急性失血性贫血对机械通气大鼠脑功能和血气的影响

王娟红; 李玉兰; 王瑞; 贾强; 王敏

doi:10.13201/j.issn.1009-5918.2018.09.010

急性失血性贫血对机械通气大鼠脑功能和血气的影响

- 兰州大学第一医院麻醉科(兰州, 730000)

详细信息

通讯作者: 李玉兰,E-mail:jasm@sina.com

中图分类号: R614

收稿日期: 2018-07-01

Effect of acute hemorrhagic anemia on cerebral function and arterial blood gas analysis in mechanically ventilated rats

- Department of Anesthesiology, the First Hospital of Lanzhou University, Lanzhou, 730000, China

More Information

Corresponding author: LI Yulan, E-mail: jasm@sina.com

Received Date: 01 July 2018

摘要

摘要: 目的:研究不同程度急性失血对机械通气大鼠感觉、记忆功能的影响及其受损的失血极限。方法:成年Wistar大鼠60只,随机分为5组(每组12只):G₀组(不放血)、G₂组(放血20%)、G₄组(放血40%)、G₆组(放血60%)、G₈组(放血80%)。大鼠麻醉后行气管插管机械通气,颈动脉插管用于放血及监测血压,股静脉插管用于液体复苏。复苏后即刻行血气分析,计算动脉血氧含量(CaO₂)。复苏结束后24 h行移除黏附物实验,测定移除黏附物时间(RAT)评价感觉功能;行水迷宫及八臂迷宫实验,测定逃避潜伏期(ELP)、穿越平台次数(CPF)、参考记忆错误(RME)和工作记忆错误(WME),评价记忆功能并计算24 h病死率。结束后取大脑海马组织,镜下观察CA1区神经元病理改变。结果:①与G₀组比较,G₂、G₄、G₆、G₈组CaO₂逐次降低(G₈642),G₄、G₆组RAT明显延长,且G₆>G₄,差异均有统计学意义(P<0.05),G₂组RAT无明显变化(P>0.05)。②水迷宫及八臂迷宫实验:与G₀组比较,G₄、G₆组ELP显著延长(G₆>G₄,P<0.05),G₂组无明显变化(P>0.05);G₆组CPF、WME均显著增加(P<0.05),其余各组无明显差异(P>0.05)。③病理切片显示G₀、G₂、G₄组CA1区神经元形态完整,排列整齐,大小均匀,G₆组和G₈组CA1区神经元发生了核固缩及核碎裂,G₈组较G₆组改变明显,部分G₈组神经元发生了核溶解。结论:急性失血40%持续24 h后,感觉、短期记忆功能显著减退,海马神经元形态无明显差异;失血60%持续24 h后,感觉及短期记忆功能显著受损,部分海马神经元出现破坏性损伤,24 h病死率为41.7%;失血80%时,24 h内病死率为100%,海马神经元出现不可逆损伤。引起大脑感觉、短期记忆功能受损的急性失血极限为40%,海马神经元损伤的急性失血极限为60%。
- 失血性贫血 /
- 机械通气 /
- 感觉 /
- 记忆
Abstract: Objective:To investigate the effect of varying degrees of acute blood loss on sensation and memory function in mechanically ventilated rats and evaluate the extreme limit of causing cerebral dysfunction. Method:Sixty adult Wistar rats were randomly assigned into 5 groups(n=12):group G₀ (sham hemorrhaged),group G₂ (20% hemorrhage),group G₄(40% hemorrhage),group G₆(60% hemorrhage),group G₈(80% hemorrhage).All rats were anesthetized and mechanically ventilated,carotid artery was cannulated for bloodletting and arterial pressure monitoring,and femoral venous cannula was used for fluid resuscitation.Arterial blood gas analysis was conducted after resuscitation,as well as calculated the blood oxygen content(CaO2).Remove adhesion experiment was conducted by measuring remove adhesive time(RAT)for evaluation of sensation function at 24 h after resuscitation.Morris water maze(MWM)and eight-arm maze experiment were conducted by measuring escape latency period(ELP),cross platform reference(CPF),reference memory errors(RME)and working memory errors(WME)for estimation of memory function 24 h after resuscitation,and mortality of 24 h was calculated.The pathological change of the neurons at hippocampal CA1 area was examined. Result:①Compared with group G₀,the CaO₂ of group G₂,G₄,G₆ and G₈ was reduced successively(G₈642,P<0.01).The RAT of group G₄ and G₆ was obviously prolonged(G₆>G₄,P<0.05),there was no significant difference in group G₂.②The MWM and eight-arm maze test:Compared with group G₀,the ELP of group G₄ and G₆ increased significantly(G₆>G₄,P<0.05),there was no significant difference in group G₂.The CPF and WME of group G₆ increased significantly(P<0.05).③Pathological section:the cellular morphology of the neurons at hippocampal CA1 area in group G₀,G₂ and G₄ did not change obviously,morphological changes including karyopyknosis and karyorrhexis was observed in the nerons of group G₆ and G₈,and karyolysis of neurons could be seen in group G₈.Conclusion:The sensation and short-term memory function decreased significantly 24 h after 40% of blood loss,but no obvious changes in hippocampal neurons.The sensation and short-term memory function significantly impaired and destructive damage of the hippocampus neurons can be seen obviously at 24 h after 60% of blood loss,and the mortality rate of 24 h was 41.7%.Irreversible damage could be observed in part of hippocampus neurons after 80% of blood loss,and the mortality rate of 24 h was 100%.The blood loss limit which cause injury of cerebral sensation and memory function is about 40%,and the blood loss limit which cause damages of hippocampus neurons is about 60%.
- hemorrhage anemia /
- mechanical ventilation /
- sensation /
- memory

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