Publication | Closed Access
Effects of neutrophil depletion and superoxide dismutase on postischemic hypoperfusion of rat brain.
25
Citations
0
References
1990
Year
Redox BiologySocial SciencesRat BrainOxidative StressNeuroinflammationInflammationThrombosisCerebral Vascular RegulationNeurovascular DiseaseFree RadicalsBrain InjuryNeurologySuperoxide DismutaseNeuroimmunologyAtherosclerosisIschemic SyndromeReversible Forebrain IschemiaMedicineHypoxia (Medicine)NeuropharmacologyVascular BiologyNeuroprotectionCerebral Blood FlowReperfusion InjuryNeutrophil DepletionNeurophysiologyPhysiologyNeurosciencePostischemic Perfusion DisturbancesStroke
In the present investigation, the involvement of PMNLs and oxygen free radicals was explored in rats with postischemic perfusion disturbances of the brain. Reversible forebrain ischemia was induced by bilateral clamping of both carotid arteries in combination with hemorrhagic hypotension. This procedure resulted in a reproducible DPH 1 hr after start of recirculation. Neutropenia was induced by sheep ANS. One group received ANS before and a second group immediately after termination of ischemia. Two additional groups received SOD before or immediately after ischemia. Regional postischemic CBF was determined by [14C]iodoantipyrine autoradiography. It was found that CBF significantly improved in cortical structures of animals treated with ANS before ischemia. Treatment with ANS at the end of ischemia had no effect on the postischemic CBF depression. Neither was injection of SOD effective to influence DPH, irrespective whether given before or after ischemia. It is concluded that PMNLs play a role in the development of DPH of the brain, whereas free radical mechanisms seem to be less relevant.