Bulletin europeen de physiopathologie respiratoire最新文献

The possibility that changes in energy metabolism are involved in oxygen sensing during hypoxic pulmonary vasoconstriction was tested indirectly by measurement of hypoxic-pressor reactivity in lungs isolated from rats with low and high levels of plasma thyroxine. In the first study, male rats were treated for one week after thyroidectomy with 50 micrograms (n = 6) or 100 micrograms (n = 6) thyroxine per 100 g body weight (b.w.) daily or with solvent (n = 6). The lungs were isolated and perfused at constant flow with salt-albumin solution. They were ventilated with air +5% CO2 in a humid chamber at 38 degrees C. The dose-pressor response to hypoxia and angiotensin II were measured. In the second study, thyroidectomized male rats were treated similarly with 100 micrograms thyroxine (n = 7) or solvent (n = 6) and isolated lungs were perfused with homologous blood obtained from thyroidectomized blood donors treated in the same manner. Then the dose-pressor responses to hypoxia and K+ were elicited. The hypoxic-pressor responses were bigger in thyroxine than in solvent-treated rats. The response to angiotensin II and K+ was not affected by thyroxine treatment. The results are consistent with the idea that hypoxic-pressor reactivity varies directly with the metabolic rate of lung tissue.

It has been suggested that patients with severe chronic airway obstruction might suffer dangerous hypoxia after administration of a beta-agonist through an air driven nebulizer. Twenty patients with severe chronic airway obstruction (12 male, mean age 71.1 (SEM 1.5) yr) were monitored with a Biox oximeter and Hewlett-Packard capnometer before and after 4 mg terbutaline was delivered through an air driven nebulizer or Nebuhaler. The eight patients with chronic hypoxia (mean PaO2 6.76 kPa, PaCO2 7.47 kPa. FEV1 0.53 l) experienced a 4.7% increase in oxygen saturation (SaO2) and 2.9% fall in transcutaneous carbon dioxide tension (PtcCO2) (p less than 0.05) during all treatments, followed by a return to initial levels. These changes were attributable to increased ventilation whilst breathing through a mouthpiece. A similar trend was seen in the SaO2 of the twelve normoxic patients (mean PaO2 9.32 kPa, PaCO2 5.34 kPa, FEV1 0.8 l), but there was a sustained fall in PtcCO2 of 3.7% (p less than 0.001) after administration of terbutaline. Inhaled terbutaline in the dosage given did not cause hypoxia in patients with severe chronic airflow obstruction, but nebulizer and Nebuhaler use was associated with a rise in SaO2 related to increased ventilation whilst breathing through a mouthpiece.

In order to assess ventilatory control in patients with chronic airflow obstruction (CAO), the present study was carried out in nine patients with chronic obstructive pulmonary disease (COPD), eight asthmatics and nine normal subjects. We analysed the components of the respiratory control system at three levels: neural, assessed by diaphragmatic electromyography (EMGd), muscular, assessed by mouth occlusion pressure (P0.1), and ventilatory, assessed by mean inspiratory flow (VT/TI). EMGd was recorded by surface electrodes. During a CO2 rebreathing test, patients showed a normal or greater EMGd response slope (EMGdS), while for a given degree of EMGdS, P0.1 response slope (P0.1S) was found to be significantly reduced; in contrast, for a given degree of P0.1S, VT/TI response slope (VT/TIS) was found to be significantly reduced in COPD patients only. These data show that, compared to normal subjects, patients with CAO have a normal or increased neural component of the respiratory activity (EMGdS) and a relatively lower neuromuscular coupling (P0.1S/EMGdS). Probably due to different parenchymal and airway involvement, musculoventilatory transfer (VT/TIS/P0.1S) was found to be reduced in COPD patients but not in asthmatics. A complementary study, showing a good agreement between surface and oesophageal EMGd seems to confirm that surface EMGd is a useful and promising tool for clinical investigation.

