脑外伤大鼠血液粘度、血液气体变化及其相关性的研究
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摘要
目的:观测高空重物自由落体致大鼠脑外伤模型血液粘度和血液气体的变化,探寻其变化规律并分析变化原因。为脑外伤临床诊治提供参考,也为脑损伤研究提供继发性损伤的血液学因素。
方法:采用高空自由落体砝码致大鼠弥散性脑外伤,建立脑外伤大鼠模型,取右心房新鲜混合静脉血,分别用血液粘度仪、血气分析仪(采用G3~+测试片)检测受伤后大鼠血液粘度和血液气体变化的指标。
结果:
1、脑外伤大鼠在伤后高切低切下的血液粘度均高于正常对照组,具有显著性差异(p＜0.05),且变化趋势明显。在伤后30分钟、1天组出现血液粘度变化的两次高峰;伤后8小时、5天组出现血液粘度的两次低峰。
2、脑外伤大鼠血液PH值、PCO_2、PO_2随着大鼠伤后持续时间不同,出现明显的变化趋势。PH值在受伤后数分钟内略有升高,30分钟、1天组出现两次低峰,在6小时组出现一次高峰,然后趋势平缓;PCO_2在30分钟,1天组出现两次高峰,6小时出现一次低峰,然后略有下降后趋于平缓;PO_2在伤后10min略有升高,然后逐渐下降,12小时组出现一次低峰,随后缓慢升高。
结论
1、大鼠脑外伤可致血液粘度增高,增高程度随着受伤后持续时间不同在伤后30分钟、1天出现两次高峰。
2、大鼠脑外伤可致血液PH值下降,伤后30分钟,1天出现两次低峰。
3、大鼠脑外伤可致PCO_2升高,伤后30分钟,1天出现两次高峰。
4、大鼠脑外伤可致PO_2下降,伤后12小时出现一次低峰。
5、血液粘度变化和血液气体变化有明显的相关性。
6、血液粘度和血液气体与脑外伤后的继发性病理生理改变可能相关。
Objective:to observe blood viscosity and blood gas variations after the rats' brain trauma were percussed by heavy free-falling,and seek its change discipline and reason for clinical treatments and hematology factor of secondary trauma.
Methods:Use weights-free-falling brain injury model to cause brain injury and take out mixed venous blood from right atrium to detect blood viscosity and blood gas variations by blood viscograph and blood-gas analysis meter.
Results:
1.The blood viscosity of high-low Shear rate of brain trauma rats group was significant higher the control(P＜0.05),and blood viscosity appeared peak after they had injured for 30 minutes and one day and seven days respectively,then the blood viscosity appeared platykurtosis after they had injured for eight hours and five days.
2.The blood pH value and PCO_2 and PO_2 were different with rats keeping different times after they injured.The pH value hoisted after they injured for several minutes,and dropped to platykurtosis after 30 minutes and one day,and then appeared peak at six hours and tow days,and then went to dropoff;The PCO_2 appeared peak at thirty minutes and one day separately,and then appeared platykurtosis at six hours and tow days,and afterwards it went down then tend to platykurtosis;The PO_2 went up at ten minutes,and then went down gradually,and went to platykurtosis at 12 hours,and afterwards went up slowly.
Conclusion:
1.The brain trauma could make rats blood viscosity increase,moreover appeared peak after they injured for thirty minutes and one day and seven days separately.
2.The brain trauma could cause pH value to drop,and appeared platykurtosis at thirty minutes and one day separately.
3.The brain trauma could make PCO_2 rise,and appeared peak at thirty minutes and one day separately.
4.The brain trauma could cause PO_2 to drop,and appeared platykurtosis at 12 hours.
5.The blood viscosity variations was obvious relativity with the blood gas variations.
6.The blood viscosity and blood gas variations may was relativity with secondary variations after traumatic brain injury.
