Role of the lung in metabolism of prostaglandin E during severe hemorrhagic shock in the dog.

The pulmonary handling of prostaglandin E (PGE) during a hemorrhagic shock procedure was evaluated in pentobarbitalized dogs. Net extraction [(V - A)/V] and turnover [(V - A) X total plasma flow] of endogenous PGE were measured. Following hemorrhage to 40 mm Hg arterial pressure, the endogenous arterial plasma PGE level rose from ca 400 to ca 700 pg/ml, and net extraction fell from 42.5% to -30%, indicating a shift from preponderant removal of endogenous PGE by the lung to net release. Reflecting this, turnover decreased from a control average of 480 ng/min to -60 ng/min. At two hours post-reinfusion, net extraction and turnover were still essentially zero. These findings support the hypothesis that changes in net metabolism of PGE by the lung in hemorrhagic shock result in increased systemic arterial blood levels of PGE, which may contribute to peripheral vasodilation during the decompensatory phase of hypotension, and to the irreversible phase of the post-infusion period.