深低温停循环后脑损伤的动物实验研究
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摘要
第一部分小预充量体外循环在深低温停循环中脑保护效果的动物实验研究
目的:建立联合兔脑微透析和体外循环(CPB)及深低温停循环(DHCA)动物实验模型,探讨小预充量体外循环在深低温停循环中的脑保护效果。
方法:成年雄性新西兰白兔19只,随机分配到假手术组(S组,n=5),小预充量CPB组(L组,n=7),大预充量CPB组(H组,n=7),预充量分别为75ml和210ml。首先在兔的脑内海马CA1区定位,埋植微透析针导轨并安装透析针保护罩。埋针36小时后开始微透析,并建立CPB和DHCA模型。CPB降温至16—18℃,停循环60min,复温30min。微透析每30min取样一次,持续到脱离CPB后2小时。整个过程中持续监测心率、动脉血压、肛温,间断血气检查PaCO_2、PaO_2、HCT。CPB术后2小时处死动物,留取脑顶叶皮层和海马CA1区组织,分别作组织病理学、电镜、TUNEL检测;对微透析样品用高效液相色谱法和CMA600分析仪进行葡萄糖、乳酸、丙酮酸和谷氨酸检测。
结果:为保证在整个实验过程中,L组和H组的血压和酸碱平衡控制在正常生理范围内,H组所用的血管活性药物多巴胺和碳酸氢钠的量明显高于L组(P＜0.05)。微透析检测显示,在H组中反映能量代谢状况指标乳酸/丙酮酸和乳酸/葡萄糖比值在脱离CPB后显著高于L组(P＜0.05);反映神经兴奋毒性作用的指标谷氨酸水平在两组DHCA后显著升高,脱离CPB后L组谷氨酸逐渐恢复到基础水平,而H组谷氨酸仍维持在高水平。组织病理学、电镜、TUNEL检测显示H组脑组织损伤程度明显重于L组(P＜0.05)。
结论:在应用DHCA情况下,小预充量CPB同大预充量CPB相比有显著的脑保护作用。
第二部分深低温停循环后脑损伤分子机制的动物实验研究
目的:探讨深低温停循环(DHCA)后脑损伤的分子机制中是否存有细胞能量障碍、兴奋性神经毒性作用、聚腺苷二磷酸核糖转移酶-1(PARP-1)过度激活及细胞坏死和(或)凋亡这些分子事件。
方法:成年雄性新西兰白兔22只,随机分配到CPB组(n=11),DHCA组(L组,n=11)。首先在兔的脑内海马CA1区定位,埋植微透析针导轨并安装透析针保护罩。埋针36小时后开始微透析,并建立CPB和DHCA模型。CPB降温至16—18℃,停循环60min,复温30min。微透析每30min取样一次,持续到脱离CPB后2小时。整个过程中持续监测心率、动脉血压、肛温,间断血气检查PaCO_2、PaO_2、HCT。CPB术后2小时处死动物,留取脑顶叶皮层和海马CA1区组织,分别进行HE染色、PARP-1活性和原位细胞凋亡检测和PARP-1的Western Blot检测。对微透析样品用高效液相色谱法和CMA600分析仪进行葡萄糖、乳酸、丙酮酸和谷氨酸检测。
结果:微透析的结果显示DHCA组的乳酸/丙酮酸和乳酸/葡萄糖比值及谷氨酸浓度较单纯CPB组和术前基础水平显著升高;组织学检测结果提示,DHCA组脑损伤程度、PARP-1激活程度和细胞凋亡发生率较单纯CPB组增高。
结论:在DHCA后脑损伤的分子机制中存有以下分子事件—细胞能量障碍、兴奋性神经毒性作用、PARP-1过度激活及细胞坏死和(或)凋亡,共同作用导致脑损伤,在DHCA后脑损伤的分子机制中发挥重要作用。
Part One Neuroprotective Effect of Deep Hypothermic Circulatory Arrest with Low Priming Volume:Study in a Rabbit Model
Objective:The aim of the study was to investigate the possible neuroprotective effects of a low priming volume following deep hypothermic circulatory arrest (DHCA) by setting up a model of cardiopulmonary bypass(CPB) and DHCA associated with cerebral microdialysis in rabbits.
