Organ allograft rejection is charcterized by cellular infiltration, reduction in blood flow arid intravascular coagulation, resulting out graft organ failure. The absolute increase in thromboxane and relative decrease in prostacyclin synthesis in allo...
Organ allograft rejection is charcterized by cellular infiltration, reduction in blood flow arid intravascular coagulation, resulting out graft organ failure. The absolute increase in thromboxane and relative decrease in prostacyclin synthesis in allograft is suspected the basic phoneme- non in prostacyclin-thromboxane system in acute rejection (1-3).
Recently ti has been suggested that the reduction in renal blood flow in cyclosporin (CyA)-induced nephrotoxicity seems to be due to inhibited endothelial production of prostncyclin (PGI_2) by CyA.^4 Several animal experiments reported that prostaglandin bought prolongation of allograt survival(5, 6). The present study was undertaken to investigate the effects of exogenous prostaglandin E, (analogue of PGI_2) upon rat cardiac allografts under CyA therapy.