方法:采用高空自由落体砝码致大鼠弥散性脑外伤,建立脑外伤大鼠模型,取右心房新鲜混合静脉血,分别用血液粘度仪、血气分析仪(采用G3~+测试片)检测受伤后大鼠血液粘度和血液气体变化的指标。
结果:
1、脑外伤大鼠在伤后高切低切下的血液粘度均高于正常对照组,具有显著性差异(p＜0.05),且变化趋势明显。在伤后30分钟、1天组出现血液粘度变化的两次高峰;伤后8小时、5天组出现血液粘度的两次低峰。
2、脑外伤大鼠血液PH值、PCO_2、PO_2随着大鼠伤后持续时间不同,出现明显的变化趋势。PH值在受伤后数分钟内略有升高,30分钟、1天组出现两次低峰,在6小时组出现一次高峰,然后趋势平缓;PCO_2在30分钟,1天组出现两次高峰,6小时出现一次低峰,然后略有下降后趋于平缓;PO_2在伤后10min略有升高,然后逐渐下降,12小时组出现一次低峰,随后缓慢升高。
结论
1、大鼠脑外伤可致血液粘度增高,增高程度随着受伤后持续时间不同在伤后30分钟、1天出现两次高峰。
2、大鼠脑外伤可致血液PH值下降,伤后30分钟,1天出现两次低峰。
3、大鼠脑外伤可致PCO_2升高,伤后30分钟,1天出现两次高峰。
4、大鼠脑外伤可致PO_2下降,伤后12小时出现一次低峰。
5、血液粘度变化和血液气体变化有明显的相关性。
6、血液粘度和血液气体与脑外伤后的继发性病理生理改变可能相关。
Objective:to observe blood viscosity and blood gas variations after the rats' brain trauma were percussed by heavy free-falling,and seek its change discipline and reason for clinical treatments and hematology factor of secondary trauma.
Methods:Use weights-free-falling brain injury model to cause brain injury and take out mixed venous blood from right atrium to detect blood viscosity and blood gas variations by blood viscograph and blood-gas analysis meter.
Results:
1.The blood viscosity of high-low Shear rate of brain trauma rats group was significant higher the control(P＜0.05),and blood viscosity appeared peak after they had injured for 30 minutes and one day and seven days respectively,then the blood viscosity appeared platykurtosis after they had injured for eight hours and five days.
2.The blood pH value and PCO_2 and PO_2 were different with rats keeping different times after they injured.The pH value hoisted after they injured for several minutes,and dropped to platykurtosis after 30 minutes and one day,and then appeared peak at six hours and tow days,and then went to dropoff;The PCO_2 appeared peak at thirty minutes and one day separately,and then appeared platykurtosis at six hours and tow days,and afterwards it went down then tend to platykurtosis;The PO_2 went up at ten minutes,and then went down gradually,and went to platykurtosis at 12 hours,and afterwards went up slowly.
Conclusion:
1.The brain trauma could make rats blood viscosity increase,moreover appeared peak after they injured for thirty minutes and one day and seven days separately.
2.The brain trauma could cause pH value to drop,and appeared platykurtosis at thirty minutes and one day separately.
3.The brain trauma could make PCO_2 rise,and appeared peak at thirty minutes and one day separately.
4.The brain trauma could cause PO_2 to drop,and appeared platykurtosis at 12 hours.
5.The blood viscosity variations was obvious relativity with the blood gas variations.
6.The blood viscosity and blood gas variations may was relativity with secondary variations after traumatic brain injury.
