| Objectives: Secondary brain insults(SBI) usually fellowstraumatic brain injury in a few hours to several days, may further theaggravation of brain injury. The particularity of the marineenvironment and treatment delays, making SBI with seawater immersioneasily, the injury is more complicated. In this study, the model of SBIwith seawater immersion was created on the bassis of SBI.Then thechanges of superoxide dismutase(SOD) and malondialdehyde(MDA) wereobserved to study possible mechanism of SBI with seawater immersion.Methods: Total of163male SD rats were randomly divided into fourgroups:control group(A,5rats), SBI group(B,32rats), SBI with salineimmersion group(C,33rats), SBI with seawater immersion group(D,93rats). DBI was produced by acceleration-deceleration model of traumaticbrain injury developed by Marmarou et al.15minutes following the impactinjury,a secondary insults was produced by right carotid occlusion for30minutes.dental drill is used to open the right skull, the dura materwas cut longitudinally.The brain is covered with cotton slice and usedinfusion set to infuse seawater over the cotton at room temperature,suture the head skin, so that local brain tissue was soaked in sea watercontinuously.Pathological changes of traumatic brain edema wasobserved by hematoxylin and eosin method at designed time points(1h,3h,6h,12h,24h,48h).Thiobarbituric acid method and xanthine oxidasemethod were used to determine the contents of malondialdehyde(MDA) andthe activities of total SOD in brain tissue,and analyses therelationship of them. Results: SBI model and SBI with seawater immersion model wereconstruct,injured brain tissue can be immersed by sea water after thedura mater cutted, the models can be satisfied the experiment.SBI withseawater immersion group mortality rate（45/93，48.93％）is much higherthan B group（8/32，25.00％）and C group（9/33，27.27％）.these werestatistically significant (P <0.05). The brain edema of SBI withseawater immersion is earlier and much serious than other groups,thebrain edema of SBI and SBI with saline immersion group were stabilizedafter24hs, but SBI with seawater immersion group is much serious until48hs（88.38±0.93％）. Pathological change by HE method indicated thatpre-injury traumatic edema was aggravated as a result of seawaterimmersion and became grid changed not the same as Spongiform change ofSBI group.SOD level in seawater immersion group were significantlydecreased at the beginging of3h（212.09±22.29）U/mgprot,and lower thanSBI group（245.31±21.26）U/mgprot;MDA level in seawater immersion groupwere incresed in seawater immersion group at the beginging of3h（9.53±0.47）nmol/mgprot,and higher than SBI groups in3h（6.16±0.34）nmol/mgprot.There is a inverse correlation in control groups of SODand MDA in brain tissue,with the result(P＜0.05) There is parallelrelationship between MDA and brain water content in B group,C group andD group.Conclusion:①SBI with seawater immersion group is more seriousthan SBI group under the corresponding time window;②the deteriorismof traumatic condition in SBI with seawater immersion became moreserious quickly;③The radical change of SBI with seawater immersion isclosely with traumatic condition. |
PDF Full Text Request