demo of Brain Damage Produced by Reperfusion After Transient Focal Ischemia in Rats
top of pageAbstractDuring reperfusion after ischemia, Deleterious biochemical processes can be triggered that may antagonize the benefits of reperfusion. Research into the perception and treatment of reperfusion injury (ri) is a vital objective in the new era of reperfusion therapy for stroke. to review RI, Permanent and relatively easy to fix unilateral middle cerebral artery/common carotid artery (MCA/CCA) Occlusion (administered by laser Doppler) Of variable duration in LongEvans (le) And in an instant hypertensive (SH) Rats and unilateral MCA and bilateral CCA occlusion in decided on LE rats was induced. In LE rats, Infarct volume after 24 hours of everlasting unilateral MCA/CCA occlusion was 31.1 34.6 mm3 and was only 28% of the infarct volume after 120 to 300 minutes of relatively easy to fix occlusion plus 24 hours of reperfusion, Indicating that 72% of the damage of ischemia/reperfusion is due to RI. When relatively easy to fix ischemia was prolonged to 480 and 1080 minutes, Infarct numbers was 39.6 mm3 as well as 16.6 mm3, Respectively, Being indistinguishable from the damage produced by permanent ischemia and very much smaller than damage after 120 to 300 minutes of ischemia. Reperfusion injury hasn't been seen in SH rats or with bilateral CCA occlusion in LE rats, In which perfusion is reduced more profoundly. Reperfusion injury was ameliorated by the protein activity inhibitor
cycloheximide or spintrap agent Ntertbutylalphaphenylnitrone pretreatment,/p>
phrases: Cycloheximide; center ischemia; brand; PBN; Reperfusion being injured; cva or cerebrocascular accident
Abbreviations: CCA, general carotid artery; clubpenguin, Cerebral perfusion; 
H hematoxylin and furthermore eosin; LDF, device Doppler flowmeter; the, LongEvans; MCA, meeting place cerebral artery; PBN, NtertButylalphaphenylnitrone; ri, Reperfusion accidents; SH, automatically hypertensive; TTC, 2,3,5triphenyltetrazolium chloride
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