Bronchial circulation and cyclooxygenase products in acute lung injury

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Abstract
The role of cyclooxygenase products in the response of the bronchial circulation to acute lung injury was examined in 30 dogs. By use of an open-chest preparation the left lower lobe (LLL) pulmonary circulation was isolated, continuously weighed, and perfused in situ. The anastomotic bronchial blood flow [.ovrhdot.Qbr(s-p)] was measured as the rate of increase in the volume of the LLL-perfusion circuit. Four groups of dogs were studied. In group A, six dogs received cyclooxygenase inhibition (COI) with either indomethacin (2 mg/kg) or ibuprofen (10 mg/kg). In group B (n = 10) lung injury was caused by airway instillation of glucose (15 mg) with glucose oxidase (500 .mu.g/kg) (G/GO) or LLL pulmonary arterial infusion of .alpha.-napthyl thiourea (ANTU, 2 mg/kg). Group C (n = 10) received COI, and 30 min later injury was induced as above with either ANTU or G/GO. Group D (n = 4) received COI immediately after anesthesia; then, 30 min after completion of the surgical preparation, injury was induced with ANTU or G/GO. After COI, .ovrhdot.Qbr(s-p) decreased to 35 .+-. 9% of the basal values (P < 0.05). After administration of ANTU or G/GO, .ovrhdot.Qbr(s-p) increased irrespective of whether COI was present. 6-Ketoprostaglandin F1.alpha. (6-keto-PGF1.alpha.) and thromboxane B2 (TxB2) were measured by radioimmunoassay in the LLL pulmonary artery and systemic venous blood, demonstrating an increase in 6-keto-PGF1.alpha. due to surgical preparation and confirming complete COI in those animals receiving COI immediately after anesthesia. These findings demonstrate that 1) the bronchial circulation is capable of a sevenfold increase in flow in response to acute lung injury; 2) surgical preparation increases .ovrhdot.Qbr(s-p), which is mediated by cyclooxygenase products; and 3) the rise in .ovrhdot.Qbr(s-p) after injury with ANTU or G/GO is due to mediators other than the cyclooxygenase products.