흰쥐의 뇌허혈에 대한 니모디핀의 보호효과

다국어 초록 (Multilingual Abstract)

Background : Accumulation of intracellular calcium is one of the main pathogenic mechanisms of cellular death in brain ischemia. We investigated to the effect of nimodipine on the size of infarction and intracellular calcium concentration in the ischemic rat brain. Methods : Cerebral ischemia was produced by bilateral carotid ligation in 30 Sprague-Dawley rats. Seventeen rats were treated with nimodipine (400 ㎍/㎏) 20 minutes before ligation, and 13 were used as controls. Intracellular calcium concentration was measured with a fluorescent dye fura-2 using a following equation: [Ca2+]i = KD[ (R-Rmin)/(Rmax-R)](Sf2/Sb2) at 30 minutes, 1 hour, 2, and 3 hours after ischemia. The size of infarction was determined by staining the three pieces of mid-coronal section of the brain with 2% 2,3,5-triphenyltetrazolium chloride (TTC) solution. Results : In the nimodipine trial goup, total sizes of infarction were 13.0±2.4%, 16.0±1.9%, 18.7±.2%, 21.0±4.4%, and 33.8±2.7% when ischemic insults were done for 30 minutes, 1 hour,2,3, and 4 hours, respectively, while those in the controls were 13.8±2.7%, 19.1±1.1%, 24.2±1.8%, 37.6±4.3%, and 39.8±2.4%. The sizes of infarction correlated with duration of the ischemia, and were smaller in thenimodipine treated rats except for the 30 minutes-carotid occlusion groups. Intracellular calcium concentrations in the nimodipine treated group were 430±49 nM, 388±19 nM, 367±22nM, and 403 ± 20 nM when ischemic insults were produced for 30 minutes, 1 hour, 2, and 3 hours, respectively, while those in the controls were 305±23 nM, 323±27 nM, 422±43 nM, and 381±55 nM. There was no significant difference in the intracellular calcium concentration between the treated rats and and controls. However, the rate of increase in intracellular calcium concentration was slower in the treated group than in the controls. Conclusions : The sizes of infarction but not intracellular calcium concentrations in cortical brain correlated with the duration of ischemia. Nimodipine did not sufficiently block calcium influx but decreased infarction size. We suggest that the calcium channel blocker can prevent ischemic damage of brain cells through vascular dilatation and blocking of calcium influx. Korean Journal of Stroke 1999;1(2): 231~239