The aim of this study was to investigate the extent to which
ischemia and reperfusion lead to oxidative damage of the
retinal tissue and investigate how ischemic and reperfused
retinal tissues react to the application of
perfluorooctylbromide (
PFOB) and, if this reaction can be influenced by
protective drugs such as
vitamin E (Vit.E). The experiments were performed with 60 male Wistar rats, divided into 12 groups using an established model of reversible
ischemia and reperfusion of the globe. Grouping of animals was carried out according to different
ischemia and reperfusion periods and different therapeutic regimens (
PFOB, Vit.E). Treatment with
PFOB and/or Vit.E was performed after 60 min of
ischemia with 60 min of reperfusion. At the end of the experiments
thiobarbituric acid reactive substances (
TBARS) were determined in the
retinal tissues and served as parameters of oxidative tissue damage.
Ischemia of up to 60 min led to a significant increase in
TBARS values. Ninety and 120 min of
ischemia led to no further significant elevation compared to the 60 min or 90 min group. Following 60 min of
ischemia, a reperfusion period of 15 min led to an increase in
TBARS values that was significant (P<0.05) after 30 and 60 min. Addition of
PFOB resulted in a further significant (P<0.05) increase in
TBARS values as compared to the respective group without treatment. Vit. E alone did not change the values significantly compared to the respective group without treatment. However, the application of Vit.E in addition to
PFOB led to a significant reduction in
TBARS values.
Ischemia resulted in severe oxidative
retinal tissue damage, which increased during reperfusion. The
reperfusion damage might be due to the known depletion of protecting substances such as
vitamin E. Enhancement of
oxygen supply by
PFOB during reperfusion without any tissue protection leads to more severe damage. Thus, additional protection of the tissue by powerful
antioxidants is necessary when providing
oxygen for better tissue recovery.