Background: Experimental data indicate that low-flow reperfusion following prolonged cardiocirculatory arrest may aggravate early cerebral microcirculatory reperfusion disorders. We investigated the influence of cerebral reperfusion flow change to the...
Background: Experimental data indicate that low-flow reperfusion following prolonged cardiocirculatory arrest may aggravate early cerebral microcirculatory reperfusion disorders. We investigated the influence of cerebral reperfusion flow change to the ischemic histopathologic damage of brain tissue after incomplete forebrain ischemia in rats.
Materials and method: Anesthetized Sprague-Dawley rats were undergone ligation of both internal carotid artery by microvascular clamp for 10 minutes. After release of the clamp, reperfusion was started with several different flow levels (0, 10, 20, 30, 50, and 100%) of internal carotid artery comparing to pre-clamping phase using flowmeter. After 15minutes of reperfusion, rat brains were prepared by perfusion-fixation with 3% formaldehyde. Under light microscopic examination of Hematoxylin-Eosin stained tissue slide, histopathologic damage was examined at cortex, putamen, and hippocampus regions. Categorical hisotopathologic damage scores were derived in each regions by manual counts of ischemic neurons.
Result: The histopathologic damage scores were 0, 10.2±0.5, 7.6±1.5, 5.9±1.4, 5.0±2.8, 3.5±0.7, and 1.0±0.0 in control, 0, 10,20, 30, 50, and 100% reperfusion groups, respectively(p<0.05).
Conclusion: Our results showed significant increment of brain histopathologic damage scores along with decreasing amount of cerebral reperfusion flow after incomplete forebrain ischemia. We believe restoration of reperfusion flow to pre-ischemic level would be a critical component in attenuation of brain ischemic damage.