Blasingham M C, Selkurt E E
Circ Shock. 1985;15(3):175-84.
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.
在戊巴比妥麻醉的犬身上评估了出血性休克过程中肺对前列腺素E（PGE）的处理情况。测量了内源性PGE的净摄取率[（V - A）/V]和周转率[（V - A）×总血浆流量]。在动脉血压降至40 mmHg的出血后，内源性动脉血浆PGE水平从约400 pg/ml升至约700 pg/ml，净摄取率从42.5%降至 -30%，表明从肺主要清除内源性PGE转变为净释放。反映这一情况的是，周转率从对照平均水平480 ng/min降至 -60 ng/min。再灌注后两小时，净摄取率和周转率仍基本为零。这些发现支持以下假设：出血性休克时肺对PGE的净代谢变化导致全身动脉血中PGE水平升高，这可能在低血压失代偿期导致外周血管舒张，并在再灌注后期导致不可逆阶段。
