Heterogeneous acute respiratory distress syndrome patients are still considered to suffer from one syndrome, and are treated in the same way. Understanding the range of different pathways that lead to pulmonary dysfunction makes it possible to better target clinical treatment.

It is generally accepted that halothane reduces airway and tissue resistance in lungs with preexisting airway tone. However, under conditions of resting airway tone, pulmonary resistance remains unaltered. In this study, we have determined the effects of halothane on respiratory system, pulmonary and chest wall resistive, elastic and viscoelastic mechanical properties, and related the results to findings from lung histology in intact normal rats. Sixteen adult male Wistar rats were allocated randomly to one of two groups (n = 8 in each group): control or halothane group. In the control group, animals were sedated with diazepam 5 mg i.p. and anaesthetized with pentobarbital 20 mg kg-1 i.p. In the halothane group, the anaesthetic was administered at an end-tidal concentration of I MAC throughout the study. Rats were paralysed and underwent mechanical ventilation. Halothane decreased airway resistance but increased the tissue component of resistance (caused by viscoelastic elements and lung inhomogeneity). Static and dynamic elastance also increased with halothane anaesthesia. Pulmonary resistance remained unchanged. Lung histopathology demonstrated airway dilatation and a greater degree of lung collapse and hyperinflation in the halothane group. We conclude that halothane anaesthesia acts both on airway and lung tissue. In airway tissue, dilatation occurs but the lung periphery stiffens. Consequently, these opposing effects result in no overall apparent change in mechanical properties, although changes are observed during halothane anaesthesia in normal animal and subjects.

SummaryWe evaluated whether isoflurane, halothane and sevoflurane attenuate the inflammatory response and improve lung morphofunction in experimental asthma. Fifty-six BALB/c mice were sensitised and challenged with ovalbumin and anaesthetised with isoflurane, halothane, sevoflurane or pentobarbital sodium for one hour. Lung mechanics and histology were evaluated. Gene expression of pro-inflammatory (tumour necrosis factor-a), pro-fibrogenic (transforming growth factor-b) and pro-angiogenic (vascular endothelial growth factor) mediators, as well as oxidative process modulators, were analysed. These modulators included nuclear factor erythroid-2 related factor 2, sirtuin, catalase and glutathione peroxidase. Isoflurane, halothane and sevoflurane reduced airway resistance, static lung elastance and atelectasis when compared with pentobarbital sodium. Sevoflurane minimised bronchoconstriction and cell infiltration, and decreased tumour necrosis factor-a, transforming growth factor-b, vascular endothelial growth factor, sirtuin, catalase and glutathione peroxidase, while increasing nuclear factor erythroid-2-related factor 2 expression. Sevoflurane down-regulated inflammatory, fibrogenic and angiogenic mediators, and modulated oxidant-antioxidant imbalance, improving lung function in this model of asthma.

M Mo od de el ll li in ng g t th he e m me ec ch ha an ni ic ca al l e ef ff fe ec ct ts s o of f t tr ra ac ch he ea al l t tu ub be es s i in n n no or rm ma al l s su ub bj je ec ct ts s On the basis of experimental data from the literature and on a previously reported mathematical model of the inspirogram, we wished to study predictions of pressures, volume, flow and work of breathing during the use of tracheal tubes.The present investigation indicates that: 1) the loss in volume is greater at the beginning of inspiration and with narrower tubes; 2) in order to preserve tidal volume the inspiratory drive must be increased at any time during inspiration with the use of diminishing internal diameter of the tubes; 3) alternatively, tidal volume can be maintained by increasing inspiratory duration; and 4) the addition of tubes with internal diameter of 9 mm (no. 9) and 8 mm (no. 8) increases the total resistive work by 115 and 154%, respectively, whilst total elastic work decreases 9 and 16% in relation to the nonintubated patient.These findings are consequent to the turbulent flow pattern that normally occurs within the tracheal tubes and connectors themselves. We believe they are relevant to the physician confronted with a patient needing tracheal intubation.