ISCHEMIA AND REPERFUSION-INDUCED INJURY IN RAT RETINA OBTAINED FROM NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS - EFFECTS OF FREE-RADICAL SCAVENGERS
Mt. Droylefaix et al., ISCHEMIA AND REPERFUSION-INDUCED INJURY IN RAT RETINA OBTAINED FROM NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS - EFFECTS OF FREE-RADICAL SCAVENGERS, International journal on tissue reactions, 15(2), 1993, pp. 85-91
The authors have studied the effects of free radical scavengers, super
oxide dismutase (SOD) and extract of Ginkgo biloba (EGb 761, flavone-r
ich extract) on ion shifts (Na, K and Ca) induced by ischaemia and rep
erfusion in rat retina obtained from normotensive and spontaneously hy
pertensive rats. Eyes were subjected to 90 min of ischaemia by occlusi
on of the retinal artery, followed by 4 and 24 hours of reperfusion, S
OD (15,000 U/kg, i.v.) or EGb 761 (50 mg/kg, per os) was administered
in a daily dose for 10 days. In the drug-free control groups, 90 min o
f ischaemia significantly increased tissue Na gains from their pre-isc
haemic control values of 63 +/- 7 muM/g dry weight (in retina obtained
from normotensive rats) and 76 muM/g dry weight (in retina obtained f
rom hypertensive rats) to 89 +/- 9 muM/g dry weight and 101 +/- 7 muM/
g dry weight, respectively. During reperfusion, a further elevation wa
s found in retinal Na in both the normotensive and hypertensive groups
, Probably, because of the ischaemia-induced inhibition of Na-K-ATPase
, retinal K loss was detected after ischaemia and reperfusion, respect
ively. An accumulation of retinal Ca was measured after ischaemia and
reperfusion in the normotensive and spontaneously hypertensive groups.
Both free radical scavengers significantly reduced the maldistributio
n of ions induced by ischaemia and reperfusion, but the effectiveness
of drugs was more evident in normotensive than hypertensive groups. Th
e present results indicate that the elimination of free radicals by fr
ee radical scavengers may reduce, probably via an indirect mode, the r
eperfusion-induced ionic imbalance and improve the ionic homeostasis i
n injured retinal cells obtained from normotensive and spontaneously h
ypertensive rats.