Method:Rabbits were randomized into three groups:DHCA with low priming volume(Group L,n=7),DHCA with high priming volume(Group H,n=7),and sham-operated goup(Group S,n=5).The priming volume of Groups L and H were 75mi and 210ml,respectively.The rabbits were simultaneously placed on CPB and brain microdialysis,cooled to 16 to 18℃with DHCA for 60 minutes.After weaning from CPB,the animals were monitored and observed up to 2 hours of recovery.The microdialysis was continuous from consciousness to recovery from CPB. Physiological parameters were regularly recorded.The extracellular levels of glutamate,glucose,lactate,and pyruvate in the hippocampus were collected by microdialysis and measured by HPLC and a microdialysis analyzer.The brain tissue sections,in parietal cortex and hippocampus(CA1),for morphological studies were stained with hematoxylin and eosin and TUNEL,simultaneously,examined by electron microscope.Brain damage was evaluated by these three means.Statistical analysis was performed with the SPSS 13.0.All data were expressed as mean+ standard deviation(SD).Different groups were compared by one-way analysis of variance(ANOVA).Repeated measures ANOVA or Kruskal-Willis analysis were used for comparisons between relevant time-points and the baseline in the same group. A p value of less than 0.05 was considered statistically significant.
Results:In order to keep the mean arterial pressure and acid-base balance within defined physiological ranges,more doses of dopamine and sodium bicarbonate were administered in Group H than in Group L(P＜0.05).The ratios of lactate/glucose and lactate/pyruvate in Group H increased significantly compared with those in Group L from the beginning of weaning from CPB(P＜0.05).The levels of extracellular glutamate in the two DHCA groups increased significantly(p＜0.05).After weaning from CPB,the glutamate values in Group H remained at higher levels compared with those in Group L(P＜0.05).The percentage of injured neurons,TUNEL positive staining,and the mitochondria score of the hippocampus CA1 in Group H were significantly higher than in Group L(P＜0.05).
Conclusions:A low priming volume during DHCA could have a neuroprotective effect compared with a high priming volume.
Part Two Molecular Events in Neuronal Injury after Deep Hypothermic Circulatory Arrest:Study in a Rabbit Model
Objective:Although deep hypothermic circulatory arrest has been known to induce neuronal injury,the molecular mechanism of this damage has not been identified.We studied the key molecular mediators through cellular energy failure, excitotoxicity,and overactivation of poly(adenosine diphosphate-ribose) polymerase 1(PARP-1) in brain tissues of a rabbit model of deep hypothermic circulatory arrest similar to clinical settings.
Method:We established 2 models of cardiopulmonary bypass(n=11) and deep hypothermic circulatory arrest(n=11) associated with cerebral microdialysis in rabbits.Deep hypothermic circulatory arrest lasted for 60 minutes.The measurements of glucose,lactate,pyruvate,and glutamate collected by means of microdialysis were quantified by using a microdialysis analyzer and high-performance liquid chromatography.The overactivation of PARP-1 was assessed by detecting immunostaining of poly(adenosine diphosphate-ribose)(PAR).Histologic studies were used to identify neuronal morphologic changes,and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling staining(TUNEL) and PARP-1 Western blotting were used to identify apoptotic cells and early apoptotic signals.
Results:Deep hypothermic circulatory arrest significantly increased the lactate/pyruvate and lactate/glucose ratios and the glutamate value,whereas cardiopulmonary bypass did not(P＜0.05).Deep hypothermic circulatory arrest significantly increased the numbers of PAR-positive and apoptotic neurons compared with cardiopulmonary bypass(P＜0.05).The cleavage of PARP-1 was only found in the deep hypothermic circulatory arrest group.More injured neurons were found in the deep hypothermic circulatory arrest group(histologic scores,P＜0.05).
Conclusions:This study demonstrated that deep hypothermic circulatory arrest results in a series of molecular events consisting of cellular energy failure, excitotoxicity,overactivation of PARP-1,and necrosis and/or apoptosis in neuronal injury.
