title: Brain damage related to hemorrhagic transformation following cerebral ischemia and the role of K ATP channels.
abstract: BACKGROUND
  Hemorrhagic transformation (HT) is a major factor limiting the use of thrombolytic treatment for stroke. Animal model can help us to understand HT. This study is to establish a HT model in rats to compare HT with uncomplicated cerebral infarction in neurobehavioral deficit, brain edema, brain adenosine triphosphatase (ATPase) activity and succinic dehydrogenase (SDH) activity, and to investigate its pathology changes as well as the impact of, Glibenclamide, a ATP-sensitive K(+) channel (K(ATP) channel) blocker, on the pathogenesis of HT.
  
  
  METHODS
  Male, Sprague-Dawley rats were randomly assigned to four groups: hemorrhagic transformation (HT), cerebral infarction (CI), Glibenclamide+HT (GH) and a control. To create HT model, right middle cerebral artery occlusion (MCAO) was conducted with intraluminal thread technique; 30 min after MCAO, 50 microL arterial blood was injected into the caudate nucleus where the infarction occurred. Neurologic deficit was evaluated by Longa test, Berderson test and Beam test. Brain water content, brain ATPase activity and SDH activity were measured. Histology was examined using light microscope and transmission electron microscope.
  
  
  RESULTS
  No significant difference in neurobehavioral deficit and brain water content was observed between HT and CI groups in all time points (P>0.05). Brain ATPase activity 12 h and 24 h after operation and brain SDH activity 24 h after the operation in HT group were both significantly increased compared with those in CI group (P<0.05); the increase of brain ATPase and SDH activity in HT group could be prevented by Glibenclamide. Neuronal degeneration and tissue edema in HT group, swollen neuropil and loosen intercellular substance in CI group were revealed by histology study. Ultrastructural changes including swollen mitochondria and interstitial edema were also observed in both HT and CI groups.
  
  
  CONCLUSIONS
  The results demonstrated that moderate hemorrhagic transformation does not significantly aggravate cerebral infarction, and that K(ATP) channels have an important role in energy metabolism.
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Yang
authors.forename: Xiang-jian
authors.initials: XJ
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Yin
authors.forename: Li-tao
authors.initials: LT
authors.lastname: Li
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001929:Brain Edema / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D020520:Brain Infarction / Q000209:etiology* / Q000378:metabolism* / Q000503:physiopathology; D002545:Brain Ischemia / Q000150:complications*; D002543:Cerebral Hemorrhage / Q000150:complications* / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology; D005905:Glyburide / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D020244:Infarction, Middle Cerebral Artery / Q000150:complications; D054086:KATP Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008297:Male; D046529:Microscopy, Electron, Transmission; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013385:Succinate Dehydrogenase / Q000378:metabolism
chemical_list: D007004:Hypoglycemic Agents; D054086:KATP Channels; D013385:Succinate Dehydrogenase; D000251:Adenosine Triphosphatases; D005905:Glyburide