Adenosine Metabolites Are a Source of Oxygen Free Radicals in the Ischemic/Reperfused Rat Brain

摘要: The pathophysiology of brain ischemia/ reperfusion injury is characterized by a complex sequence events, including biochemical, hemodynamic, and electrophysiologic processes, which frequently lead to neuronal death. Decreases in cerebral blood flow (CBF) below critical threshold result energy failure, tissue acidosis, disturbed ion homeostasis with cellular Na+ Ca2+ influx K+ efflux, membrane depolarization, cytotoxic edema. There massive release the excitatory amino acid neurotransmitters, glutamate aspartate, can trigger further cell depolarization intracellular calcium accumulation. increased level free cytosolic appears play pivotal role progression events that irreversible injury, it precipitates series neurotoxic radical generation, lipid peroxidation, activation proteolytic enzymes, induction potentially injurious protooncogene expression.