引文
[1]金惠铭,陈达信,闫友珍,等.静脉注射高分子右旋糖酐复制家兔急性微循环障碍模型的实验研究[J].中国急救医学杂志.1982,2(3):37-41
[2]吴云鹏等.临床血液流变学问答.南京大学出版社.1991,108
[3]余猛进,杨瑞和.血液流变学及其临床应用.上海医学.1997,20(2):117
[4]邸氏,高立达,陈槐卿。脑伤后血液流变学变化对脑微循环影响的临床研究[J].中华神经外科杂志,1994,10(2):82-82
[5]刘信桥,钱冠清,金惠铭.血液流变性障碍在血栓形成中的作用[J].微循环技术杂志,1993,1(2):104-104
[6]Pearson TG Vascular occlusive episodes and venous hematocrit in primary polycythem ia[J].Lancet,1978,2:1219
[7]徐新民,戴文光,李全珍.重型脑损伤患者血液流变学变化及临床意义[J].中国危重病急救医学,1997,9(11):673-673
[8]戚仁铎,王友赤.诊断学,人民卫生出版社,1996,4,263-264
[9]钱东翔,黄东健.何炳威等甘油果糖和甘露醇对脑损伤后血流变影响的对比,广州医学院学报1999,第27卷,第3期
[10]黄东健,钱东翔,王智坚,等.氦氖激光血管内照射治疗脑损伤对血液流变学的影响[J].中华理疗杂志,1999,第22卷,第5期
[11]姜明辉,刘多三。实验性脑缺血微血管超微结构的观察.中华神经精神科杂志,1990,23(6):342-344
[12]陈晔,王文字,王致喻,等.局部缺血猫脑的透射电镜观察。中国神经精神疾病杂志,1991,17:139-141
[13]徐如祥,易声禹.脑损伤后神经细胞Ca2+通道变化及其对BBB和脑水肿的影响.第一军医大学学报,1994,第14卷第1期
[14]Weyer F B.Calcium,neuronal hyperexitability and is chemic injury.Brain Res Rev 1989;14:227-243
[15]张萍,李立.脑损伤与神经细胞钙通道变化.国外医学神经病学神经外科学分册,1994,第21卷第1期,15-17
[16]Kristian T,Siesj BJ.Calcium-related damage in ischemia.Life Sci,1996,59(516):357-367
[17]Swartz KJ.Modulation of Ca2+channels by kinase C in rat centra and peripheral neurons:distribution of G protein-mediated inhibition.Neuron,1993,11(2):305-320
[18]Silver IA,Erecinska M.Intracellular and extracelluar changes of (Ca2+) in hypoxia and ischemia in rat brain in vivo J Gen physiol,1990,95(5):837-866.
[19]Yamazakl M,et al.The effect of nicardiping on morphological changes and calcium accumulation during hypoxia in pyramidal nervecell in the rat cerebral cortex.Masui,1989,38(10):1264-1270.
[20]Lewen A,Matz p,Chan PH,Free radical pathways in CNS injury J Neurotrauma,2000,17(10):871-890
[21]李鸣皋,郝唯蔚,俞启福,等.急性缺氧对大鼠血浆内皮素前体原影响 的研究.中华航空航天医学杂志,1999,10(1):32-34
[22]Burmester T,weich B,Reinhardt S,et al.A vertebrate globin expressed in the brain.Nature,2000,407:520-523
[23]Stoltz JF.Introduction to hemorheology:theoretical aspects and hyperviscosity syndromes(J).Int Angiol,1987,6(2):119-132.
[24]张荣军,游潮,等.Feeney法建立大鼠闭合性脑损伤模型及评估.中国修复重建外科杂志,2005,第19卷第12期
[25]吴桂荣,张云然,等.猴头部冲击性脑损伤的判别.航天医学与医学工程,1998,12第11卷第六期。
[26]Veleev EK.The microcirculatory bed and blood rheological properties in the acute period of severe craniocerebral trauma.Zh Vopr Neirokhir,1989,3:24.
[27]潘亚文,康笃伦,裘明德,骆力.中国血液流变学杂志,1999,年、第9卷、第4期
[28]黄东健,钱东翔,王智坚,等.氦氖激光血管内照射治疗脑损伤对血液流变学的影响[J].中华理疗杂志,1999,第22卷,第5期
[29]钱东翔,黄东健,何炳威,等.广州医学院学报1999,第27卷,第3期
[30]刘佰运,王忠诚,富壮,等.脑外伤后血液流变学变化的相关因素分析.中国急救医学2000年2月第20卷第2期
[31]李哲由.脑外伤患者呼吸道不全阻塞原因浅探.实用医技杂志,2007,12月14卷35期。
[32]刘卫平,章翔,易声禹,等.大鼠急性颅脑损伤后脑微循环变化的实验研究.创伤外科杂志第3卷增刊[J]