目的:建立联合兔脑微透析和体外循环(CPB)及深低温停循环(DHCA)动物实验模型,探讨小预充量体外循环在深低温停循环中的脑保护效果。
方法:成年雄性新西兰白兔19只,随机分配到假手术组(S组,n=5),小预充量CPB组(L组,n=7),大预充量CPB组(H组,n=7),预充量分别为75ml和210ml。首先在兔的脑内海马CA1区定位,埋植微透析针导轨并安装透析针保护罩。埋针36小时后开始微透析,并建立CPB和DHCA模型。CPB降温至16—18℃,停循环60min,复温30min。微透析每30min取样一次,持续到脱离CPB后2小时。整个过程中持续监测心率、动脉血压、肛温,间断血气检查PaCO_2、PaO_2、HCT。CPB术后2小时处死动物,留取脑顶叶皮层和海马CA1区组织,分别作组织病理学、电镜、TUNEL检测;对微透析样品用高效液相色谱法和CMA600分析仪进行葡萄糖、乳酸、丙酮酸和谷氨酸检测。
结果:为保证在整个实验过程中,L组和H组的血压和酸碱平衡控制在正常生理范围内,H组所用的血管活性药物多巴胺和碳酸氢钠的量明显高于L组(P＜0.05)。微透析检测显示,在H组中反映能量代谢状况指标乳酸/丙酮酸和乳酸/葡萄糖比值在脱离CPB后显著高于L组(P＜0.05);反映神经兴奋毒性作用的指标谷氨酸水平在两组DHCA后显著升高,脱离CPB后L组谷氨酸逐渐恢复到基础水平,而H组谷氨酸仍维持在高水平。组织病理学、电镜、TUNEL检测显示H组脑组织损伤程度明显重于L组(P＜0.05)。
结论:在应用DHCA情况下,小预充量CPB同大预充量CPB相比有显著的脑保护作用。
第二部分深低温停循环后脑损伤分子机制的动物实验研究
目的:探讨深低温停循环(DHCA)后脑损伤的分子机制中是否存有细胞能量障碍、兴奋性神经毒性作用、聚腺苷二磷酸核糖转移酶-1(PARP-1)过度激活及细胞坏死和(或)凋亡这些分子事件。
方法:成年雄性新西兰白兔22只,随机分配到CPB组(n=11),DHCA组(L组,n=11)。首先在兔的脑内海马CA1区定位,埋植微透析针导轨并安装透析针保护罩。埋针36小时后开始微透析,并建立CPB和DHCA模型。CPB降温至16—18℃,停循环60min,复温30min。微透析每30min取样一次,持续到脱离CPB后2小时。整个过程中持续监测心率、动脉血压、肛温,间断血气检查PaCO_2、PaO_2、HCT。CPB术后2小时处死动物,留取脑顶叶皮层和海马CA1区组织,分别进行HE染色、PARP-1活性和原位细胞凋亡检测和PARP-1的Western Blot检测。对微透析样品用高效液相色谱法和CMA600分析仪进行葡萄糖、乳酸、丙酮酸和谷氨酸检测。
结果:微透析的结果显示DHCA组的乳酸/丙酮酸和乳酸/葡萄糖比值及谷氨酸浓度较单纯CPB组和术前基础水平显著升高;组织学检测结果提示,DHCA组脑损伤程度、PARP-1激活程度和细胞凋亡发生率较单纯CPB组增高。
结论:在DHCA后脑损伤的分子机制中存有以下分子事件—细胞能量障碍、兴奋性神经毒性作用、PARP-1过度激活及细胞坏死和(或)凋亡,共同作用导致脑损伤,在DHCA后脑损伤的分子机制中发挥重要作用。
Part One Neuroprotective Effect of Deep Hypothermic Circulatory Arrest with Low Priming Volume:Study in a Rabbit Model
Objective:The aim of the study was to investigate the possible neuroprotective effects of a low priming volume following deep hypothermic circulatory arrest (DHCA) by setting up a model of cardiopulmonary bypass(CPB) and DHCA associated with cerebral microdialysis in rabbits.
