Abstract

The effects of ibuprofen (I) were studied in the Pseudomonas (P) porcine ARDS model. Pigs, 14–26 kg (5 in each group), were anesthetized and ventilated with 0.5 FiO 2 and 5 cm H 2O PEEP. A control (C) group received saline only, a second group was given P, 1 × 10 8 org/ml at 0.3 cc/20 kg/min, and a third group was given P followed by 12.5 mg 1 at 20 and 120 min. Pulmonary arterial (PAP), wedge (PWP) and systemic arterial pressures, cardiac output (CO), and thermal-cardiogreen extravascular lung water (EVLW), thromboxane (TxB 2), 6- keto-PGF 1α, P a O 2, P a CO 2 were determined every 30 min. Albumin flux was measured with scintigraphic determination of lung:heart radioactivity ratios versus time, called slope index (SI). At 3 hr, P produced marked ( P < 0.05) increases in PAP (18 ± 7 to 37 ± 2 mm Hg), TxB 2 (471 ± 513 to 9216 ± 3615 pg/ml), 6- keto-PGF 1α, EVLW (6.4 ± 1.4 to 14.6 ± 5.7 mg/kg), and SI (0.4 ± 0.2 to 1.7 ± 0.5 × 10 −3 U/min) with decreases in P a O 2 (214 ± 47 to 101 ± 41 torr), CO and SAP. Ibuprofen caused a rapid clearing of TxB 2 and 6- keto-PCF 1α, associated with a transient decrease in PAP; P a O 2 was considerably improved compared to P; however, CO, SAP, EVLW, and SI were unaffected. Prostaglandin blockage temporarily ameliorated the pulmonary hypertension and markedly improved oxygenation in this porcine septic ARDS model, but failed to alter increased permeability, confirming other studies that the increased pulmonary shunt in ARDS is not only dependent upon capillary leak.

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