No abstract

Influence of atopy on exhaled nitric oxide in patients with stable asthma and rhinitis. Ch. Gratziou, M. Lignos, M. Dassiou, Ch. Roussos. #ERS Journals Ltd 1999. ABSTRACT: The level of exhaled NO is increased in patients with allergic asthma and seasonal rhinitis. The aim of this study was to investigate the significance of atopy on NO production in the lower airways.Measurements of exhaled NO were performed in 131 stable asthmatic patients with chronic mild asthma (95 atopics and 36 nonatopics), 72 patients with perennial rhinitis (57 atopics and 15 nonatopics) and 100 healthy controls (20 atopics and 80 nonatopics).Patients with either asthma or rhinitis had higher exhaled NO values (13.3& 1.2 parts per billion (ppb) and 11.7 1.1 ppb) than control subjects (4.8 0.3 ppb, p<0.01). Exhaled NO levels were significantly higher in atopic asthmatics (19 3.6 ppb) compared with nonatopic patients (5.6 0.8 ppb, p<0.001). Similar findings were observed in patients with rhinitis (13.3 1.3 ppb in atopics and 5.8 1.2 ppb in nonatopics, p<0.001). No difference was found in NO levels between atopic and nonatopic control subjects (4.8 0.8 ppb, and 4.5 0.3 ppb).In summary, this study has shown that increased exhaled NO levels are detected only in atopic patients with asthma and/or rhinitis and not in nonatopic patients. These findings may suggest that it is rather the allergic nature of airways inflammation, which is mainly responsible for the higher NO production in the lower airways. Eur Respir J 1999; 14: 897±901.

No abstract

The effect of endotoxic shock on the respiratory muscle performance was studied in spontaneously breathing dogs given Escherichia coli endotoxin (Difco Laboratories, 10 mg/kg). Diaphragmatic (Edi) and parasternal intercostal (Eic) electromyograms were recorded using fishhook electrodes. The recorded signals were then rectified and electrically integrated. Pleural, abdominal, and transdiaphragmatic (Pdi) pressures were recorded by a balloon-catheter system. After a short control period, the endotoxin was administered slowly intravenously (within 5 min). Death was secondary to respiratory arrest in all animals. All animals died within 150-270 min after the onset of endotoxic shock. Within 45-80 min of the endotoxin administration, mean blood pressure and cardiac output dropped to 42.1 +/- 4.1 and 40.1 +/- 6.0% (mean +/- SE) of control values, respectively, with little change afterward. Mean inspiratory flow rate and Pdi increased from control values of 0.27 +/- 0.03 l X s-1 and 5.75 +/- 0.7 cmH2O to mean values of 0.44 +/- 0.3 l X s-1 and 8.70 +/- 1.05 cmH2O and then decreased to 0.17 +/- 0.03 l X s-1 and 3.90 +/- 0.30 cmH2O before the death of the animals. There were no major changes in the mechanics of the respiratory system. Edi and Eic increased progressively to mean values of 360 +/- 21 and 263 +/- 22% of control, respectively, before the death of the animals. None of the dogs were hypoxic. Arterial PCO2 decreased from a control value of 42.9 +/- 1.7 Torr to a mean value of 29.9 +/- 2.8 Torr and then increased to 51 +/- 4.3 Torr before the death of the animals.(ABSTRACT TRUNCATED AT 250 WORDS)

R Re es sp pi ir ra at to or ry y m mu us sc cl le es s a an nd d w we ea an ni in ng g f fa ai il lu ur re e ABSTRACT: Weaning failure is, unfortunately, a rather common phenomenon for mechanically-ventilated patients (especially those with chronic obstructive pulmonary disease (COPD)), and the respiratory muscles play a pivotal role in its development.Weaning fails whenever an imbalance exists between the ventilatory needs and the neurocardiorespiratory capacity. This can happen if there is an increase in the energy demands of the respiratory muscles, a decrease in the energy available, a decrease in neuromuscular competence, or if the respiratory muscles pose an impediment to the heart and blood flow.The imbalance created will lead to weaning failure through the development of respiratory muscle fatigue, hypercapnia, dyspnoea, anxiety and organ dysfunction.

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.

It is known that, in stable asthmatics at rest, tidal expiratory flow limitation (EFL) and dynamic hyperinflation (DH) are seldom present. This study investigated whether stable asthmatics develop tidal EFL and DH during exercise with concurrent limitation of maximal exercise work rate (WRmax).A total of 20 asthmatics in a stable condition and aged 32 ¡ 13 yrs (mean ¡ SD) with a forced expiratory volume in one second (FEV1) of 101¡21% of the predicted value were studied. Only three patients exhibited an FEV1 below the normal limits. On a first visit, patients performed a symptom-limited incremental (20 W?min -1 ) bicycle exercise test. On the second visit, the occurrence of EFL (using the negative expiratory pressure technique) and DH (via reduction in inspiratory capacity) were assessed at rest and when cycling at 33, 66 and 90% of their predetermined WRmax. FEV1 was measured to detect exercise-induced asthma, 5 and 15 min after stopping exercise at 90% WRmax.Only one patient showed EFL at rest, whereas 13 showed EFL and DH during exercise. In these 13 asthmatics, exercise capacity was significantly reduced (WRmax 75¡9% pred) compared to the seven non-EFL patients (WRmax 95¡13% pred). Moreover, a significant correlation of WRmax (% pred) to the change in inspiratory capacity (percentage of resting value) from rest to 90% WRmax was found. Tidal EFL during exercise was not associated with exercise-induced asthma, which was detected in only three patients.In conclusion, tidal expiratory flow limitation and dynamic hyperinflation during exercise are common in stable asthmatics with normal spirometric results and without exercise-induced asthma, and may contribute to reduction in exercise capacity.

Dynamic hyperinflation (DH) contributes importantly to the limitation of constant-load exercise (CLE) in patients with chronic obstructive pulmonary disease (COPD). However, its role in the limitation of interval exercise (IE) remains to be explored. The change (Delta) in inspiratory capacity (IC) was measured to reflect changes in DH in 27 COPD patients (forced expiratory volume in one second mean+/-SEM % predicted: 40+/-3) at the end of a symptom-limited CLE test at 80% of peak work capacity (WRmax) and an IE test at 100% WRmax (30 s of work, alternated with 30 s of unloaded pedalling). At the limit of tolerance in both IE and CLE, patients exhibited similar DH (DeltaIC: 0.39+/-0.05 L and 0.45+/-0.05 L, respectively). However, exercise endurance time (t end) for IE (32.7+/-3.0 min) was significantly greater than for CLE (10.3+/-1.6 min). The IE t end correlated with resting IC, expressed as % pred normal. At 30 and 90% of total IE t end, DeltaIC (0.43+/-0.06 and 0.39+/-0.05 L, respectively) and minute ventilation (31.1+/-1.6 and 32.7+/-2.2 L.min(-1), respectively) were not significantly different. Resting hyperinflation helps to explain the limitation of interval exercise. Implementation of interval exercise for rehabilitation should provide important clinical benefits because it prolongs exercise endurance time and allows sustaining higher stable ventilation.