Changes in peripheral chemoreflex sensitivity during sustained, isocapnic hypoxia.

One hypothesis concerning the origin of hypoxic ventilatory decline is that hypoxia acts centrally to depress peripheral chemoreflex loop activity. To investigate possible changes in peripheral chemoreflex loop activity during sustained, isocapnic hypoxia, the ventilatory responses to four one minute pulses of either extra hypoxia (45 Torr) or carbon dioxide (8 Torr above resting levels) were measured in man at minutes 2, 7, 12, and 17 of a 23 min isocapnic, hypoxic period (50 Torr). For hypoxia, the first pulse response (130%) was significantly greater (P less than 0.05) than the fourth response (74%). For CO2, pulse responses 2 and 3 (101 and 103%, respectively) were significantly greater (P less than 0.05) than the fourth response (91%). A central depression of peripheral chemoreflex loop activity should affect peripheral sensitivities to CO2 and hypoxia equally. Our results suggest that the peripheral sensitivity to hypoxia declined more than that to CO2, implying a peripheral chemoreceptor origin for hypoxic ventilatory decline.

[1]  N. Anthonisen,et al.  Recovery of the ventilatory response to hypoxia in normal adults. , 1988, Journal of applied physiology.

[2]  N H Edelman,et al.  Ventilatory responses to transient hypoxia and hypercapnia in man. , 1973, Respiration physiology.

[3]  J. Severinghaus,et al.  Proposed standard determination of ventilatory responses to hypoxia and hypercapnia in man. , 1976, Chest.

[4]  M. Hanson,et al.  Breathing pattern of kittens during hypoxia. , 1984, Journal of applied physiology: respiratory, environmental and exercise physiology.

[5]  J. V. van Beek,et al.  Effects of brain stem hypoxaemia on the regulation of breathing. , 1984, Respiration physiology.

[6]  G D Swanson,et al.  Central and peripheral chemoreflex loop gain in normal and carotid body-resected subjects. , 1979, Journal of applied physiology: respiratory, environmental and exercise physiology.

[7]  N. Anthonisen,et al.  Depression of hypoxic ventilatory response in humans by somatostatin. , 1988, Journal of applied physiology.

[8]  P. Robbins,et al.  The Transients in Ventilation Arising from a Period of Hypoxia at Near Normal and Raised Levels of End-Tidal CO2 in Man , 1989 .

[9]  G D Swanson,et al.  A prediction-correction scheme for forcing alveolar gases along certain time courses. , 1982, Journal of applied physiology: respiratory, environmental and exercise physiology.

[10]  J. Weil,et al.  Biphasic ventilatory response of adult cats to sustained hypoxia has central origin. , 1987, Journal of applied physiology.

[11]  R G DeLaney,et al.  Stimulus interaction in the responses of carotid body chemoreceptor single afferent fibers. , 1975, Respiration physiology.

[12]  P. Robbins,et al.  Hypoxic depression of ventilation in humans: alternative models for the chemoreflexes. , 1990, Respiration physiology.

[13]  Statistical Methods in Biology. , 1983 .

[14]  M. Jukes,et al.  The relation between alveolar oxygen pressure and the respiratory response to carbon dioxide in man. , 1958, Quarterly journal of experimental physiology and cognate medical sciences.

[15]  R A Gabel,et al.  Depression of ventilation hypoxia in man. , 1975, Journal of applied physiology.

[16]  N. Anthonisen,et al.  Increased chemoreceptor output and ventilatory response to sustained hypoxia. , 1989, Journal of applied physiology.

[17]  P A Easton,et al.  Ventilatory response to sustained hypoxia in normal adults. , 1986, Journal of applied physiology.