Portal de Periódicos da CAPES

P4–164: Neuroprotective role of ATP dependent potassium channel regulators following ischemia–reperfusion in parietal cerebral cortex of rat

2006; Wiley; Volume: 2; Issue: 3S_Part_18 Linguagem: Inglês

10.1016/j.jalz.2006.05.1903

1552-5279

Mehdi Mehdizadeh, Mansoureh Slimany, Hammid Pasouki, Mohammad Taghi Joghataei,

Anesthesia and Neurotoxicity Research

Cells in Nervous system in general and neurons of Central nervous system in particular are highly vulnerable to diverse forms of injury, including ischemia, hypoxia, hypoglycemia, infection and trauma. Oxidative stress has been clearly established to contribute to ischemia–reperfusion injury. ROS may act as signaling molecules in hypoxia but can also directly damage intracellular components and cell. Mitochondria are central to brain cell response to ischemia–reperfusion with critical roles in generation of ATP, production of free radicals, and regulation of cell death. Changes in the permeability of the outer mitochondrial membrane can control ischemic cell death. In this study we have used ATP dependent potassium channel regulators to see their effects on neuronal cell death following ischemia–reperfusion. Male wistar rats weighing 180–200 g were used. They were kept on a 12 h light/dark cycle and were caged in pairs with food and water ad libitum. There were 8 groups of 6 rats: those with a sham unoperated group and a vehicle ischemia group and 3 experimental groups treated with different doses of gliben clamide and 3 experimental groups treated with different doses of diazoxide. 24 hours after 15 minutes global ischemia animals were anesthetized and the brains were removed from the skull and placed in formalin as fixative and were embedded in paraffin. Serial 7 μm cross–sections were cut and stained with crysil violet. Cell counts were performed in 4 subregion of cerebral cortex. Normal population of neurons in groups treated with 5 mg/kg and 25 mg/kg of gliben clamide was decreased significantly. Diazoxide in doses of 6 mg/kg and 18 mg/kg showed an increase in number of neurons. Treatment with diazoxide as a potassium channel opener can decrease neuronal loss following ischemia–reperfusion but Gliben clamide as a potassium channel blocker can lead to increased neuronal loss.Related Neurodegenerative Conditions Vascular dementia/multi–infarct dementia