Why the study?
Does intravenous adrenaline or noradrenaline stimulate respiration and alter CO2 elimination in humans?
Does intravenous adrenaline or noradrenaline stimulate respiration and alter CO2 elimination in humans?
Intravenous adrenaline and noradrenaline stimulate respiration in humans, likely driven by increased metabolic CO2 production and oxygen consumption.
Answers are grounded in this paper and cite their sources.
Adrenaline may increase ventilation via metabolic drive; leaves open relevance to catecholamine dosing in shock or respiratory failure.
Adrenaline infused intravenously at a rate of 0.15 μ g/kg/min increased the ventilation and CO 2 ‐elimination by a maximum of 45% in experiment on man. Since adrenaline increased the CO 2 tension and decreased the pH in the plasma of arterial blood, the respiratory increase after adrenaline was assumed to depend, at least in part, on an increased CO 2 ‐production of metabolic origin. About half of the increase in CO 2 ‐production was estimated to be due to raised oxygen consumption and the remaining half to have come from the plasma and tissue bicarbonate. The reduction of tissue bicarbonate was to a large part caused by an increased lactic acid and FFA concentration. The stimulating effect on respiratin of noradrenaline was initially associated with a decrease in plasma pCO 2 and an increased plasma pH. The initial increase in CO 2 ‐elimination which took place was assumed ro result from washing out of CO 2 The possibility that noradrenaline had stimulated O 2 ‐sensitive chemoreceptors is discussed. In a later stage noradrenaline probably stimulated the respiration through an increased oxygen consumption and CO 2 ‐production.
No takes yet. Share an insight, caveat, or question.
Lundholm et al. (1966) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: