摘要
目的:在全脑缺血-再灌注后,尽早施行头部重点低温取得了较好的脑复苏效应。为阐明其机理,近10年来,我院和各家兄弟单位研究表明头部重点低温脑复苏是通过多途径起作用的。基于近年来的研究发现,脑缺血后因脑组织NO明显升高,因而参与神经损伤。本研究意在观察低温对脑缺血再灌注后产生NO的效应,并探讨其可能机制。方法:SD大鼠66只,均用腹腔麻醉,分为正常对照组(组Ⅰ),按Pulsineli大鼠脑缺血模型制作的缺血对照组(组Ⅱ),常温再灌注组(组Ⅲ),头部重点低温再灌注组(组Ⅳ),给药(L-NAME)组(组Ⅴ)。在完成实验条件后处死,用硝酸还原酶法测定脑组织NO3-/NO2-,另外用MDA测定试剂盒检测MDA含量,按Eliot公式计算脑水含量。结果:缺血常温再灌注后,NO产生增多,MDA和脑水含量相应增加,提示NO参与了再灌注损伤过程。头部重点低温不仅抑制再灌注NO的产生,也抑制MDA和脑水含量增幅,而L-NAME仅对NO有较强的抑制作用。结论:全脑缺血再灌注后NO大量升高,头部重点低温抑制NO产生有利于脑复苏作用。
ackground: Selective head cooling (SHC)may exert multifaceted benificial effects,both biochemically and histomorphologically,for brain resuscitation,as shown by animal experiments conducted in recent years.It ameliorates the neuronal ischemiareperfusion damage by inhibiting the release of toxic mediators and enhancing the recruitment of substances (e.g.Na+-K+ATPase) required for cellrepairing .Recently,it has been implied that overproduction of NO during cerebral ischemia may take part in neuronal damage.In order to explore the effect of SHC on NO production and its possible mechanism,this study was undertaken.Methods:66 SpragueDawley rats were allocated into normal control group(group Ⅰ),simple global ischemia group (groupⅡ),normothermic reperfusion group (group Ⅲ),SHC hypothermic reperfusion group (group Ⅳ)and LNAME treated reperfusion group (group Ⅴ).Group Ⅲ、Ⅳ、Ⅴ were divided further,according to the duration of reperfusion for 30、120 and 240min,into subgroups 1、2 and 3,with 6 rats in each subgroup.Global ischemia lasting 30 min was accomplished by Pulsinelli model.Rats were sacrificed and brain specimens were taken as requirements were fulfilled.Brain NO was measured in form of NO3-/NO2- by means of nitrate reductase method.Brain MDA was used to assay for radicals,according the method introduced by MDA box.Brain water content was calculated by Elliot method.Results:NO was overproduced during positischemic normothermic reperfusion,in association with rising of MDA and brain water content.Conclusion:NO takes part in the process of reperfusion damage.SHC not only attenuates the NO production,but also decreases the increments of MDA and brain water content,while LNAME has only the inhibitory effect on NO production.NO is overproduced during postischemic normothermic reperfusion.SHC seems to be effective to ameliorate the reperfusion damage,thus favorable for brain resuscitation.
出处
《临床麻醉学杂志》
CAS
CSCD
1998年第1期1-4,共4页
Journal of Clinical Anesthesiology
关键词
脑复苏
再灌注损伤
低温
NO
脑缺血
Brain resuscitation Hypothermia NO LNAME Ischemia reperfusion damage