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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 observe the effects of different liquid resuscitation on the levels of EAA and IAA in brain tissue of traumatic brain injury combined with acute hemorrhagic shock in rats. Methods Nineteen male SD rats were randomly divided into three groups: 0.9% saline group (NS group, n = 7), 10% hydroxyethyl starch group (HES group, n = 6) Colloid Inhalation Mixture (HHS group, n = 6). In accordance with the Feeney modified method of making a model of traumatic brain injury, bleeding through the femoral artery, so that MAP reduced to about 40mmHg, to maintain this blood pressure 1h. One hour after craniocerebral trauma combined with acute hemorrhagic shock model, NS group received 3 times the amount of bleeding 0.9% NaCl through the femoral vein, HES group received 10% hydroxyethyl starch equal to the amount of bleeding, HHS group Enter a mixture of 7.5% NaCl and 10% hydroxyethyl starch (1: 1) 4ml / kg. The microdialysis technique was used to collect the peripheral brain extracerebral fluid before traumatic brain injury in traumatic brain injury (1 h) and traumatic brain injury (2 h), and the excitatory amino acids [Glutamic acid (Glu), aspartic acid (Asp)], inhibitory amino acids [Cly, γ-aminobutyric acid (GABA) and taurine (Tau)]. Results Acute hemorrhagic shock combined with traumatic brain injury resulted in the increase of 5 kinds of amino acid concentrations in brain extracellular fluid. The resuscitation of physiological saline led to further increase of extracellular Glu in brain cells. HES and HHS resuscitation could maintain the levels of GABA and Tau in brain extracellular fluid Higher level, HES can inhibit the increase of brain extracellular Glu, HHS can inhibit brain extracellular fluid Glu, Asp, Gly increased. Conclusions For acute traumatic brain injury combined with acute hemorrhagic shock, resuscitation with normal saline increases the release of brain EEA. Both HES and HHS can inhibit the brain EEA release, while the effect of HHS is stronger than that of HES.