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Biomedical subjects

D Murciano

Publications and source records attributed to D Murciano.

52 records · Page 3Linked to original sources
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↗
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

[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

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

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

[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↗
PubMed1980

[Assessment of chemoprophylaxis with intermittent tetracycline in chronic bronchitis. A functional follow-up for 3 years (author's transl)].

This study is a reappraisal for the value of intermittent tetracycline therapy in the reduction of the rate of pulmonary function alteration in patients with chronic obstructive lung disease. Two groups of patients with chronic bronchitis were randomly divided and followed up for three years. No significant differences in pulmonary function were observed between these two groups.

Adult↗
PubMed1979

[Interest of helium-oxygen flow volume and isoflow volume curves in chronic obstructive lung disease (author's transl)].

We have compared changes in maximal flows induced by breathing gases of different density in 54 patients suffering from emphysema and chronic bronchitis. We considered as positive responders those subjects displaying an increase by at least 20% of maximal expiratory flows while breathing gases of lower density. Such a response was demonstrated in 21 cases, the remainder (33 cases) being non-responders. Hence, in such patients, airways obstruction may primarily be localised in central or peripheral airways. There was no correlation between the nature of this response and the clinical diagnosis, but non-responders, in general, were those in whom respiratory insufficiency was more severe. There seemed to be no additional information gained by measuring isoflow-volume (iso V vol.) in comparison with measuring differences in maximal flows at 50% of vital capacity.

Bronchitis↗