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This Article Full Text Full Text (PDF) All Versions of this Article: 563/3/883    most recent jphysiol.2004.080085v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bin-Jaliah, I Articles by Kumar, P Search for Related Content PubMed PubMed Citation Articles by Bin-Jaliah, I Articles by Kumar, P

¹ Department of Physiology, Division of Medical Sciences, The Medical School, University of Birmingham, Birmingham B15 2TT, UK

We have utilized an anaesthetized rat model of insulin-induced hypoglycaemia to test the hypothesis that peripheral chemoreceptor gain is augmented during hypermetabolism. Insulin infusion at 0.4 U kg ^–1min^–1 decreased blood glucose concentration significantly to 3.37 ± 0.12 mmol l^–1. Whole-body metabolism and basal ventilation were elevated without increase in P_a,CO2 (altered non-significantly from the control level, to 37.3 ± 2.6 mmHg). Chemoreceptor gain, measured either as spontaneous ventilatory airflow sensitivity to P_a,CO2 during rebreathing, or by phrenic minute activity responses to altered P_a,CO2 induced by varying the level of artificial ventilation, was doubled during the period of hypermetabolism. This stimulatory effect was primarily upon the mean inspiratory flow rate, or phrenic ramp component of breathing and was reduced by 75% following bilateral carotid sinus nerve section. In vitro recordings of single carotid body chemoafferents showed that reducing superfusate glucose concentration from 10 mM to 2 mM reduced CO₂ chemosensitivity significantly from 0.007 ± 0.002 Hz mmHg^–1 to 0.001 ± 0.002 Hz mmHg^–1. Taken together, these data suggest that the hyperpnoea observed during hypermetabolism might be mediated by an increase in the CO₂ sensitivity of the carotid body, and this effect is not due to the insulin-induced fall in blood glucose concentration.

(Received 25 November 2004; accepted after revision 18 January 2005; first published online 20 January 2005)
Corresponding author P. Kumar: Department of Physiology, Division of Medical Sciences, The Medical School, University of Birmingham, Birmingham B15 2TT, UK. Email: p.kumar{at}bham.ac.uk

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