The Effects of Prostaglandin E1 and N-Acetyl-L-Cysteine for Ischemic Renal Reperfusion Injury in the Rat.
- Author:
Min Young CHO
1
;
Suk In JUNG
;
Won Yong CHO
;
Hyung Kyu KIM
;
Nam Hee WON
;
Sang Yong CHOI
;
Cheung Wung WHANG
Author Information
1. Department of Surgery, College of Medicine, Korea University, Korea.
- Publication Type:Original Article
- Keywords:
Reperfusion;
Prostaglandin E1;
N-acetyl-L-cystein;
Acute renal failure
- MeSH:
Acetylcysteine*;
Acute Kidney Injury;
Adenosine Triphosphate;
Alprostadil*;
Animals;
Blotting, Western;
Constriction;
Creatinine;
Humans;
Kidney;
Male;
Microscopy;
Oxygen;
Rats*;
Regeneration;
Reperfusion Injury*;
Reperfusion*;
Veins
- From:The Journal of the Korean Society for Transplantation
1999;13(2):229-242
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Some studies has showed that even though reperfusion is essential for the recovery of renal function, it, itself, might be caused of renal injury through liberation of oxygen free radical due to surplus oxygen following reperfusion. If it is so, it can be presumed that oxygen free radical scavenger during reperfusion might be useful drugs to protect renal injury during reperfusion. On the base of this hypothesis, we selected prostaglandin E1 (PGE1) which is vasodilator and cellular protector which act through decreased demand of ATP and N-acetyl-L-cystein (NAC) which is oxygen radical scavenger for the purpose to see oxygen free radical scavenger related drugs will work on protection from renal injury during reperfusion. MATERIALS AND METHODS: To define the efficacy of these drugs, It was evaluated by a serial check of the serum creatinine level, and pathologic change on the light microscopy. And also to investigate the role of HSP 70 and HSP 72 on reperfusion injury, immunohistochemical study and Western blot analysis were performed on the experiment rats. The experimental ischemic renal model was made by clamping hilum of both kidney for 60 minutes on Wistar male rats. After declamping, PGE1, NAC and saline through a tail vein: PGE1 35 microgram/kg/hr, NAC 6 mM/kg/hr and 0.9% saline 1 ml/kg/hr were infused for 60 minutes and then blood samples were obtained from IVC at 1st hour, 2nd hour, 1st day hour, 2nd day and 5th day after reprefusion for creatinine. RESULTS: The serum creatinine was normalized in group receiving PGE1 at 5th day after reperfusion. But creatinine was not normalized in group receiving saline and NAC at 5th day after reperfusion: serum creatinine at 5th day after reperfusion were 0.58 0.08 mg/dl in group receiving PGE1, 2.85 0.65 mg/dl in group receiving saline and 2.96 0.51 mg/dl in group receiving NAC. There was expression of HSP 72 in group receiving PGE1 at 5th day after reperfusion. But not in group receiving NAC and saline at 5th day after reperfusion. It was noted to have prominent expression of HSP 70 in renal cortex in group receiving PGE1 at 2nd and 5th day. On contrary, there were prominent expression of HSP 70 in renal cortex in group receiving NAC at 1st and 2nd hour. CONCLUSION: It is clear that PGE1 has a protective effect for ischemic renal reperfusion injury by showing early regeneration of renal tubule, persistent expression of HSP 72 and HSP 70 and normalization of serum creatinine at 5th day after reperfusion.
