Apoptotic Study In The Regions Of Hippocampal And Thalamencephalon Based On A Model Of Ventricular Fluid Impacting The Periventriclular Structure.

Cell death after cerebral trauma can be divided into two forms:necrosis and apoptosis. Some studies have raised the idea that apoptosiswas the major form in the secondary cerebral trauma. Recently,researches on apoptosis mechanism have demonstrated that apoptosisparticipated in the whole process of secondary pathophysiologic changesafter cerebral trauma, and apoptosis could be found in diverse traumaticmodel. In our study, we first time used the model of ventricular fluidimpacting the periventriclular structure, and observed the pathologicchanges in the regions of hippocampal and thalamencephalon after HEand TUNEL stained. Moreover, we investigated the association ofventricular fluid impact power with apoptosis after cerebral trauma.Methods: 80 rabbits were divided into 5 groups, including controlgroup(n=8), sham operation group(n=8), mild injury group(n=24, thepower of impact was 0.23J), moderate injury group(n=24, the power ofimpact was 0.52J) and severe injury group(n=24, the power of impactwas 0.92J). We randomly selected 8 rabbits from each injury group andmeasured the recovery time (the survival in each group were 8, 7 and 3respectively), and recorded pathophysiologic changes. The other 16rabbits in each group were given cerebral perfusion and observed thepathologic changes (the survival in each group were 15, 13 and 10respectively). All groups of rabbits were killed at different times(2h, 8h, 24h, 48h, 72h and 7d) after impact. Each were examined thepathological changes of the regions of hippocampal andthalamencephalon after HE and TUNEL stained under light microscope.Results: 1. The mortality of each injury group were significantlydifferent (the rates were 4.16%, 16.67% and 48.53%, respectively;P＜0.05), while no death was found in control group and sham operationgroup. 2. The physiological responses after impact were observed in alltraumatic animals, including a sudden rise or reduction of blood pressure,deep and fast breath and apnea etc. The responses were the most obviousin the severe injury group. 3. The recovery times were significantlydifferent in each injury group (T=2.11±0.40h, 5.85±1.23h and 7.83±0.40h,respectively; P＜0.05). 4. Necrosis could be found in the regions ofhippocampal and thalamencephalon after HE stained. 5. TUNEL stainingshowed the apoptosis in the regions of hippocampal andthalamencephalon. Firstly, we examined the results of the apoptosis in thehippocampal region. In the mild group, apoptosis positive neurocyteswere found 48h after cerebral contusion(8.19±2.13) and got to peak at72h (12.8±1.96); in the moderate injury group, apoptosis positiveneurocytes were found 24h after cerebral contusion(6.21±2.37) and gotto peak at 72(18.44±3.97), then decreased on 7d(8.93±2.51); in thesevere injury group, apoptosis positive neurocytes were found 24h aftercerebral contusion(8.23±1.81) and got to peak at 72 (27.18±5.05), thendecreased on 7d (9.12±3.04). Secondly, we observed the results of theapoptosis in the thalamencephalon. In the mild group, apoptosis positiveneurocytes were found 48h after cerebral contusion (16.38±5.92) andgot to peak at 72h (27.29±8.93); in the moderate injury group, apoptosispositive neurocytes were found 24h after cerebral contusion (17.45±6.73) and got to peak at 72h (34.25±6.25), then decreased on 7d (12.88±3.27);in the severe injury group, apoptosis positive neurocytes were found 24hafter cerebral contusion (20.17±8.84) and got to peak at 72h (43.47±10.29), then decreased on 7d (13.15±6.78). The apoptosis positiveneurocytes found 72h after cerebral contusion were significantly in thehippocampal region and in the thalamencephalon (P＜0.05). 5. Theelectron microscope showed reduction or disapperance of microtubule inaxons, neurofilements ranging disorderly, medullary sheath bleeding,pyknosis of chorioidal epithelium cells.Conclusion: The model in our study can effectively induceapoptosis in the region of hippocampal and thalamencephalon in eachinjury group. Besides, the degree and the appearing time of neurocytesapoptosis closely correlate with the impact power, in another word, thegreater impact power obtained, the earlier appearing time and the moreapoptosis positive neurocytes observed. The ventricular fluid whichhave obtained some power in the process of cerebral trauma candamage the periventricular structure and produce a series ofpathophysiological changes. This model is simple and cheap, and has agood ability of classifying and repeating.