Catecholamines reduce pulmonary blood volume via alpha-receptor-mediated constriction of capacitance vessels, an effect dissociated from changes in pulmonary vascular resistance.
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Does not support clinical changes in pulmonary hemodynamics; leaves open human translation of alpha-mediated capacitance effects.
The effect of arterially injected adrenaline and noradrenaline on lung blood volume has been examined in isolated, blood‐perfused lung preparations from rabbit and cat. Both substances caused rapid and relatively marked reductions in the weight of the preparations, which was followed continuously. This weight reduction is interpreted as being due to constriction of capacitance vessels. This effect on the capacitance vessels was mediated via α‐receptors, as addition of the α‐inhibitor phentolamine abolished the response. Addition of the β‐inhibitor propranolol did not interfere with the effect of the catecholamines on the capacitance vessels. Noradrenaline usually gave an increase, adrenaline usually a decrease in pulmonary vascular resistance in this preparation. The effect of the catecholamines on capacitance vessels was dissociated from the effects of these drugs on the vascular resistance in the organ.
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Hauge et al. (1967) studied this question.
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