Flynn J T
Prostaglandins. 1979 Jan;17(1):39-52. doi: 10.1016/0090-6980(79)90073-x.
Studies were undertaken to determine the effect of arachidonic acid, the precursor of bisenoic prostanoic acid derivatives, on the response of the isolated, perfused rabbit liver to hypoxia. Two and one half hours of severe hypoxia resulted in significant increases in hepatic vascular perfusion pressure, tissue wet weight, and the rates of cellular loss of lactic dehydrogenase, malic dehydrogenase, and acid phosphatase into the perfusing medium. Hypoxia also increased the rate of hepatic PGF2 alpha production by 25% after 2 1/2 hours (p less than 0.05, hypoxia vs sham). The addition of arachidonic acid (0.1 microgram/g/min for 150 minutes) to the perfusion medium of hypoxic livers significantly attenuated the changes in perfusion pressure, tissue wet weight, and loss of cellular enzymes. Arachidonic acid administration increased the rate of PGF2 alpha production by 100% (p less than 0.05, sham vs hypoxia + arachidonic acid) within 30 min after hypoxia and maintained this rate for the duration of the study. These results demonstrate that hypoxia mediated prostaglandin F2 alpha synthesis in the rabbit liver can occur in the absence of neural and blood borne components and that significant activation of the arachidonic acid cascade via the administration of exogenous arachidonic acid has a salutary effect on hepatic hemodynamics and cellular integrity during hypoxia.
开展了多项研究以确定花生四烯酸（双烯前列腺酸衍生物的前体）对离体灌注兔肝缺氧反应的影响。两小时半的严重缺氧导致肝血管灌注压、组织湿重以及乳酸脱氢酶、苹果酸脱氢酶和酸性磷酸酶向灌注液中的细胞丢失率显著增加。缺氧还使肝PGF2α的生成率在两小时半后增加了25%（p<0.05，缺氧组与假手术组相比）。向缺氧肝脏的灌注液中添加花生四烯酸（0.1微克/克/分钟，持续150分钟）可显著减轻灌注压、组织湿重和细胞酶丢失的变化。给予花生四烯酸使缺氧后30分钟内PGF2α的生成率增加了100%（p<0.05，假手术组与缺氧+花生四烯酸组相比），并在研究期间维持该生成率。这些结果表明，兔肝中缺氧介导的前列腺素F2α合成可在无神经和血源性成分的情况下发生，并且通过给予外源性花生四烯酸显著激活花生四烯酸级联反应对缺氧期间的肝脏血流动力学和细胞完整性具有有益作用。
