CAJ | 학술논문

目的探讨颅脑损伤后早期应用不同剂量糖皮质激素对大鼠继发性脑损伤和死亡率的影响. 方法将成年雄性Wistar大鼠220只按随机数字表法分为正常组、地塞米松正常给药组、甲基强的松龙正常给药组、创伤对照组、小剂量地塞米松组、中剂量地塞米松组、大剂量地塞米松组、小剂量甲基强的松龙组、中剂量甲基强的松龙组和大剂量甲基强的松龙组(后7组统称损伤组),每组各22只.损伤组通过液压打击方法制备成颅脑损伤模型且分别给予生理盐水或不同剂量不同类型糖皮质激素处理,并于伤后24 h进行改良神经功能缺损评分.采用TUNEL法于伤后24h、48h、7d和14d时检测各组大鼠损伤侧海马组织的细胞凋亡情况.观察伤后14d内各组大鼠的死亡率,并通过尸检和常规HE染色观察死亡大鼠脑组织、垂体、心脏和肺脏的变化. 结果损伤组间伤后24h神经功能缺损评分比较差异无统计学意义(P＞0.05).损伤组大鼠海马组织中凋亡细胞于伤后24h开始出现,48 h达到高峰,7～14d内降至正常,其中大剂量地塞米松组和大剂量甲基强的松龙组凋亡细胞数在伤后48 h时均明显高于创伤对照组,差异均有统计学意义(P=0.000,P=0.002).大剂量地塞米松组和大剂量甲基强的松龙组的大鼠死亡率也均明显高于创伤对照组,差异均有统计学意义(P=0.012,P=0.038).尸检发现大剂量地塞米松组和大剂量甲基强的松龙组的死亡大鼠均有不同程度的间质性肺炎及垂体淤血. 结论颅脑损伤可以导致海马神经细胞凋亡,而伤后早期应用大剂量糖皮质激素可进一步加重其凋亡,同时增加死亡率,其原因可能为间质性肺炎和垂体淤血的发生.
목적 탐토로뇌손상후조기응용불동제량당피질격소대대서계발성뇌손상화사망솔적영향. 방법 장성년웅성Wistar대서220지안수궤수자표법분위정상조、지새미송정상급약조、갑기강적송룡정상급약조、창상대조조、소제량지새미송조、중제량지새미송조、대제량지새미송조、소제량갑기강적송룡조、중제량갑기강적송룡조화대제량갑기강적송룡조(후7조통칭손상조),매조각22지.손상조통과액압타격방법제비성로뇌손상모형차분별급여생리염수혹불동제량불동류형당피질격소처리,병우상후24 h진행개량신경공능결손평분.채용TUNEL법우상후24h、48h、7d화14d시검측각조대서손상측해마조직적세포조망정황.관찰상후14d내각조대서적사망솔,병통과시검화상규HE염색관찰사망대서뇌조직、수체、심장화폐장적변화. 결과 손상조간상후24h신경공능결손평분비교차이무통계학의의(P＞0.05).손상조대서해마조직중조망세포우상후24h개시출현,48 h체도고봉,7～14d내강지정상,기중대제량지새미송조화대제량갑기강적송룡조조망세포수재상후48 h시균명현고우창상대조조,차이균유통계학의의(P=0.000,P=0.002).대제량지새미송조화대제량갑기강적송룡조적대서사망솔야균명현고우창상대조조,차이균유통계학의의(P=0.012,P=0.038).시검발현대제량지새미송조화대제량갑기강적송룡조적사망대서균유불동정도적간질성폐염급수체어혈. 결론 로뇌손상가이도치해마신경세포조망,이상후조기응용대제량당피질격소가진일보가중기조망,동시증가사망솔,기원인가능위간질성폐염화수체어혈적발생.
Objective To investigate the effect of glucocorticoids of different dosages on mortality and hippocampal neuron apoptosis in rats after traumatic brain injury (TBI).Methods All the adult male Wistar rats were allocated into normal control group,dexamethasone (DXM) treatment group,methylprednisolone (MP) treatment group,injury control group,low-dose DXM treatment group,moderate-dose DXM treatment group,high-dose DXM treatment group,low-dose MP treatment group,moderate-dose MP treatment group,and high-dose MP treatment group (n=22).Rats in the later seven groups (the injuried groups) accepted fluid percussion injury to induce TBI models,and then,treatments were given.The injury severity was evaluated with modified Neurological Severity Scale 24 h after injury.The number ofhippocampal neuron apoptosis was examined using TUNEL after 24 and 48 h,and 7 and 14 d of injury.The mortality of rats in each group was also observed during a 14-day-follow-up period.The changes of brains,pituitaries,hearts and lungs in the dead rats were examined by H.E.staining.Results No significant difference on the scores of modified Neurological Severity Scale was noted in the injuried groups 24 h after the injury (P＞0.05).The hippocampal neuron apoptosis began to appear 24 h after inju~,peaked at 48 h,and declined in 7 to 14 d.At 48 h after injury,the number of hippocampal neuron apoptosis in high-dose DXM treatment and high-dose MP treatment groups was significantly higher than that in the injury control group (P＜0.05).The mortality of rats in high-dose DXM treatment and high-dose MP treatment was significantly higher than that in the injury control group (P＜0.05).The autopsy of dead rats in each group revealed various degrees of interstitial pneumonia and hypophysial congestion in rats receiving high-dose glucocorticoids.Conclusion TBI could induce hippocampal neuron apoptosis,and early administration of high-dose glucocorticoids aggravates the apoptosis and increases the mortality,for which interstitial pneumonia and hypophysial congestion would account.