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(REVERSE ORDER). Instructions for questions 1- ALCPT Form
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them to.Effect of prolonged adrenaline infusion on mitochondrial
function and metabolism. beta-Adrenergic blockade with
propranolol does not influence the development of the hypoxic
ventilatory response. This indicates that beta-adrenergic
stimulation is only indirectly involved in stimulating ventilation
during hypoxia. The hypothesis is that there is a direct betaadrenergic effect on ventilatory muscle metabolism. The authors
investigated this possibility by infusing epinephrine for 4-8 days
into the arterial circulation of dogs. Ventilatory response tohypoxia was recorded by plethysmography. Phosphorylcreatine
kinase activity and oxygen uptake by isolated mitochondria weremeasured to monitor energy metabolism of the dogs' ventilatory
muscles. Prolonged, steady-state, hypotensive doses ofpage 2 / 3

epinephrine do not increase oxygen uptake by isolated
mitochondria. Phosphorylcreatine kinase activity in the ventilatory
muscles, a measure of ATP availability, increases during hypoxia
for 2-3 days and then decreases when prolonged infusion iscontinued. In acute experiments hypoxia alone increases
phosphorylcreatine kinase activity. Propranolol does not influence
the initial increase in phosphorylcreatine kinase activity observedin response to hypoxia. Results indicate that prolonged infusion ofadrenaline is not associated with a direct metabolic effect onventilatory muscles. The ability of epinephrine to induce a positive
ventilatory response to hypoxia is probably due to an indirect, beta
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