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杂种犬10只,随机分为失血性休克组(HS)和失血性休克地塞米松予治疗组(HSD)。放血至血压降至并维持于40—50mmHg。结果表明,ASD组血清过氧化脂质含量逐渐降低,失血后4.5小时测定值显著地低于HS组(P<0.05);SOD活力,HSD组逐渐增高,失血后2小时HSD组酶活力高于HS组(P<0.05)。HSD组SOD活力与血清过氧化脂质含量呈明显负相关(r=-0.795,P<0.01),HS组无相关。肺过氧化脂质含量HSD组低于HS组(P<0.05)。PaO_2,HSD组高于HS组(P<0.05)。HS组失血后3小时呈浅而快呼吸,光镜观察发现弥漫性肺不张,HSD组显著地较HS组轻。
Ten hybrid dogs were randomly divided into hemorrhagic shock group (HS) and hemorrhagic shock dexamethasone treatment group (HSD). Bleeding to blood pressure dropped to and maintained at 40-50mmHg. The results showed that the content of lipid peroxidation in ASD group decreased gradually, the value of 4.5 hours after blood loss was significantly lower than that in HS group (P <0.05); the activity of SOD increased gradually in HSD group, and the enzyme activity in HSD group was higher than that in HSD group HS group (P <0.05). There was a significant negative correlation between SOD activity and serum lipid peroxidation in HSD group (r = -0.795, P <0.01), but no correlation in HS group. The level of lipid peroxidation in HSD group was lower than that in HS group (P <0.05). PaO2, HSD group was higher than HS group (P <0.05). HS group was shallow and fast breathing 3 hours after blood loss, diffuse atelectasis was observed by light microscopy, HSD group was significantly lighter than HS group.