic acidosis were studied in anesthetized, spontaneously breathing, dogs. The phrenic nerves were stimulated supramaximally at 10, 20, 50, and 100 Hz during 2 s with electrodes placed around the fifth roots, and the resulting transdiaphragmatic pressure (Pdi) was measured with balloon catheters. The dogs were occluded before the stimulations at functional residual capacity. The latter was monitored by measuring the end-expiratory transpulmonary pressure, which remained constant throughout the experiment. Diaphragmatic fatigue was produced by resistive loaded breathing. At the end of the runs, which lasted 15 +/- 2 min, all the dogs were severely hypoxemic (30 +/- 5 mmHg), hypercapnic (65 +/- 4 mmHg), and acidotic (7.1 +/- 0.05). During the fatigue runs, phrenic stimulation resulted in a marked decrease in Pdi, which amounted at 20 Hz to 70 +/- 8% and 45 +/- 12% of the control values 5 min after the onset of the fatigue runs and at the end, respectively. After recovery (3 h), Pdi and arterial blood gas determinations returned to control values. Identical fatigue runs were repeated with aminophylline infusion (loading dose, 6 mg/kg in 10 min and maintenance dose, 1 mg/kg/h), leading to a plasmatic concentration of 16.4 +/- 2 mg/l. Aminophylline protected the diaphragm against fatigue, and despite the presence of hypoxemia and hypercapnic acidosis, the Pdi generated for a 20 Hz stimulation of the phrenic nerves at identical times of the preceding run amounting to 100 +/- 15% and 85 +/- 10% of control values, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1983

Diaphragmatic contractility enhanced by aminophylline: role of extracellular calcium.

We have studied the effects of aminophylline on diaphragmatic contractility in 12 anesthetized dogs. The phrenic nerves were stimulated supramaximally (20 Hz, 0.1 ms) with electrodes placed around the fifth roots, and the transdiaphragmatic pressure (Pdi) generated at functional residual capacity (FRC) was measured with balloon catheters. Constancy of FRC was monitored by measuring the end-expiratory transpulmonary pressure, the dogs being occluded at FRC before the stimulations. The electrical activity of the diaphragm (Edi) during the stimulations was recorded with electrodes inserted in both hemidiaphragms. Phrenic stimulations during an infusion of aminophylline (10 mg/kg in 5 min) increased Pdi by 25 +/- 8% of control values, whereas the Edi remained unchanged. This potentiating effect of aminophylline was abolished when an identical dose was injected during a continuous infusion of a calcium blocker (verapamil, 0.1 mg X kg-1 X min-1). Infusion of another methylxanthine compound, caffeine (10 mg/kg), also increased Pdi for an identical electrical phrenic nerve stimulation by 21 +/- 6% compared with control values. However, the potentiating effect of caffeine was not abolished by verapamil. We conclude that aminophylline in vivo increases diaphragmatic contractility and that extracellular calcium is necessary for this action, a mechanism not shared by another methylxanthine compound, caffeine.

Aminophylline↗