The Effect of Albumin Therapy for Reperfusion Injury Following Transient Focal Cerebral Ischemia in Rats

OBJECTIVE: Albumin is a very useful drug for the improving of cerebral blood volume and the oncotic effect in cerebral ischemia or cerebral vasospasm. The purpose of this study was to examine the morphological and neurological effect of albumin therapy on reperfusion injury following transient focal cerebral ischemia. MATERIALS AND METHODS: 18 Male Sprague-Dawley rats weighing 270-320g were used. The ischemia model was produced by 2-hour period of transient middle cerebral artery occlusion with a poly-L-lysin coated intraluminal suture. The agent(20% human serum albumin[HSA]) or control solution(NaCl 0.9%) was administered intravenously at a dosage of 1% of body weight immediate after reperfusion following a 2-hour period occlusion. Neurological function was evaluated by the postural reflex and the forlimb placing test during occlusion(at 60 min) and daily for 3 days thereafter. The brain was perfusion-fixed, and infarct volumes and brain edema were measured. RESULTS: The HSA significantly improved the neurological score in treated group. The rats of albumin treatment group showed significantly reduced total infarct volume(by 34%) and brain edema(by 81%) compared with saline-treated rats. CONCLUSION: HSA showed a substantial effect on the transient focal cerebral ischemia and reperfusion injury model. These results may indicate its usefulness in treating reperfusion injury patients after thrombolysis treatment for the thrombo-embolic major cerebral artery occlusions.

Neuroprotective Effect of Focal Ischemic Preconditioning in Transient Focal Ischemia Animal Model

BACKGROUND: The term 'ischemic preconditioning', which implies the first, brief, sublethal ischemia before the next ischemia, is widely accepted to have protective effect in the myocardium, and recently with a specified circumstances, in the brain also. However, the existence of this 'ischemic tolerance' phenomenon is not yet clarified in the repeated transient focal cerebral ischemia model. This study was performed to test whether the ischemic preconditiong has protective effect also in this TIA-mimicking condition. METHODS: Using intraluminar suture technique, initial transient focal ischemia was maintained for 30 minutes in the rat brain. After this ischemic preconditioning, second ischemia of 120 minutes duration was performed using the same method at 1, 3, 5, and 7 days after the 1st ischemia (n=20). The resulting brain infarct volume was assessed and compared to that of previously sham-operated paired controls(n=20). RESULTS: Using the infarct volume as parameters, there was no significant difference between the ischemia and control group in all pairs. But when the percent of infarct volume compared to the hemispheric volume was used instead, neocortical infarct percent was significantly smaller at day 3 after preconditiong (p<0.05). But such difference was not found at 1, 5, and 7th day in the neocotex. Neither the percent of total infarct nor the subcortical infarct showed any statistical difference. CONCLUSION: It could be concluded that transient focal cerebral ischemic preconditioning have neuroprotective effect. The optimal interval between ischemia for this 'ischemic tolerance' to happen is 3 days, and this phenomenon seems to be the function of cerebral cortex, but not the subcortex.