Dobutamine increases alveolar liquid clearance in ventilated rats by beta-2 receptor stimulation

Fred A. Tibayan, Asha N. Chesnutt, Hans G. Folkesson, Jon Eandi, Michael A. Matthay

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    Abstract

    Although it is well known that beta-adrenergic agonist stimulation increases alveolar epithelial sodium and fluid transport, it is not known whether the beta-1 or the beta-2 receptor mediates this effect. Two clinically relevant beta-adrenergic agonists, dopamine (beta-1 agonist) and dobutamine (beta-1 and beta-2 agonist) were used to define the contribution of these two beta-receptors to beta-adrenergic stimulated fluid clearance from the air spaces of the lungs. Alveolar fluid clearance was measured in anesthetized, ventilated rats over one hour after instilling an isosmolar 5% albumin solution in Ringer's lactate with 3 μCi 125I-albumin. The concentrations of the labeled and unlabeled albumin were used to quantify alveolar liquid clearance. Dopamine, whether given intra-alveolar (10-4 M) or intravenously (5-10 μg/kg/min), had no effect. However, both intra- alveolar (10-4 M) and intravenous (5 μg/kg/min) dobutamine increased alveolar liquid clearance by approximately 50% over one hour compared to controls. ICI 118,551, a potent and specific beta-2 antagonist, blocked the effect of dobutamine. The dobutamine effect was blocked by amiloride (10-3 M), an inhibitor of sodium uptake. In summary, the beta-2 receptor mediates beta-adrenergic stimulation of alveolar epithelial sodium and fluid transport.

    Original languageEnglish (US)
    Pages (from-to)438-444
    Number of pages7
    JournalAmerican journal of respiratory and critical care medicine
    Volume156
    Issue number2 I
    DOIs
    StatePublished - Jan 1 1997

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    ASJC Scopus subject areas

    • Pulmonary and Respiratory Medicine
    • Critical Care and Intensive Care Medicine

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