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作 者:梅弘勋[1] 王恩真[1] 张绍东[2] 万虹[3] 王保国[1]
机构地区:[1]首都医科大学附属北京天坛医院麻醉科,100050 [2]中国医学科学院 [3]北京市神经外科研究所
出 处:《中华麻醉学杂志》2006年第4期322-325,共4页Chinese Journal of Anesthesiology
摘 要:目的观察不同液体复苏对颅脑外伤合并急性失血性休克大鼠脑细胞外液兴奋性氨基酸(EAA)和抑制性氨基酸(IAA)浓度的影响。方法 19只雄性SD大鼠,随机分为3组:0.9%生理盐水组(NS组,n=7);10%羟乙基淀粉组(HES组,n=6);高晶体-高胶体渗透压混合液组(HHS组,n= 6)。按照Feeney改良法制作颅脑外伤模型,经股动脉放血,使MAP降至40mm Hg左右,维持此血压1 h。制作颅脑外伤合并急性失血性休克模型后1 h,NS组经股静脉输入3倍于放血量的0.9%NaCl, HES组输入等于放血量的10%羟乙基淀粉,HHS组输入7.5%NaCl与10%羟乙基淀粉(1:1)混合液 4ml/kg。采用微透析技术收集脑外伤前(基础值)、脑外伤合并急性失血性休克期(1 h)、复苏期(2h)内脑外伤周边脑细胞外液,采用高效液相色谱法测定兴奋性氨基酸[谷氨酸(Glu)、天冬氨酸(Asp)]、抑制性氨基酸[甘氨酸(Cly)、γ-氨基丁酸(GABA)和牛磺酸(Tau)]的浓度。结果脑外伤合并急性失血性休克导致上述脑细胞外液5种氨基酸浓度均升高,生理盐水复苏导致脑细胞外液Glu进一步升高, HES和HHS复苏均能维持脑细胞外液GABA和Tau在较高水平,HES能抑制脑细胞外液Glu升高, HHS能抑制脑细胞外液Glu、Asp、Gly升高。结论对脑外伤合并急性失血性休克大鼠,生理盐水复苏增加脑EEA的释放,HES和HHS复苏均能抑制脑EEA释放,而HHS的作用强于HES。Objective To compare the effects of 0.9% NaCl (normal saline, NS), 10% hydroxyethyl starch (HES, 200/0.5) and hypertonic-hyperoncotic solution (HHS, 7.5% NaCl-10% HES 1:1) on cerebral extracellular excitatory amino acids (EAA) and inhibitory amino acids (IAA) in a rat model of traumatic head injury (THI) combined with acute hemorrhagic shock (AHS). Methods Nineteen healthy adult male SD rats weighing 300-350 g were randomized into 3 groups : NS group ( n = 7 ) ; HES group ( n = 6 ) and HHS group ( n = 6). THI was produced by modified Feeney method (a 20g weight drops from a height of 40 cm on the parietal region) and AHS was induced by modified Wiggers method (Blood was removed from femoral artery and MAP was maintained at 40 mm Hg for 1 hour). Fluid resuscitation was started at 1 hour of AHS with 0.9% NS (3 times the volume of the removed whole blood) or 10% HES (in a one to one ratio) or HHS 4 ml·kg^-1 administered over 15 min. The extracellular fluid of njured brain tissue was collected using intracerebral microdialysis before head injury (baseline) during THI + AHS (1h) and resuscitatin (2h) for determination of the levels of EAA (glutamate, aspartate) and IAA (glycine, GABA, taurine) by HPLC.Results The 5 amino acids were significantly increased during THI + AHS as compared with their baseline values. Glutamate level was further increased during resuscitation with NS. GABA and taurine concentrations were maintained at high level during resuscitation with HES or HHS. The increase in glutamate was inhibited by resuscitation with HES and the increase in glutamate, aspartate and glycine were inhibited by HHS. Conclusions In a rat model of THI combined with AHS, resuscitation with NS can increase cerebral extracellular EAA. Both HES and HHS resuscitation can inhibit the increase in cerebral extracellulaar EAA and HHS is more effective.
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