240

Proc. roy. Soc. Med. Volume 68 April 1975

Dr D C Flenley, Dr A G Leitch, Dr L Clancy, Dr A Critchley, Dr A Ungar, Dr P K Wraith and Dr H M Brash (Departments of Medicine andPharmacology, University ofEdinburgh) The Hypoxic Drive to Breathing in Man, Studied During Exercise Our previous observation (Flenley et al. 1970), that a ventilatory drive from hypoxia may be absent in some patients suffering from severe hypoxic bronchitis has led us to seek a safe noninvasive method of studying variations in the intensity of this hypoxic drive in an apparently normal population. Potentiation of the drive by exercise, in both normal subjects and bronchitic patients (King et al. 1973) provides a useful tool for such a study. In 4 of 37 Scottish mine rescue workers we were unable to convincingly demonstrate such a hypoxic drive during walking at 3 miles per hour, using measurements of the transient ventilatory response to 2 or 3 breaths of nitrogen (Flenley et al. 1973). We believe that a transient increase in ventilation following this stimulus on exercise depends upon intact carotid chemoreceptors (Lugliani et al. 1971), but this response may also depend upon afferents from exercising muscle (Dejours 1959), or from oscillations in arterial gas tensions (Bhattacharyya etal. 1970). In recent studies using an on-line computer, we find that depression of ventilation on exercise is maximal immediately after switching from the breathing of 14% to 30% oxygen, as the end tidal P02 rises from 50 to over 150 mmHg, with a latter return of ventilation towards the higher levels which prevailed with the low oxygen mixture, despite maintenance of a higher oxygen tension with the 30% os. We suggest that this response could result from compensatory changes in cerebral blood flow following relief of hypoxia, which would tend to increase the central ventilatory stimulation acting via the acidity of the cisternal CSF. In a comparison of the ventilation during steady state walking when breathing 14% oxygen, with that on the same exercise breathing 30 % oxygen, we find a consistently higher ventilation in the hypoxic exercise. Furthermore, the differences in ventilation are greater for exercise with an oxygen uptake of 1.5 l/min than for 1.0 1/min, and these ventilatory differences are associated with changes in similar direction in levels of noradrenalin in the arterial blood. These results lead us to suggest that circulating catecholamines may play a role in potentiating the ventilatory response to hypoxia in exercise, particularly at higher work loads. Finally, in preliminary studies of the ventilatory response to static muscular exercise (Lind et al.

10 1964), it appears that this response is also potentiated by hypoxia. This observation may yet provide a method of determining what role, if any, is played by afferents from muscle in the mechanism of interactions between hypoxia and exercise in determining the level of ventilation. REFERENCES Bhattacharayya N K, Cunningham D J C, Goode R C, Howson M G & Lloyd B B (1970) Respiration Physiology 9, 329-347 Dejours P (1959) Journal ofPhysiology (Paris) 51, 163-261 Flenley D C, Franklin D H & Millar J S (1970) Clinical Science 38, 503-518 Flenley D C, Cooke N J, King A J, Leitch A G & Brash H M (1973) Bulletin de Physio-Pathologie Respiratoire 9,689-691 King A J, Cooke N G, Leitch A G & Flenley D C (1973) Clinical Science 44, 151-162 Lind A R, Taylor S H, Humphreys P W, Kenelly B M & Donald K W (1964) Clinical Science 27, 229-244 Lugliani R, Whipp B J, Seard C & Wasserman K (1971) New England Journal of Medicine 285, 1105 DISCUSSION

Dr Cunningham said that in the interpretation of a reduction in ventilation effected by administration of oxygen an allowance should be made for a secondary increase due to the rise in Pco,. He agreed that at low levels of exercise (Po,< 1.0 1/min) the effect of noradrenaline was unimportant. It might contribute at higher levels. Dr Weil cited evidence that the response to hypoxia in the cat was uninfluenced by beta adrenergic blockade, but was greatly attenuated by phenoxybenzamine; thus it might be due to stimulation of a receptors. Dr T J H Clark asked if there was evidence for patients who had no ventilatory response to hypoxia being particularly vulnerable to CO2 narcosis during oxygen

breathing.

Dr Flenley replied that they were not.

Dr K D Lee

(Department of Medicine, University of 'Birmingham, Queen Elizabeth Hospital, Birmingham, B15 2TH) Oxygen Tests and the Determination of Hypoxic Respiratory Drive in Patients With Chronic Lung Disease The size of the reflex hypoxic respiratory drive in patients who are hypoxemic because of chronic lung disease is of considerable practical importance and theoretical interest. In the present work oxygen tests, originally developed in an attempt to estimate the reflex hypoxic drive in normal subjects (Dejours 1962) were applied to such patients. Patients who were hypoxwmic because of chronic bronchitis breathed air which was

The hypoxic drive to breathing in man, studied during exercise.

240 Proc. roy. Soc. Med. Volume 68 April 1975 Dr D C Flenley, Dr A G Leitch, Dr L Clancy, Dr A Critchley, Dr A Ungar, Dr P K Wraith and Dr H M Brash...
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