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Carbon dioxide sensitivity during hypoglycaemia‐induced, elevated metabolism in the anaesthetized rat
Author(s) -
BinJaliah I.,
Maskell P. D.,
Kumar P.
Publication year - 2005
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2004.080085
Subject(s) - hypermetabolism , medicine , endocrinology , respiration , ventilation (architecture) , carotid body , control of respiration , peripheral chemoreceptors , chemoreceptor , anesthesia , chemistry , insulin , carbohydrate metabolism , respiratory system , electrophysiology , anatomy , mechanical engineering , receptor , engineering
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 −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 P a,CO 2(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,CO 2during rebreathing, or by phrenic minute activity responses to altered P a,CO 2induced 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 m m to 2 m m reduced CO 2 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 CO 2 sensitivity of the carotid body, and this effect is not due to the insulin‐induced fall in blood glucose concentration.