Deckmyn H, Proesmans W, Vermylen J
Thromb Res. 1983 Apr 1;30(1):13-8. doi: 10.1016/0049-3848(83)90392-4.
The capacity of leukocytes to produce prostacyclin (PGI2) from endogenous and from platelet-derived endoperoxides was tested in whole blood. During the acute phase of the hemolytic uremic syndrome (H.U.S.), the PGI2-production was lower than the controls, whereas the blood from children with chronic renal failure produced higher amounts. Production of PGI2 by blood from children 3/12 to 6 years after the acute phase of H.U.S. was normal, as was the case with blood from their parents. Furthermore, in two H.U.S.-patients studied serially, the decreased PGI2-production capacity normalized 2 1/2 months after the acute phase.
在全血中检测白细胞从内源性和血小板衍生的内过氧化物产生前列环素(PGI2)的能力。在溶血性尿毒症综合征(H.U.S.)的急性期,PGI2生成低于对照组,而慢性肾功能衰竭儿童的血液产生量更高。H.U.S.急性期后3/12至6岁儿童的血液中PGI2生成正常,其父母的血液也是如此。此外,对两名H.U.S.患者进行连续研究,急性期后2个半月,PGI2生成能力下降恢复正常。