Akademik Veri Yönetim Sistemi
Biochemical Society Transactions, cilt.24, sa.4, 1996 (SCI-Expanded)
The resumption of blood flow to organs following ischemia may cause further increase in tissue damage through an increase in peroxidation of lipids in cell membranes. This experimental study was conducted to investigate the reperfusion injury after brain ischemia induced in rats, through changes in the lipid peroxide content and the Na+/K+ ATPase activity of the cortex and medulla portion of the brain and to observe the probable effects of pentoxifylline on the reperfusion injury. Adult male wistar rats were divided into 7 groups, each containing 7 rats. 1 group underwent sham operation as a control. The other groups were subjected to bilateral brain ischemia lasting 30 minutes. 3 groups were subjected to 0,60,120 minutes of reperfusion thereafter; 3 groups were treated with pentoxifylline before inducing ischemia and were subjected to 0, 60, 120 minutes of reperfusion thereafter. Thiobarbituric acid reactive products of lipid peroxidation (TBARS) and Na+/K+ ATPase were assessed in cortex and medulla. Brain ischemia reperfusion caused significant increase in brain TBARS level (p<0.01). Na+/K+ ATPase activity decreased significantly in both the cortex and medulla portions of the brain (p<0.01). Pretreatment with pentoxifylline did not effect the biochemical reperfusion in the brain, neither in medulla, nor the cortex, assessed through the increase in TBARS levels. Both the non-medicated and the pentoxifylline treated group showed significantly highest TBARS levels in the 120-minute reperfusion period. However, pretreatment with pentoxifylline had the effect of augmenting the Na+/K+ ATPase activity in both the cortex and medulla portions ot the brain (p<0.01), starting with 60 minutes of reperfusion. We conclude that intra-abdominal administered pentoxifylline was not effective in reducing TBARS levels but pentoxifylline plays an important role in the reversal of the ischemiareperfusion injury induced in a rat-model through the mechanism of acting on the Na+/K+ ATPase activity in the brain.