Defreyn G, Proesmans W, Machin S J, Lemmens F, Vermylen J
Clin Nephrol. 1982 Jul;18(1):43-9.
In a child with the hemolytic uremic syndrome, plasma 6 keto-prostaglandin F1 alpha levels remained undetectable throughout the acute phase of the disease. The patient's plasma failed to stimulate prostacyclin production by "exhausted" rat aorta rings. In vitro study of the patient's vessels indicated that they retained the capacity to synthesize prostacyclin from exogenous arachidonic acid but that their endogenous arachidonic acid stores were either depleted or non-available. The response to repeated infusion of exogenous prostacyclin was equivocal, suggesting that abnormal prostacyclin metabolism in the hemolytic uremic syndrome may not be the only factor in its pathogenesis.
在一名溶血尿毒综合征患儿中,在疾病的急性期,血浆6-酮-前列腺素F1α水平始终无法检测到。该患者的血浆未能刺激“耗尽”的大鼠主动脉环产生前列环素。对该患者血管的体外研究表明,它们保留了从外源性花生四烯酸合成前列环素的能力,但内源性花生四烯酸储备要么耗尽,要么无法利用。对外源性前列环素重复输注的反应不明确,这表明溶血尿毒综合征中异常的前列环素代谢可能不是其发病机制中的唯一因素。