重组链激酶早期应用对脑出血血肿周围脑组织的影响

目的　研究重组链激酶早期应用对脑出血 (ICH)血肿周围脑组织的影响。方法　 72只SD雄性大鼠制成ICH模型 ,随机分为对照组、重组链激酶组、水蛭素组 ,各组分别在ICH后 4、8、12、16h于血肿腔中注入生理盐水、重组链激酶、或重组链激酶加水蛭素。ICH后 2 4h处死大鼠 ,观察脑组织中的含水量、Na+、K+以及血脑屏障通透性的变化。结果　在ICH后 4、8、12、16h应用重组链激酶 ,可引起脑组织含水量增加以及Na+升高、K+的降低 (P <0 .0 5 ) ,在ICH后 4、8、12h应用重组链激酶 ,脑组织中伊文思蓝 (Evensblue,EB)含量明显升高(P <0 .0 5 )。如同时加用水蛭素 ,与对照组比较脑组织的含水量在 4、8、12h明显降低 (P <0 .0 5 ) ,而脑组织中EB含量则在 4、8、12、16h明显降低 (P <0 .0 5 )。结论　ICH血肿腔中早期应用重组链激酶可加重ICH血肿周围脑组织的损伤 ,联合应用水蛭素不但可防治重组链激酶溶化血块时对脑组织的损伤 ,而且还可降低血肿本身所释放的毒性物质所引起的脑水肿及血脑屏障的破坏

Effect of Early Using Recombinant Streptokinase on the Perihematomal Brain Tissue of Intracerebral Hemorrhage

Purpose To investigate the effect of early using recombinant streptokinase on the perihematomal brain tissue of intracerebral hemorrhage(ICH). Methods Seventy-two adult male SD rats made to be intracerebral hemorrhage models were divided randomizedly to 3 groups:contrast?r-sk(recombinant streptokinase) and hirudin.The hematomal cavity were injected with normal saline?r-sk?hirudin plus r-sk,at the 4?8?12?16 h after ICH.The rats were decapitated at 24 h after ICH,then the brain water content and K +?Na + contents and blood brain barrier permeability were measured. Results In r-sk groups,the water content of the perihematomal tissue were increased at the 4?8?12?16 h after ICH;The K +?Na + contents were changed obviously at 4?8?12 h(P<0.05);The evens blue contents were increased obviously at 4?8?12 h(P<0.05).While in hirudin groups,the water content of the perihematomal tissue was not only decreased,but was decreased obviously at 4?8?12 h compared to the contrast groups.The EB contents were decreased obviously at 4?8?12?16 h compared to the contrast groups. Conclusions The early using recombinant streptokinase in the hematomal cavity will damage the perihematomal brain tissue after ICH,while r-sk plus hirudin used in the hamatomal cavity will not only prevent the damage produced by the early using of plasminogen activator for lysis the hematomas,but also can reduced the damage to the brain tissue produced by toxin released from hematomal itself.