周围神经缺血再灌注损伤的实验研究

IschemicInjuryandReperfusionofthePeripheralNervesinRabbits-anExperimentalStudy

采用暂时阻断家兔髂总动脉起始处血流的实验模型观察不同缺血再灌注时间周围神经电生理，超微结构和自由基含量的变化。结果表明：１．缺血时间越长，再灌注损伤越重。２．在一定时间范围内，再灌注时间越长，神经传导速度、潜伏期和波幅等电生理指标及神经超微结构改变越明显，再灌注损伤越重。３．缺血后自由基含量增高（Ｐ值＞０．０５），再灌注后进一步明显增高（Ｐ值＜０．０１）。这是再灌注损伤的根本原因。４．应用氯丙嗪、当归、甘露醇后神经组织内自由基含量明显下降（Ｐ值＜０．０１）。三者均有一定自由基清除能力，可用于治疗周围神经的缺血再灌注损伤。

Modelsofunilateralsciaticnerveischemiawereproducedinrabbitsbyclippingthecom-moniliacarteryandreperfusionwasdonebyremovingtheclipsat1,3and6hoursinthe3groupseachof11experimentalanimals.Thechangesofthecontentsoffreeradicals,electrophysiologyandultra-structureinthediferentperiodsofischemiaandreperfusionwereobservedinthespecimensofthepe-ripheralnerves.Thefindingswere:1.thelongertheischemicperiod,thelargerthelesionsofreperfu-sion.2.withinacertainperiod,thelongerthedurationofreperfusion,thechangesoftheelectrophysi-ologicalparameterssuchastheconductionvelocity,thelatentperiodandamplitudeaswelastheultra-structureofthenervebecamemoreevidentindicatingamoreseverereperfusionlesion.3.thecontentsoffreeradicalswereclosetothoseofthenormalcontrolgroupafter6hoursofischemia(P>0.05).After30minofreperfusion,therewasasignificantincreaseintheproductionoffreeradicalsinthenerves(P<0.01).Thisisthebasicreasonofreperfusioninjury.4.afteradministrationofchloropro-mazine,danggui(aChineseherbagent)ormannitol,thecontentsoffreeradicalsinthenerveswerere-ducedsignificantlyincomparisonwiththeuntreatedcontrols.Alofthethreedrugshavetheabilitytopreventtheproductionoffreeradicals.Theyseemtobeusefultotreatthereperfusioninjuryofthepe-ripheralnerves.