الفهرس | Only 14 pages are availabe for public view |
Abstract The renal ischaemia-reperfusion injury (IRI) in clinical practice occurs as a consequence of both systemic hypo perfusion with subsequent circulatory resuscitation and local renal hypo perfusion following aortic cross -clamping or renal transplantation. The renal IRI is an important cause of early graft dysfunction after renal transplantation and may adversely affect the long- term survival of the allograft. The L-arginine is the precursor of nitric oxide, which is formed by the action of a group of enzymes known as nitric oxide synthases (NOSs) acting on L-arginine. Also prostaglandin E1 is a potent vasodilator prostaglandin, which prevents neutrophil adhesion and platelet aggregation. The present work aimed to investigate the effects of L-arginine and prostaglandin E1 in renal ischaemia-reperfusion injury in rats. This was achieved through 80 male Sprague Dwaley rats. In this study it was observed that L-arginine caused a significant improvement in creatinine clearance by 175% on the 2nd day and by 110% on the 7th day; while prostaglandin E1 caused a significant improvement in creatinine clearance by 90% on the 2nd day and 7th days. Also it was observed that both L-arginine and PGE1 caused a significant improvement in creatinine clearance by 170% on the 2nd day and by 100% on the 7th day.and L-NAME worsened the kidney functions by 33% on the 2nd day and by 60% on the 7th day.and finally indomethacin caused improvement in creatinine clearance by 44% on the 2nd day and by 10% on the 7th day. The results of this study are analyzed and the following conclusions can be drawn: 1) Ischaemia-reperfusion-induced by clamping the rat renal artery causes renal impairment and histological damage.2) Pretreatment with L-arginine (NO precursor) has a protective effect on renal ischaemia by increasing NO production.3) Pretreatment with L-NAME (NOS inhibitor) further depressed the renal functions. 4) There is an endogenous NO, which has some protective effect in renal IRI.5) The exogenous PGE1 (vasodilator prostaglandin) is protective in renal IRI.6) The indomethacin may be protective in renal IRI probably by inhibiting the vasoconstrictor prostaglandins, which are increased during IRI.7) Adding of PGE1 to L-arginine gives no more improvement in the renal impairment during renal IRI than giving L-arginine alone. |