地塞米松对失血性休克犬酸碱平衡和血清过氧化脂质的影响

本实验用8只杂种犬复制了失血性休克的病理模型,按体重随机分为失血性休克(SH)组和失血性休克——地塞米松(SH—C)组。在实验过程中,通过调整血容量使动脉血压维持于5.3～6.7kPa,定期取动脉血测pH、PCO_2、HCO_3-BE和测血清中过氧化脂质的含量。结果表明:SH—D组的存活时间显著地长于SH组,动脉血pH、PCO_2,HCO~-_3和BE检测的结果是,随着失去性休克的进展,SH组和SH—D组均发生了强度相似的代谢性酸中毒;血清过氧化脂质的含量,随失血时间的延长,SH组逐渐增高,而SH—D组则逐渐降低,至失血后4.5小时,两组比较差异显著(P<0.05)。

Effect of dexamethasone on the acid-base balance and the amount of serum lipid peroxides in hemorrhagic shock dogs

Hybrid dogs were randomly divided into hemorrhagic shock group (HS) and similar but pretreated with dexamethasone group (HS-D) . The arterial blood pressure was kept at 5.3-6.7Kpa by means of bloodletting and infusion through the femoral artery. Arterial blood was collected at different times after bleeding and examined for pH, PCO2, HCO3-,BE and serum lipid peroxides. The survival period was significantly longer in the HS-D group than the HS group. Analyses of pH, PCO2. HCO3 and BE values showed that metabolic acidosis developed in both groups with development of hemorrhagic shock. The content of serum lipid peroxides was gradually increasing in the HS group and decreasing in the HS-D group. Difference in the serum lipid peroxide contents between these 2 groups became obvious after 4.5 hours(P<0.05).The above results show that one of the mechanisms of dexamethasone in protecting dogs from hemorrhagic shock may be that it blocks the production of lipid peroxides.