THE CAPACITY OF DOG LUNG TO RELEASE PROSTAGLANDIN I2 AS A BIOCHEMICAL PARAMETER FOR EVALUATING LUNG DAMAGE DURING PRESERVATION1

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Abstract

The release of prostaglandin I2 (PGI2) from the vasculature is thought to reflect damage to the vessels. Basal and bradykinin (BK)-stimulated release of PGI2 from isolated dog lungs after 6-hr preservation were investigated to evaluate lung damage after preservation. Maximal PGI2 release induced by BK decreased significantly after preservation at 24$dGC (room temperature), but not after hypothermic preservation at 4$dGC, although basal PGI2 release without BK stimulation did not change in either group of lungs after preservation. The function of allotransplanted lungs assessed by arterial oxygen tension was impaired by preservation at room temperature but not by hypothermic preservation. No differences were observed by light microscopy in either group in the pulmonary tissues, including the pulmonary artery, after preservation.

In summary, damage to the lung after preservation may be reflected by the maximal PGI2 release from the lung after BK infusion. Therefore the maximal PGI2 releasing capacity induced by BK may be a useful biochemical parameter for estimating the viability of preserved lungs.

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