Short-latency ventilatory responses to sudden withdrawal of hypoxia at normal and raised body temperature in man

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Abstract
Approximately isopneic conditions (.ovrhdot.VE = 40 1/min) were achieved by the inhalation of asphyxial gas mixtures (PAO2 [arterial O2 partial pressure] 60 torr, PACO2 [arterial CO2 arterial pressure] 40-45 torr) in normothermia and after a rise in rectal temperature of 1.6.degree. C had been induced by a heated flying suit. Arterial chemoreceptor drive was transiently reduced by either isocapnic removal of hypoxia (type (1) tests: 2 breaths of CO2 in O2) or simultaneous withdrawal of both hypercapnia and hypoxia (type (2) tests: 2 breaths of O2). Tests [8-13] of each type were performed at both temperature conditions in 6 experiments on 4 healthy human subjects. Expired volume, total breath duration and inspiratory time were recorded and minute ventilation and expiratory time subsequently computed breath by breath. In hyperthermia the steady-state ventilation of 40 1/min (at a relatively higher respiratory frequency and a correspondingly lower tidal volume) was achieved at a PACO2 which was 5 torr lower than in normothermia. Ventilation decreased significantly in all tests. Tested with a 3 way analysis of variance significant differences between the ventilatory responses at the 2 temperature conditions and between the 2 test types were found. The rate of change of ventilation was greater in hyperthermia than in normothermia and also greater in type (2) tests than in type (1) tests. Since isopneic conditions existed prior to the tests, it implies that the arterial chemoreceptor contribution to the total ventilatory drive is increased in hyperthermia. In type (2) tests a significant lengthening of expiratory time was observed in the 1st test breath. The effect in man of changes in airway PCO2 in lung stretch receptor discharge was confirmed.