Namura Y, Shio H, Kimura J
Department of Neurology, Kyoto University School of Medicine, Japan.
Acta Neurochir Suppl (Wien). 1994;60:296-9. doi: 10.1007/978-3-7091-9334-1_79.
LTC4, which enhances vascular permeability and promotes tissue edema, and LTB4, which is a potent chemotactic and activating factor for leukocytes, were measured in rat brain after ischemia and several time periods of reperfusion. Forebrain ischemia was induced by 4-vessel occlusion. LTC4/LTB4 in the brain were measured by RIA. We also studied the effects of a 5-lipoxygenase inhibitor, AA-861 and a PAF antagonist, CV-3988 on LTC4/LTB4 concentrations. LTC4 in brain tissue increased during 30 min forebrain ischemia (p < 0.001). After reperfusion, LTC4 increased further, but at 15 min reperfusion LTC4 returned to the control level. Tissue levels of LTB4 in the brain increased during 30 min ischemia and remained high until 5 min after reperfusion (p < 0.01) returning at 15 min reperfusion to the control level. AA-861 inhibited elevation of LTC4/LTB4 in the reperfusion phase, but was not effective during ischemia. CV-3988 had a similar effect. LTC4 and LTB4 may be involved in the pathogenesis of ischemia brain edema and leukocyte infiltration. Further, PAF and LTs have many similarities of their pathophysiological properties, and may interact therefore in pathologic process.
在缺血及几个再灌注时间段后，检测大鼠脑内可增强血管通透性并促进组织水肿的白三烯C4（LTC4）以及作为白细胞强效趋化和激活因子的白三烯B4（LTB4）。通过四血管闭塞诱导前脑缺血。采用放射免疫分析法测定脑内的LTC4/LTB4。我们还研究了5-脂氧合酶抑制剂AA-861和血小板活化因子拮抗剂CV-3988对LTC4/LTB4浓度的影响。在前脑缺血30分钟期间，脑组织中的LTC4增加（p<0.001）。再灌注后，LTC4进一步增加，但在再灌注15分钟时LTC4恢复到对照水平。脑内LTB4的组织水平在缺血30分钟期间升高，并在再灌注后5分钟内保持较高水平（p<0.01），在再灌注15分钟时恢复到对照水平。AA-861抑制再灌注期LTC4/LTB4的升高，但在缺血期间无效。CV-3988有类似作用。LTC4和LTB4可能参与缺血性脑水肿和白细胞浸润的发病机制。此外，血小板活化因子和白三烯在病理生理特性上有许多相似之处，因此可能在病理过程中相互作用。
