CAJ | 학술논문

目的评价异氟醚后处理对缺血缺氧性脑损伤新生大鼠脑组织线粒体通透性转换孔(mPTP)的影响.方法新生SD大鼠120只,7日龄,体重12～ 16 g,采用随机数字表法分为4组(n=30):假手术组(S组)、异氟醚组(I组)、缺血缺氧性脑损伤组(HIBI组)及缺血缺氧性脑损伤+异氟醚后处理组(HI组).HIBI组和HI组永久性结扎左颈总动脉后,置于低氧环境(8％O2-92％N2混合气体)2h,以制备缺血缺氧性脑损伤模型.HI组于缺氧缺血性脑损伤模型制备后即刻吸入1.5％异氟醚30 min.I组仅吸入1.5％异氟醚30 min,不制备模型.于缺氧缺血性脑损伤模型制备后24h时,随机取10只大鼠,处死后取脑组织,测定线粒体mPTP开放程度;于缺氧缺血性脑损伤模型制备后7d,记录大鼠生存情况,处死后取脑,计算丘脑腹后内侧核及海马CA3区左右侧正常神经元密度比值;分离左侧和右侧大脑半球并称重,计算左右侧大脑半球质量百分比.结果 4组大鼠生存率比较差异无统计学意义(P＞0.05);与S组比较,HIBI组和HI组丘脑腹后内侧核及海马CA3区左右侧正常神经元密度比值、左侧大脑半球质量及左右侧大脑半球质量百分比降低,脑组织mPTP开放程度升高(P＜0.05),I组上述各项指标差异无统计学意义(P＞0.05);与HIBI组比较,HI组丘脑腹后内侧核及海马CA3区左右侧正常神经元密度比值、左侧大脑半球质量及左右侧大脑半球质量百分比升高,脑组织mPTP开放程度降低(P＜0.05).结论异氟醚后处理减轻新生大鼠脑缺血缺氧性脑损伤的机制可能与抑制脑组织mPTP开放有关.
목적 평개이불미후처리대결혈결양성뇌손상신생대서뇌조직선립체통투성전환공(mPTP)적영향.방법 신생SD대서120지,7일령,체중12～ 16 g,채용수궤수자표법분위4조(n=30):가수술조(S조)、이불미조(I조)、결혈결양성뇌손상조(HIBI조)급결혈결양성뇌손상+이불미후처리조(HI조).HIBI조화HI조영구성결찰좌경총동맥후,치우저양배경(8％O2-92％N2혼합기체)2h,이제비결혈결양성뇌손상모형.HI조우결양결혈성뇌손상모형제비후즉각흡입1.5％이불미30 min.I조부흡입1.5％이불미30 min,불제비모형.우결양결혈성뇌손상모형제비후24h시,수궤취10지대서,처사후취뇌조직,측정선립체mPTP개방정도;우결양결혈성뇌손상모형제비후7d,기록대서생존정황,처사후취뇌,계산구뇌복후내측핵급해마CA3구좌우측정상신경원밀도비치;분리좌측화우측대뇌반구병칭중,계산좌우측대뇌반구질량백분비.결과 4조대서생존솔비교차이무통계학의의(P＞0.05);여S조비교,HIBI조화HI조구뇌복후내측핵급해마CA3구좌우측정상신경원밀도비치、좌측대뇌반구질량급좌우측대뇌반구질량백분비강저,뇌조직mPTP개방정도승고(P＜0.05),I조상술각항지표차이무통계학의의(P＞0.05);여HIBI조비교,HI조구뇌복후내측핵급해마CA3구좌우측정상신경원밀도비치、좌측대뇌반구질량급좌우측대뇌반구질량백분비승고,뇌조직mPTP개방정도강저(P＜0.05).결론 이불미후처리감경신생대서뇌결혈결양성뇌손상적궤제가능여억제뇌조직mPTP개방유관.
Objective To evaluate the effects of isoflurane postconditioning on mitochondrial permeability transition pore (mPTP) in brain tissues of neonatal rats with hypoxic-ischemic brain injury.Methods One hundred and twenty 7-day-old Sprague-Dawley rats,weighing 12-16 g,were randomly divided into 4 groups (n =30 each) using a random number table:sham operation group (group S),isoflurane group (group I),hypoxicischemic brain injury group (group HIBI),and hypoxic-ischemic brain injury + isoflurane postconditioning group (group HI).To establish hypoxic-ischemic brain injury model in the neonatal rats,the left common carotid artery ligation was carried out,and then the rats were exposed to 8％ O2 + 92％ N2 at 37 ℃ for 2 h in HIBI and HI groups.The rats inhaled 1.5 ％ isoflurane for 30 min after the model was established in group HI.The rats only inhaled 1.5％ isoflurane for 30 min in group I.At 24 h after the model was established,10 rats taken out randomly in each group were sacrificed and brains were removed to detect mPTP opening.At 7 days after the model was established,the survival rate was recorded in the rest rats.The rats were then sacrificed and brains were removed and the right and left cerebral hemispheres were weighed separately,and the ratio between left/right cerebral hemispheres was calculated.The density of normal neurons in ventral posterior inferior thalamic nucleus and hippocampal CA3 region in the left and right cerebral hemispheres were measured and the ratios of the density of normal neurons in the left to right cerebral hemisphere were calculated.Results There was no significant difference in the survival rate between the four groups (P ＞ 0.05).Compared with group S,the ratios of the density of normal neurons in the left to right cerebral hemisphere,weight of left cerebral hemisphere,and ratio between left/right cerebral hemispheres were significantly decreased,and mPTP opening was increased in group HIBI (P ＜ 0.05),and no significant changes were found in the parameters mentioned above in group I (P ＞ 0.05).Compared with group HIBI,the ratios of the density of normal neurons in the left to right cerebral hemisphere,weight of left cerebral hemisphere,and ratio between left/right cerebral hemispheres were significantly increased,and mPTP opening was decreased in group HI (P ＜ 0.05).Conclusion The mechanism by which isoflurane postconditioning reduces hypoxic-ischemic brain injury may be related to inhibition of mPTP opening in brain tissues of neonatal rats.