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Received November 25, 2004
Revised December 22, 2004
Accepted after revision January 18, 2005
1 University of Birmingham, The Medical School
* To whom correspondence should be addressed. E-mail: p.kumar{at}bham.ac.uk.
We have utilized an anaesthetized rat model of insulin-induced hypoglycaemia to test the hypothesis that peripheral chemoreceptor gain is augmented during a hypermetabolism. Insulin infusion at 0.4 U kg-1 min-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 Pa,CO2 (altered non-significantly to 37.3 ± 2.6 mmHg from 40 mmHg). Chemoreceptor gain, measured either as spontaneous ventilatory airflow sensitivity to Pa,CO2 during rebreathing, or by phrenic minute activity responses to altered Pa,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] from 10mM to 2mM 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 an increase in the CO2 sensitivity of the carotid body occurs during periods of increased metabolism.
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