Mechanism for brain injury of hemorrhagic infarction in rats and roles of adenosine triphosphate sensitive potassium channels

AIM: To determine whether adenosine triphosphate sensitive potassium(KATP) channels participates in the histological progress of hemorrhagic infarction(HI) and to explore the mechanism of brain injury following HI. METHODS: Ninety-six healthy male Sprague-Dawley rats were divided randomly into HI group, cerebral infarction(CI) group, Glibenclaimide(Gli)+HI(GH) group and sham operation group. Two-step method was used to develop the HI model in rats. Then changes in neurobehaviour, brain water content, brain adenosine triphosphatase(ATPase) activity, succinic dehydrogenase(SDH) activity and malondialdehyde(MDA) content were measured at 3,6,12 and 24 hours after operation. RESULTS: On neurobehavioral deficit and brain water content test, HI group presented no aggravation compared with CI group(P0.05). Brain ATPase activity of HI group was higher than that of CI group at 12 and 24 h(P0.05). Brain SDH activity of HI group was higher than that of CI group at 24 h(P0.05). And brain MDA content of HI group was lower than that of CI group at 12 h(P0.05). All the above-mentioned changes were cancelled by Gli. CONCLUSION: The HI model in rat established by two-step method is reproducible and stable. A medium volume of hemorrhagic transformation after CI does not aggravate the brain injury at early stage, in which KATP channels play an important role.