The Effect of Nimodipine on the Content of Leukotriene C4 in Brain Tissue after Experimental Subarachnoid Hemorrhage in Rats

Park, In Woo; Yim, Man Bin; Lee, Jang Chull; Park, Byung Kyu; Son, Eun Ik; Kim, Dong Won; Kim, In Hong; Lee, In Kyu

Abstract

In order to find out whether a calcium entry blocker, nimodipine, prevents or decreases the arachnoid acid(AA) metabolism of the brain cell membrane after a subarachnoid hemorrhage(SAH), in a series of 35 adult rats, we injected through a catheter autologus blood(0.3 ml) into the cisterna magna in 30 rats of the SAH group and saline in 5 rats in the control group. Half of the SAH group was treated with an injection of nimodipine(4 times per day of 1.2 mg/kg until sacrifice) intraperitoneally after inducing the SAH. Each SAH group of 10 aminals(5:non-treatment with nimodipine=group a, 5:treatment with nimodipine=group b) were sacrifieced at 24 hours(group Ia & Ib), 48 hours(group IIa & IIb) and 7 days(group IIIa & IIIb) after the induction of the SAH and brain tissue was obtained from the temporal lobe. Levels of leukotriene(LT) C4 in the specimens were determined by the radioimmunoassay method. We observed the change of the average levels of LT C4 after SAH in the nontreated groups with nimodipine, and we also compaired the average levels of LT C4 among the control group, the non-treatment groups and the treatment groups with nimodipine after the SAH. The results showed that the content of LT C4 in the brain tissue increased after experimental SAH. The degree of increase content of LT C4(+/-standard deviation) in the non-treatment groups was the most prominent at 48 hours after the SAH(group Ia vs. IIa vs. IIIa:61.31+/-22.28 vs. 120.38+/-24.18 vs. 66.84+/-28, respectively. Group Ia vs. IIa, and IIa vs. IIIa;p<0.05). However, in the treatment groups with nimodipine, no significant difference was noted(group Ib vs. Iib vs. IIIb:49.19+/-8.19 vs. 42.04+/-14.66 vs. 47.19+/-17.84, respectively). Levels of LT C4 in the treatment groups were lower than those of the non-treatment groups, especially at 48 hours after the SAH(group IIa vs. Iib:120.38+/-24.18 vs. 42.04+/-14.66, respectively. p<0.05). This study showed that nimodipine suppressed the release of LT C4 in brain tissue after the SAH and its protective effect was the most prominent at 48 hours after the SAH. We conclude that nimodipine, aside from its vascular effect, may exert a protective role against the damage of neurons after the SAH with a decrease in the release of the lipoxygenase pathway metabolites of AA.