Thoracic epidural anesthesia reduced respiratory distress induced by airway occlusion. This effect is most likely caused by the systemic effect of lidocaine, rather than by the reduced afferent information from the chest wall.

Inhaled furosemide suppressed the behavioral response to airway occlusion in anesthetized animals without affecting the response to somatic noxious stimulus. The authors' animal model of respiratory distress may be applicable to the study of dyspnea in regard to its mechanism and treatment.

1. Respiratory load compensation plays an important role in the maintenance of an appropriate level of ventilation. We investigated the ventilatory and behavioural responses to a severe load causing both hypercapnia and hypoxaemia in a rat model. 2. A thin silicone tube (15 mm in length, 1 mm ID) was implanted surgically in the trachea. Arterial blood gases and ventilatory and motor activities were assessed serially and non-invasively over a period of 8 weeks. 3. Ventilatory loading produced severe respiratory acidosis with concomitant hypoxaemia immediately after imposition of the load, but there was a considerable improvement of arterial blood gases at 1 day after the start of respiratory loading. Ventilatory loading also caused a gradual increase in ventilatory activity, requiring 7 days to reach the maximum level. There was a reduction in daily motor activity immediately after the ventilatory loading, but this reduction recovered gradually, together with recovery of reduced food and water intake. Administration of a hyperoxic gas mixture during the ventilatory loading decreased ventilatory activity while improving reduced motor activity. 4. These observations suggest that severe chronic ventilatory loading may induce adaptive responses that compensate rapidly for the disturbed acid-base balance with slow and gradual increases in ventilatory activity while matching the increase in motor activity/metabolic rate.

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