Method:Rabbits were randomized into three groups:DHCA with low priming volume(Group L,n=7),DHCA with high priming volume(Group H,n=7),and sham-operated goup(Group S,n=5).The priming volume of Groups L and H were 75mi and 210ml,respectively.The rabbits were simultaneously placed on CPB and brain microdialysis,cooled to 16 to 18℃with DHCA for 60 minutes.After weaning from CPB,the animals were monitored and observed up to 2 hours of recovery.The microdialysis was continuous from consciousness to recovery from CPB. Physiological parameters were regularly recorded.The extracellular levels of glutamate,glucose,lactate,and pyruvate in the hippocampus were collected by microdialysis and measured by HPLC and a microdialysis analyzer.The brain tissue sections,in parietal cortex and hippocampus(CA1),for morphological studies were stained with hematoxylin and eosin and TUNEL,simultaneously,examined by electron microscope.Brain damage was evaluated by these three means.Statistical analysis was performed with the SPSS 13.0.All data were expressed as mean+ standard deviation(SD).Different groups were compared by one-way analysis of variance(ANOVA).Repeated measures ANOVA or Kruskal-Willis analysis were used for comparisons between relevant time-points and the baseline in the same group. A p value of less than 0.05 was considered statistically significant.
Results:In order to keep the mean arterial pressure and acid-base balance within defined physiological ranges,more doses of dopamine and sodium bicarbonate were administered in Group H than in Group L(P＜0.05).The ratios of lactate/glucose and lactate/pyruvate in Group H increased significantly compared with those in Group L from the beginning of weaning from CPB(P＜0.05).The levels of extracellular glutamate in the two DHCA groups increased significantly(p＜0.05).After weaning from CPB,the glutamate values in Group H remained at higher levels compared with those in Group L(P＜0.05).The percentage of injured neurons,TUNEL positive staining,and the mitochondria score of the hippocampus CA1 in Group H were significantly higher than in Group L(P＜0.05).
Conclusions:A low priming volume during DHCA could have a neuroprotective effect compared with a high priming volume.
Part Two Molecular Events in Neuronal Injury after Deep Hypothermic Circulatory Arrest:Study in a Rabbit Model
Objective:Although deep hypothermic circulatory arrest has been known to induce neuronal injury,the molecular mechanism of this damage has not been identified.We studied the key molecular mediators through cellular energy failure, excitotoxicity,and overactivation of poly(adenosine diphosphate-ribose) polymerase 1(PARP-1) in brain tissues of a rabbit model of deep hypothermic circulatory arrest similar to clinical settings.
Method:We established 2 models of cardiopulmonary bypass(n=11) and deep hypothermic circulatory arrest(n=11) associated with cerebral microdialysis in rabbits.Deep hypothermic circulatory arrest lasted for 60 minutes.The measurements of glucose,lactate,pyruvate,and glutamate collected by means of microdialysis were quantified by using a microdialysis analyzer and high-performance liquid chromatography.The overactivation of PARP-1 was assessed by detecting immunostaining of poly(adenosine diphosphate-ribose)(PAR).Histologic studies were used to identify neuronal morphologic changes,and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling staining(TUNEL) and PARP-1 Western blotting were used to identify apoptotic cells and early apoptotic signals.
Results:Deep hypothermic circulatory arrest significantly increased the lactate/pyruvate and lactate/glucose ratios and the glutamate value,whereas cardiopulmonary bypass did not(P＜0.05).Deep hypothermic circulatory arrest significantly increased the numbers of PAR-positive and apoptotic neurons compared with cardiopulmonary bypass(P＜0.05).The cleavage of PARP-1 was only found in the deep hypothermic circulatory arrest group.More injured neurons were found in the deep hypothermic circulatory arrest group(histologic scores,P＜0.05).
Conclusions:This study demonstrated that deep hypothermic circulatory arrest results in a series of molecular events consisting of cellular energy failure, excitotoxicity,overactivation of PARP-1,and necrosis and/or apoptosis in neuronal injury.
引文
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