Thromboxane synthesis inhibition and renal allograft function.
These data indicate that chronic administration of CGS-12970 to renal allograft recipients maintains renal allograft function. These effects are probably due to selective inhibition of local tissue TXA2 production. These data also suggest that elevations in renal allograft tissue prostacyclin production may be secondary to ischemia since improving renal blood flow and GFR with selective thromboxane synthesis inhibitors leads to normalization of renal prostacyclin synthesis. The possible utility of using CGS-12970 as an adjunct therapy in human renal allotransplantation should be strongly considered.
Anderson
C
C
Department of Surgery, University School of Medicine, St. Louis, Missouri.
Jendrisak
M
M
Brunt
E
E
Tobimatsu
M
M
Murphy
M
M
Sicard
G
G
Mangino
M
M
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000818:Animals; D004285:Dogs; D005919:Glomerular Filtration Rate / Q000187:drug effects; D066298:In Vitro Techniques; D007668:Kidney / Q000187:drug effects / Q000502:physiology; D016030:Kidney Transplantation; D011725:Pyridines / Q000494:pharmacology*; D012079:Renal Circulation; D013929:Thromboxane B2 / Q000096:biosynthesis*; D013930:Thromboxane-A Synthase / Q000037:antagonists & inhibitors; D014182:Transplantation, Autologous; D014184:Transplantation, Homologous
D011725:Pyridines; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; C049113:3-methyl-2-(3-pyridyl)-1-indoleoctanoic acid; D013930:Thromboxane-A Synthase