[33]邓美玉,张成岗,等.大鼠缺氧缺血性脑损伤脑组织中脑红蛋白基因表达的变化.中华病理学杂志,2002,6月第31卷第3期。
[2]吴云鹏等.临床血液流变学问答.南京大学出版社.1991,108
[3]余猛进,杨瑞和.血液流变学及其临床应用.上海医学.1997,20(2):117
[4]邸氏,高立达,陈槐卿。脑伤后血液流变学变化对脑微循环影响的临床研究[J].中华神经外科杂志,1994,10(2):82-82
[5]刘信桥,钱冠清,金惠铭.血液流变性障碍在血栓形成中的作用[J].微循环技术杂志,1993,1(2):104-104
[6]Pearson TG Vascular occlusive episodes and venous hematocrit in primary polycythem ia[J].Lancet,1978,2:1219
[7]徐新民,戴文光,李全珍.重型脑损伤患者血液流变学变化及临床意义[J].中国危重病急救医学,1997,9(11):673-673
[8]戚仁铎,王友赤.诊断学,人民卫生出版社,1996,4,263-264
[9]钱东翔,黄东健.何炳威等甘油果糖和甘露醇对脑损伤后血流变影响的对比,广州医学院学报1999,第27卷,第3期
[10]黄东健,钱东翔,王智坚,等.氦氖激光血管内照射治疗脑损伤对血液流变学的影响[J].中华理疗杂志,1999,第22卷,第5期
[11]姜明辉,刘多三。实验性脑缺血微血管超微结构的观察.中华神经精神科杂志,1990,23(6):342-344
[12]陈晔,王文字,王致喻,等.局部缺血猫脑的透射电镜观察。中国神经精神疾病杂志,1991,17:139-141
[13]徐如祥,易声禹.脑损伤后神经细胞Ca2+通道变化及其对BBB和脑水肿的影响.第一军医大学学报,1994,第14卷第1期
[14]Weyer F B.Calcium,neuronal hyperexitability and is chemic injury.Brain Res Rev 1989;14:227-243
[15]张萍,李立.脑损伤与神经细胞钙通道变化.国外医学神经病学神经外科学分册,1994,第21卷第1期,15-17
[16]Kristian T,Siesj BJ.Calcium-related damage in ischemia.Life Sci,1996,59(516):357-367
[17]Swartz KJ.Modulation of Ca2+channels by kinase C in rat centra and peripheral neurons:distribution of G protein-mediated inhibition.Neuron,1993,11(2):305-320
[18]Silver IA,Erecinska M.Intracellular and extracelluar changes of (Ca2+) in hypoxia and ischemia in rat brain in vivo J Gen physiol,1990,95(5):837-866.
[19]Yamazakl M,et al.The effect of nicardiping on morphological changes and calcium accumulation during hypoxia in pyramidal nervecell in the rat cerebral cortex.Masui,1989,38(10):1264-1270.
[20]Lewen A,Matz p,Chan PH,Free radical pathways in CNS injury J Neurotrauma,2000,17(10):871-890
[21]李鸣皋,郝唯蔚,俞启福,等.急性缺氧对大鼠血浆内皮素前体原影响 的研究.中华航空航天医学杂志,1999,10(1):32-34
[22]Burmester T,weich B,Reinhardt S,et al.A vertebrate globin expressed in the brain.Nature,2000,407:520-523
[23]Stoltz JF.Introduction to hemorheology:theoretical aspects and hyperviscosity syndromes(J).Int Angiol,1987,6(2):119-132.
[24]张荣军,游潮,等.Feeney法建立大鼠闭合性脑损伤模型及评估.中国修复重建外科杂志,2005,第19卷第12期
[25]吴桂荣,张云然,等.猴头部冲击性脑损伤的判别.航天医学与医学工程,1998,12第11卷第六期。
[26]Veleev EK.The microcirculatory bed and blood rheological properties in the acute period of severe craniocerebral trauma.Zh Vopr Neirokhir,1989,3:24.
[27]潘亚文,康笃伦,裘明德,骆力.中国血液流变学杂志,1999,年、第9卷、第4期
[28]黄东健,钱东翔,王智坚,等.氦氖激光血管内照射治疗脑损伤对血液流变学的影响[J].中华理疗杂志,1999,第22卷,第5期
[29]钱东翔,黄东健,何炳威,等.广州医学院学报1999,第27卷,第3期
[30]刘佰运,王忠诚,富壮,等.脑外伤后血液流变学变化的相关因素分析.中国急救医学2000年2月第20卷第2期
[31]李哲由.脑外伤患者呼吸道不全阻塞原因浅探.实用医技杂志,2007,12月14卷35期。
[32]刘卫平,章翔,易声禹,等.大鼠急性颅脑损伤后脑微循环变化的实验研究.创伤外科杂志第3卷增刊[J]
[33]邓美玉,张成岗,等.大鼠缺氧缺血性脑损伤脑组织中脑红蛋白基因表达的变化.中华病理学杂志,2002,6月第31卷第3期。