During reperfusion after
ischemia, deleterious biochemical processes can be triggered that may antagonize the beneficial effects of reperfusion. Research into the understanding and treatment of
reperfusion injury (RI) is an important objective in the new era of reperfusion
therapy for
stroke. To investigate RI, permanent and reversible unilateral middle cerebral artery/common carotid artery (MCA/CCA) occlusion (monitored by
laser Doppler) of variable duration in Long-Evans (LE) and spontaneously hypertensive (SH) rats and unilateral MCA and bilateral CCA occlusion in selected LE rats was induced. In LE rats,
infarct volume after 24 hours of permanent unilateral MCA/CCA occlusion was 31.1 +/- 34.6 mm3 and was only 28% of the
infarct volume after 120 to 300 minutes of reversible occlusion plus 24 hours of reperfusion, indicating that 72% of the damage of
ischemia/reperfusion is produced by RI. When reversible
ischemia was prolonged to 480 and 1080 minutes,
infarct volume was 39.6 mm3 and 16.6 mm3, respectively, being indistinguishable from the damage produced by permanent
ischemia and significantly smaller than damage after 120 to 300 minutes of
ischemia.
Reperfusion injury was not 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 synthesis inhibitor cycloheximide or spin-trap agent
N-tert-butyl-alpha-phenylnitrone pretreatment.