ANGIOTENSIN-II-INDUCED PULMONARY-EDEMA IN A RABBIT MODEL

We conducted the present study to propose a rabbit model of puImonary edema (PE) induced by angiotensin II (AII) and to test the preventive effect of losartan on this form of PE. AII was administered to rabbits intravenously at 50, 100, 150 or 300 mu g/kg, either by continuous in fusion (10 min) or by bolus injection (30 sec). Continuously administe red AII (150 mu g/kg) induced PE in most cases, while a bolus injectio n of the same dosage did not. Additionally, the incidence of PE increa sed with higher dosages of AII when it was infused continuously. A new ly established parameter, the area under the systolic blood pressure-t ime curve corrected by baseline (cAUC), was prone to rise as the incid ence of PE increased. Moreover, cAUC significantly correlated with the wet-dry lung weight ratio (r=0.66, P <0.05). Subsequently, 0.5 or 3.0 mg/kg of losartan was given before continuous infusion of 150 mu g/kg of AII. The higher dosage of losartan prevented PE completely, while the lower one did so moderately. We concluded that intravenous adminis tration of AII induces PE, probably as a result of increasing afterloa d. Furthermore, an adequate dosage of losartan can prevent PE because it reduces the presser effect of AII.