Isoproterenol (ISU) has been shown to strikingly reduce the pulmonary edema following acid lung injury (Circ. 68, III p234 1983). We investigated the effect of ISU in an autologous blood perfused isolated pig lung model exposed to E. coli endotoxin in doses known to cause pulmonary hypertension and increased vascular permeability. The animals were anesthetized, exsanguinated, and the lungs ventilated in-situ with 21% O2, 5% CO2 gas mixtures. A constant perfusion was maintained with a recirculating system. Pulmonary artery pressure (P(pa) was recorded throughout, and lung weight change (Ẇ) was measured continuously as the inverse of reservoir weight. Left atrial pressure P(la) was kept negative (O) but was transiently increased to +5 following a control period and after each intervention. A separate group of animals received endotoxin wihout ISU pretreatment. Data was analyzed using ANOVA. Pretreatment with ISU does not prevent, but reduces, the pulmonary hypertensive response to endotoxin. Cyclooxygenase mediators (TxB2, 6 keto PGF1(α)) increased and remained elevated after exposure to endotoxin in both groups. ISU significantly reduced Ẇ following return of P(pa) to baseline. Differences in Ẇ between the groups is most striking with P(1a) is increased to stress the pulmonary vasculature. We conclude that ISU treatment reduces lung fluid conductivity after endotoxin injury.
|Original language||English (US)|
|Pages (from-to)||No. 8728|
|State||Published - Jan 1 1985|
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