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Abstract
What is the central question of this study? Hyperoxia blunts hypoglycaemia counterregulation
in healthy adults. We hypothesized that this effect is mediated by the carotid bodies
and that: (i) hyperoxia would have no effect on hypoglycaemia counterregulation in
carotid body-resected patients; and (ii) carotid body-resected patients would exhibit
an impaired counterregulatory response to hypoglycaemia. What is the main finding
and its importance? Our data indicate that the effect of hyperoxia on hypoglycaemic
counterregulation is mediated by the carotid bodies. However, a relatively normal
counterregulatory response to hypoglycaemia in carotid body-resected patients highlights:
(i) the potential for long-term adaptations after carotid body resection; and (ii)
the importance of redundant mechanisms in mediating hypoglycaemia counterregulation.
Hyperoxia reduces hypoglycaemia counterregulation in healthy adults. We hypothesized
that this effect is mediated by the carotid bodies and that: (i) hyperoxia would have
no effect on hypoglycaemia counterregulation in patients with bilateral carotid body
resection; and (ii) carotid body-resected patients would exhibit an impaired counterregulatory
response to hypoglycaemia. Five patients (three male and two female) with bilateral
carotid body resection for glomus tumours underwent two 180 min hyperinsulinaemic,
hypoglycaemic (∼ 3.3 mmol l(-1)) clamps separated by a minimum of 1 week and randomized
to either normoxia (21% fractional inspired O2 ) or hyperoxia (100% fractional inspired
O2). Ten healthy adults (seven male and three female) served as control subjects.
Hypoglycaemia counterregulation in carotid body-resected patients was not significantly
altered by hyperoxia (area under the curve expressed as a percentage of the normoxic
response: glucose infusion rate, 111 ± 10%; cortisol, 94 ± 6%; glucagon, 107 ± 7%;
growth hormone, 92 ± 10%; adrenaline, 89 ± 26%; noradrenaline, 79 ± 15%; main effect
of condition, P > 0.05). This is in contrast to previously published results from
healthy adults. However, the counterregulatory responses to hypoglycaemia during normoxia
were not impaired in carotid body-resected patients when compared with control subjects
(main effect of group, P > 0.05). Our data provide further corroborative evidence
that the effect of hyperoxia on hypoglycaemic counterregulation is mediated by the
carotid bodies. However, relatively normal counterregulatory responses to hypoglycaemia
in carotid body-resected patients highlight the importance of redundant mechanisms
in mediating hypoglycaemia counterregulation.