Hypoxic apnoea induced by N2 inhalation can be reversed by the aspiration reflex in anaesthetized cats.

Various cardiorespiratory and electrophysiological parameters were analysed in a model of acute respiratory failure induced by inhalation of pure nitrogen in approximately 150 anaesthetized cats. Initial hyperventilation leading to apnoea was characterized by extreme hypoxaemia, marked bradycardia and flattening of electrocortical (ECoG) activity. Artificial ventilation applied at the stage of marked mydriasis usually spontaneously prevented cardiovascular failure and normalized vital functions. Up to seven successive apnoeic attacks could be induced in the same cat. During the first 30 or 60 s of apnoea, nasopharyngeal stimulation usually elicited a typical gasp-like aspiration reflex, while tracheobronchial stimulation provoked a weak cough only in 28 and 34% of cases for 30- and 60-s apnoea, respectively. The aspiration reflex could be elicited at very low and even isoelectric ECoG activity, and its periodic provocation (without artificial ventilation) resulted, more frequently than did gasping, in recovery from hypoxic apnoea. Arousal and resuscitation induced by the aspiration reflex can provide a useful model to study the mechanisms of reversible respiratory failure and restitution of vital functions.