不同剂量Vit C对严重烧伤延迟复苏大鼠血清cTnⅠ的影响

Effects of different doses of vitamin C on serum cardiac troponin Ⅰ in delayed resuscitative rats with severe burn

目的研究不同剂量维生素C(Vit C)对烧伤后延迟复苏大鼠血清肌钙蛋白Ⅰ(cTnⅠ)的影响,以了解Vit C对烧伤后延迟复苏心肌的保护作用。方法 40只Wistar大鼠随机分成4组:假手术组、延迟复苏组、Vit C低剂量组及Vit C高剂量组。复制烧伤模型30 h后,检测血清cTnⅠ、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性变化。结果使用Vit C可以降低烧伤后延迟复苏大鼠血清中cTnⅠ和MDA的含量、升高SOD活性(P<0.01);Vit C高剂量组降低烧伤后延迟复苏大鼠血清cTnⅠ和MDA的含量,升高SOD活性作用较Vit C低剂量组明显(P<0.05)。结论烧伤后延迟复苏时使用Vit C对心肌具有保护作用,大剂量Vit C的保护作用优于低剂量Vit C,其保护机制可能与抗氧自由基、抑制膜脂质过氧化有关。

Objective To study the effects of different doses of vitamin C （ Vit C） on serum cardiac troponin I （ cTn I ） in delayed resuscitative rats with severe burn. Methods 40 Wistar rats were randomly divided into four groups （n = 10） ：sham - operated group, delayed resuscitative group,low - dose Vit C group and high - dose Vit C group. Animals were anesthetized by intraperitoneal injection of sodium pentobarbital at 30 mg/kg, and then depilated by 10% sodium sulfide. 24 h later, the same anesthesia was conducted again,and rats in sham - operated group received water bath below waist at 37 ℃ for 18 s,while those in the other three groups were burned by hot water bath at 92 ℃. 6 h later,all burn rats were injected with Ringer lactate solution at 40 mg/kg to cause delayed resuscitation. In two Vit C groups, additional Vit C was injected at 30 mg/kg or 250 mg/kg. After that, blood samples were obtained for the measurement of serum cTn I, malondaildehyde （MDA） content, superoxide dismutase （SOD） activity. Results cTn I and MDA contents decreased while SOD activity increased significantly in the two Vit C groups compared with delayed resuscitative group （P 〈 0.01 ）. These changes were more obvious in high - dose group than those in low - dose group （ P 〈 0.05 ）. Conclusion Vit C treatment during the period of delayed resuscitation following sever burn can protect myocardium, and high - dose Vit C is of protective effects superior to low - dose one. The mechanisms may be related to its inhibition of oxygen free radicals and lipid peroxidation.