Oxygen metabolites formed during reperfusion of ischemic kidneys prevent re
covery of renal function after short periods of renal ischemia. The adminis
tration of ATP-MgCl2 is beneficial to the survival of animals after hemorrh
agic shock, severe burns, septicemia-peritonitis, post-ischemic hepatic fai
lure, bowel ischemia, and endotoxic shock. In this study, the effect of ATP
-MgCl2 on lipid peroxidation and its curative effect were evaluated by meas
uring the decomposition products of lipid peroxidation, detected as thiobar
bituric-acid reactive substances in homogenized kidney tissues in ischemic
and reperfused rabbit kidneys. Ischemia was performed by clamping the right
renal artery for 60 minutes followed by 30 minutes of reperfusion. Thirty-
six rabbits were classified into 6 groups containing 6 rabbits in each. In
the first group, no renal ischemia-reperfusion (I-R) was designed (Sham gro
up), the right kidney was removed 90 minutes later. In the second group, I-
R was established but nothing given. Saline 0.25 cc/kg was given into the r
ight renal artery in group 3 two minutes before ischemia, and in group 4 tw
o minutes before reperfusion. ATP-MgCl2 17.5 mu mol/kg (0.25 cc/kg) was giv
en two minutes before ischemia in group 5, and before reperfusion in group
6. The right kidneys of the rabbits were removed and thiobarbituric-acid re
active substances in the homogenates were measured. In addition, histopatho
logical evaluation was performed. High lipid peroxidation products were rec
orded in groups 2-5, whereas in group 6, these levels were low similar to t
hose obtained in Sham group (76.72 +/- 1.01 nmol/g tissue). On histopatholo
gical evaluation, a considerable cell damage resulting from I-R trauma espe
cially in proximal; tubules was observed. In groups which were under saline
effect, no histopathological damage was found. Histophatological preservat
ion was better in group 6 rather than in group 5. The results of this study
indicate that ATP-MgCl2 is remarkably effective for preventing the lipid p
eroxidation if given before reperfusion but not before ischemia in experime
ntal I-R injury in rabbit kidneys.