Abstract

Phenylephrine, norepinephrine, epinephrine or isoprenaline (5 μmoles/kg) was administered to anesthetized mice. All of these treatments, except isoprenaline, caused a loss of about 35 per cent of the ascorbic acid content of lung tissue and an increase of about 20 per cent in lung weight within 15 min. Increases in lung weight were interpreted as being due to the development of pulmonary edema. In some experiments, either phenoxybenzamine or propranolol was given prior to catecholamine administration. These experiments showed that both the loss of lung ascorbic acid and the development of pulmonary edema depended on α-receptor activity and was potentiated by β-receptor activity. The results suggest an association between the loss of lung ascorbate and the development of catecholamine-induced pulmonary edema in mice.

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