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Experimental Physiology 89.3 pp 287-292
DOI: 10.1113/expphysiol.2003.026682
© The Physiological Society 2004
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The effect of changes in arterial PCO2 on neuroendocrine function in man

R. M. Leach and M. L. Forsling

Department of Respiratory Medicine and Allergy, St Thomas' Hospital Centre for Neuroscience Research, Guy's, King's and St Thomas' School of Medicine, Guy's Campus, London SE1 1UL, UK

There is evidence that changes in arterial PCO2 (Pa,CO2), as well as PO2, influence neuroendocrine function. The hyponatraemia and fluid retention (cor pumonale) seen in chronic obstructive pulmonary disease (COPD) and type II respiratory failure is associated with increased vasopressin release. This study examines the specific effects of altered Pa,CO2 on hormone release from the posterior and anterior pituitary. The study was performed in 20 ventilated ICU patients in the late recovery phase of their illness. None had primary respiratory disease. Control blood samples were taken and the alveolar ventilation was then adjusted to allow the Pa,CO2 increase or decrease for a period of 3 h, during which time further blood samples were taken for the determination, by radioimmmunoassy of vasopressin, oxytocin, growth hormone and cortisol. Urine output and electrolyte concentrations were also measured. Circulating concentrations of growth hormone and oxytocin increased with increasing Pa,CO2. Vasopressin release showed a similar pattern up to a Pa,CO2 of approximately 6.0 kPa, above which vasopressin concentrations were inversely related to Pa,CO2. There was no significant effect on cortisol concentrations. No significant effects were established in urinary parameters during the short period of this study. Thus an increase in CO2 is associated with stimulated pituitary hormone release. The effect on the neurohypophysial hormones may account for the fluid retention and hyponatraemia seen in COPD and hence provide a rationale for treatment.

(Received 22 October 2003; accepted after revision 18 February 2004; first published online 17 February 2004)
Corresponding author M. L. Forsling: 2-38A Neuroendocrine Laboratories, New Hunt's House, GKT School of Medicine, Guy's Campus, London Bridge, London, SE1 1UL UK. Email: mary.forsling{at}kcl.ac.uk







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