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Hypoglycaemia‐induced hyperpnoea: a role for epinephrine and the carotid body?
Author(s) -
Thompson Emma L,
Ray Clare J,
Coney Andrew,
Kumar Prem
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1137.18
Subject(s) - epinephrine , hyperoxia , propranolol , medicine , endocrinology , anesthesia , concomitant , ventilation (architecture) , lung , engineering , mechanical engineering
Hypoglycaemia in vivo induces a carotid body‐dependent increase in ventilation suggested to reflect a direct action of reduced blood glucose on the CB, but an indirect effect via an action of counter‐regulatory hormones, including epinephrine, has not been discounted. Ventilation (VE) was recorded during insulin‐induced hypoglycaemia (2.9±0.08mM) and during normoglycaemic epinephrine infusion (1μg.kg‐1.min‐1), in Alfaxan‐anaesthetized, male Wistar rats. All procedures were carried out in accordance with current UK legislation. Epinephrine mimicked the increased VE (ca.15–20%) observed during hypoglycaemia, without significant change in PaCO2 in either condition. Hyperoxia reduced baseline VE and decreased the VE response to both stimuli. Propranolol reduced baseline VE, reduced the VE response to epinephrine and abolished the VE response to hypoglycaemia, with concomitant increase in PaCO2 in both conditions. Hyperoxia and propranolol in combination produced additive effects. Both hypoglycaemia and epinephrine increased the hypercapnic ventilatory response, which was blocked by propranolol. These data show that the increased VE observed in hypoglycaemia is, in large part, a hyperpnoea associated with a β‐mediated, but O2‐independent effect of epinephrine. We propose that hypoglycaemia acts to increase VE via an epinephrine‐mediated change in CO2 chemosensitivity in the carotid body.