Pulmonary valve echography was technically possible in 44 of 120 patients with chronic lung disease (CLD). Mean pulmonary arterial pressure (Ppa) was significantly correlated with right ventricular isovolumetric relaxation ratio (RVIRT/RVET) as derived from the movement of cusps in valves of the right heart (r = 0.842; p less than 0.001). Prolonged RVIRT was found in 52% of patients with Ppa greater than 20 mmHg and in all ten patients with Ppa greater than 35 mmHg. Other echographic signs, including abnormal right ventricular systolic time intervals (STI), 'a' wave amplitude, right to left ventricular ratio (RV/LV) and interventricular septum diastolic bulging (IVS-B), were less sensitive, but found more often; when higher Ppa was recorded at catheterization in a given patient (r = 0.869; p less than 0.001). Approximate echographic estimation of Ppa in patients with chronic lung disease is possible if right ventricular systolic and diastolic time intervals can be measured and if abnormalities in right ventricular dimensions, interventricular septum motion and pulmonary valve echogram are considered. In contrast to pulmonary fibrosis, technical problems in adequate visualization of right heart valves in chronic obstructive lung disease limit the use of M-mode echo assessment of Ppa to a clinically unacceptable 22% of subjects.

Obligatory nasal breathing has been suggested in the past as a contributor to sudden infant death syndrome (SIDS): nasal obstruction would result in death as infants were unable to breathe orally. To test this hypothesis, we studied 55 normal and 14 near-miss for SIDS infants during a whole-night polysomnography. On several occasions, the infant nares were gently occluded by the fingertips of the investigator. Infants continued to make respiratory efforts against the occluded nose for a variable time (apnoea time), then opened the mouth and started to breathe through it. Mean apnoea time in normal infants was 4.76 +/- 3.41 s (means +/- SD), and 6.54 +/- 4.25 s in near-miss for SIDS ones. These figures were not significantly different. Analysis according to sleep stage (quiet sleep: 4.08 +/- 3.24 s in normals and 6.50 +/- 4.18 s in near-miss for SIDS ones; active sleep: 6.54 +/- 3.67 s in normals and 6.58 +/- 4.76 s in near-miss for SIDS ones) did not disclose any significant difference between groups. There was no significant relationship between apnoea time and age in either group. In many cases, an arousal preceded the resumption of (oral) flow. However, in almost half of the occlusions, oral breathing was initiated during continuing sleep. We conclude: 1) infants are not obligatory nasal breathers, and 2) the nasal obstruction hypothesis should be discarded in the etiology of SIDS.

When considering the therapeutic potential of calcium antagonists in asthma, attention should be paid to the existence of marked differences among these compounds. In the present study, we have compared the effect of verapamil, diltiazem, nifedipine and trifluoperazine on contractions generated by different mechanisms (CaCl2 acting on K+ depolarized preparation, depolarization by KCl, receptor activation by acetylcholine) in lung parenchyma strips isolated from control and actively sensitized guinea-pigs. It was found that verapamil and diltiazem need higher concentrations in the sensitized specimens to elicit the same degree of inhibition obtained in controls. The reverse was found for trifluoperazine while nifedipine had an intermediate position. In conclusion, acute sensitization reveals differences between the various groups of calcium antagonists in their ability to influence agonist-induced lung parenchyma strip contraction, a finding that suggests that these drugs may also behave diversely in the clinical setting.

The aim of this publication is to contribute to the establishment of reference values for the forced expiratory flow between 25 and 75% of the vital capacity (FEF25-75) among black females in West Africa. 316 of them, aged between 10 and 70 years, were submitted to this test. They were considered free from cardiopulmonary disease after a questionnaire and clinical examination. FEF25-75 in absolute value was lower than in the white Euro-americans. It increased up to 18-19 years of age, then decreased steadily thereafter. The main equations of regression for the FEF25-75 (l X s-1) were: 10-18 years, 0.177A + 1.058 and 0.157A + 0.826H + 0.005; 19-70 years, -0.028A + 4.211 and -0.025A + 2.206H + 0.512, (where A is the age in years and H the height in metres). The results are compared with the reference values published in Black Africa, Europe and the United States.

A 17-year old boy presented with severe, predominantly central sleep apnoeas secondary to structural damage in the medulla. At low O2 saturation, the electroencephalogram showed the sudden onset of slow waves. Hypercapnic ventilatory response was low and hypoxic ventilatory response was absent. Low flow oxygen therapy dramatically improved the apnoea score, probably by relieving hypoxic brain depression. Slow waves also disappeared with oxygen therapy. Aminophylline was effective on apnoea score and duration (p less than 0.001). This beneficial effect could be explained by an improvement of the normal oscillations of respiration at the onset of sleep, a change in arousability or a stimulation of the ascending reticular system. These findings suggest a possible role of hypoxic depression in the manifestations of central sleep apnoeas and demonstrate the beneficial effect of low flow oxygen and aminophylline in treating certain central sleep apnoeas.