Enhanced prostacyclin synthesis in acute human kidney transplant rejection.
In acute and chronic kidney transplant rejection renal cortical and medullary tissue samples were examined for their prostacyclin (PGI2) generation by bioassay and compared with normal tissue. In acute rejection PGI2 formation was significantly enhanced, particularly in the cortex. In chronic rejection the PGI2 formation was comparable with control tissue. Since PGI2 is a very potent platelet aggregation inhibitor and vasodilator, it is concluded that the increase in PGI2 generation in acute rejection might be a self protecting mechanism which is, however, overwhelmed in irreversible rejection.
D015121:6-Ketoprostaglandin F1 alpha; D000208:Acute Disease; D002908:Chronic Disease; D011464:Epoprostenol / Q000096:biosynthesis*; D006084:Graft Rejection; D006801:Humans; D007672:Kidney Cortex / Q000378:metabolism*; D007679:Kidney Medulla / Q000378:metabolism*; D016030:Kidney Transplantation; D011453:Prostaglandins / Q000096:biosynthesis*; D011460:Prostaglandins F / Q000097:blood; D014184:Transplantation, Homologous
D011453:Prostaglandins; D011460:Prostaglandins F; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol