THE ROLE OF THE BLOOD OXYGEN IN PROTECTIVE MECHANISM OF ISCHEMIC PRECONDITIONING DURING HEPATIC ISCHEMIA-REPERFUSION
The role of blood oxygen in the protective mechanism of ischemic preconditioning (IPC) was investigated in rabbits during hepatic ischemia-reperfusion (HIR). Animals were divided into 2 experimental groups: in the 1<sup>st</sup> group (n = 11) hepatic ischemia (30 min) was induced by Pringle maneuver, reperfusion was lasted 120 min; in the 2nd group (n = 8) the short period of vascular clamping (10 min) and reperfusion (10 min) were performed before HIR. The parameters of blood oxygen (рО<sub>2</sub>, p50, Hb), acid-base balance (рН, рСО<sub>2</sub>, TCO<sub>2</sub>, ABE, SBE, SBC and etc.), lipid peroxidation (Schiff bases, conjugated dienes), antioxidant system (catalase, α-tocopherol), plasma transaminases (ALT, AST) and nitrite/nitrate concentration (NO<sub>x</sub>) were measured. HIR in the 1<sup>st</sup> group leads to elevation of p50, lipid peroxidation, ALT and AST accompanied by reduction of рН, TCO<sub>2</sub>, ABE, SBE, SBC, catalase activity, α-tocopherol and NO<sub>x</sub> levels. IPC significantly reduces p50, lipid peroxidation, ALT and AST simultaneously improves рН, TCO<sub>2</sub>, ABE, SBC, catalase activity, α-tocopherol and NO<sub>x</sub> levels. These findings indicate that IPC prevents oxidative stress in liver trough increased blood hemoglobin-oxygen affinity and limitation of oxygen participation in free radical processes during reperfusion.