in the pulmonary vascular bed.2 In fact, PGFa was more than 10 times as active as serotonin in increasing resistance to flow in the canine pulmonary vascular bed.2 In subsequent studies, it was shown that prosta- glandin synthesis and release by the lung were enhanced by a number of pathophysiologic conditions including anaphylaxis, pulmonary embolization and pulmonary edema.2 In addition to the findings that the lung had a marked capacity to synthesize prostaglandins and that these substances had marked vasomotor activity in this organ, it has been documented that the lung is the major organ for metabolism of prostaglandins in the body.2 Therefore, alterations in synthesis and metabo- lism of prostaglandins in the lung would affect function, not only in the airways and pulmonary vascular bed,
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