The Preliminary Studies On The Apoptosic Mechanism Of Global Cerebral Ischemia Reperfusion Injury And The Effects Of Hyperbaric Oxygenation In Rats

BACKGROUND AND PURPOSEI Neuronal death after global cerebral ischemia reperfusion injury (CIRI) has long been considered to represent necrosis, but it now appears that many brain neurons undergo apoptosis. The mechanism of apoptosis remains unclear. Hyperbaric oxygenation (HBO) has been considered for many years for the treatment of CIRI. However, its efficacy has not been proven. The aim of this study was to approve the existence of apoptosis and the effect of 1-130 after CIRI. IMETUODSI 72 SD rats were randomly divided into 4 groups: sham operation group, atmospheric pressure group, hyperbaric air group and HBO group. CIRI was induced by four-vessel occlusion (4-V0). Reperfusion followed 1 5mm ischemia Followed 2h reperfusion, HBO group was exposured to 2.5ATA (O.25mpa) pure oxygen for 7Orninld and Hyperbaric air group was managed by 2.5ATA (O.25mpa), 21% 2 concentration for 7Omin/d. All rats were killed after 72h reperfitsion. Their brains were examined by Flow Cytometry (FCM) (P1 staining), terminal deoxynuclLeotidyl-transferase-mediated dUTP nick end-labeling (TUNEL), DNA Electrophoresis and electron microscope (EM). [RESULTS]: In atmospheric pressure group and hyperbaric air group, The counted numbers of TUNEL stained cells in hippocampal CA 1(103 5 and 96 12 ) were markedly more than those in sham operation group and HBO group(5 , 17,P<0.O1) . FCM showed obvious Sub-G1 peak. Apoptosic percents were 1.06 0.48% and 0.78 0.50% in atmospheric pressure group and hyperbaric air group. These data re obviously higher than those in sham operation group and H130 group(0.52 0.17, 0.57 0.37,P<0.0 1) . DNA Electrophoresis exhibited a DNA laddering pattern in approximately 200-bp multiples. EM demonstrated high condensation and clumping of cbromatin in shrunken neurons. [CONCLUSIONS] Features of apoptosis are present in the described model of CIRJ. Apoptosis mechanism may play an important role in :he hippocampus CAl after cerebral ischemia reperfusion. It may provMe novel therapeutic approaches for prevention of CIRI. HBO reduce apoptosis in the hippocampus CAl. The preventive mechanism of H130 against CIRI is likely correlated with apoptosis. This experimental system is useful to investigate the preventive mechanism of HBO against apoptosis in the SD rats, and to determine the clinical indications and the most effective protocol for RHO for cerebral resuscitation in the burran brain.