CAJ | 학술논문

目的观察硫化氢(H2S)对兔心肺复苏后早期NSE、S100B以及海马神经元凋亡的影响.方法 25只日本大耳白兔随机(随机数字法)分为3组:假手术组(S组)、心搏骤停组(CA组)和H2S处理组(H2S组).兔吸入5％氟烷麻醉后,气管切开,右股静脉置管用于给药,右颈动脉穿刺置管用于血压监测和采血.CA组和H2S组夹闭家兔气管导管8 min制备心搏骤停模型,并分别在恢复自主循环后吸入30％ O2或体积分数为80 x 10-6 H2S.于夹闭气管导管前(基础值)及恢复自主循环后30 min、60 min采动脉血检测血浆中神经元特异性烯醇化酶(neuronspecific enolase,NSE)和S100B的质量浓度.恢复自主循环后60 min处死家兔,取脑后分离海马固定于4％多聚甲醛中,待做组织病理学检查.计量资料以均数±标准差((x)±s)表示,采用单因素方差分析,组间比较采用SNK-q检验,以P＜0.05为差异有统计学意义.结果与S组同时点比较,CA组和H2S组NSE和S100B的质量浓度均明显增高(P＜0.05),海马CA1区存活神经元减少,活化型caspase-3阳性神经元增多(P＜0.05)；与CA组比较,H2S组恢复自主循环后60 min时S100B质量浓度显著降低(P＜0.05),海马CA1区存活神经元增多,活化型caspase-3阳性神经元显著减少(P＜0.05).结论 H2S抑制海马CA1区神经元凋亡,增加存活神经元数目,降低血浆中S100B的水平,进而减轻心搏骤停复苏后神经功能的损伤.
목적 관찰류화경(H2S)대토심폐복소후조기NSE、S100B이급해마신경원조망적영향.방법 25지일본대이백토수궤(수궤수자법)분위3조:가수술조(S조)、심박취정조(CA조)화H2S처리조(H2S조).토흡입5％불완마취후,기관절개,우고정맥치관용우급약,우경동맥천자치관용우혈압감측화채혈.CA조화H2S조협폐가토기관도관8 min제비심박취정모형,병분별재회복자주순배후흡입30％ O2혹체적분수위80 x 10-6 H2S.우협폐기관도관전(기출치)급회복자주순배후30 min、60 min채동맥혈검측혈장중신경원특이성희순화매(neuronspecific enolase,NSE)화S100B적질량농도.회복자주순배후60 min처사가토,취뇌후분리해마고정우4％다취갑철중,대주조직병이학검사.계량자료이균수±표준차((x)±s)표시,채용단인소방차분석,조간비교채용SNK-q검험,이P＜0.05위차이유통계학의의.결과 여S조동시점비교,CA조화H2S조NSE화S100B적질량농도균명현증고(P＜0.05),해마CA1구존활신경원감소,활화형caspase-3양성신경원증다(P＜0.05)；여CA조비교,H2S조회복자주순배후60 min시S100B질량농도현저강저(P＜0.05),해마CA1구존활신경원증다,활화형caspase-3양성신경원현저감소(P＜0.05).결론 H2S억제해마CA1구신경원조망,증가존활신경원수목,강저혈장중S100B적수평,진이감경심박취정복소후신경공능적손상.
Objective To explore the effects of hydrogen sulfide (H2S) on neuron specific-enolase (NSE),neurotrophic protein S100B and neurons apoptosis in hippocampus CA1 region in the early stage of cardiopulmonary resuscitation (CPR) in rabbits. Methods Twenty-five Japanese white rabbits were randomly divided into three groups:sham group (S group),cardiac arrest group (CA group) and H2S treatment group (H2S group). Rabbits were anaesthetized with 5％ halothane,trachea was exposed and intuhated,right femoral vein was cannulated for medical agent administration,and right carotid artery was cannulated for monitoring of blood pressure and blood samples taken. Cardiac arrest was produced by suffocation with clamping the endotracheal tube and turning off mechanical ventilation.Mter 8 min of the endotracheal tube clamping, rabbits received CPR. After the restoration of spontaneous circulation (ROSC),rabbits in groups CA and H2S inhaled 30％ O2 or 30％ O2 containing 80 × 10-6 H2S,respectively.Blood samples were taken before,and 30 min and 60 min after ROSC for detection of the concentrations of NSE and S100B in the plasma. As 60 min after ROSC,rabbits were decapitated after perfusion with 500 ml phosphate-buffered saline and followed by 4％ paraformaldehyde 500 ml through aortic artery,and then the hippocampus was removed rapidly and fixed in 4％ paraformaldehyde for the histological examination.All values were expressed in mean ± standard deviation ((x) ± s).Comparisons were carried out among different groups with SNK-q test of one-way analysis of variance ( One-Way ANOVA plus SNK).Results In comparison with group S,the concentrations of NSE and S100B were significantly increased 30 min and 60 min after ROSC (P ＜ O.05),the viable neurons were decreased and cleaved caspase-3 positive neurons in hippocampus CA1 region increased 60 min after ROSC in groups CA and H2S (P ＜0.05).In comparison with group CA,the concentration of S1OOB decreased 60 min after ROSC (P ＜ 0.05) ; the viable neurons were increased while cleaved caspase-3 positive neurons in hippocampus CA1 region decreased 60 min after ROSC in group H2S ( P ＜ 0.05 ). Conclusions H2S can inhibit the neurons apoptosis in hippocampus CA1 region,increase the viable neurons,decrease the concentration of S100B in the plasma,and then attenuate the cerebral injury after cardiopulmonary resuscitation in rabbits.