摘要
目的运用化学去神经法阻断辣椒素敏感的C类神经纤维(CapsCF),观察对肺缺血再灌注损伤(IR)的影响,并探讨氧化应激反应在其中的作用。方法新西兰大白兔32只随机分为4组:假手术组(S组)、肺缺血再灌注组(IR组)、辣椒素组(CS组)、辣椒素肺缺血再灌注组(CIR组)。分别予以辣椒素(100mg/kg)或其载液皮下注射,5d后建立肺IR模型。实验终末检测血气分析,氧化应激指标〔丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)〕、肺组织湿干比,HE染色观察肺组织病理学改变。结果与S组和CS组比,IR组和CIR组动脉血氧分压降低(P<0.05),肺泡动脉氧分压差升高(P<0.05),肺组织湿干比升高,氧化应激反应加重(P均<0.05),病理学损伤加重。CIR组指标改变均较IR组加重(血气学指标除外)。结论化学去神经法阻断CapsCF,加重肺IR损伤,其机制可能与加重氧化应激反应有关。
Objective To investigate the role of Capsaicin sensitive C fibers (CapsCF) denervation in lung ischemia-reperfusion (IR) injury and the possible mechanism related to oxidative stress. Methods Thirty two male New Zealand rabbits were randomized into four groups.. IR group (IR), sham group (S), capsaicin pretreated IR group (CIR), and capsaicin pretreated sham group (CS). The rabbits in CIR and CS groups were pretreated with capsaicin (100mg/kg) to induce functional ablation of CapsCF, and then subjected to lung ischemia and reperfusion. The rabbits in IR group were not treated with capsaicin before lung ischemia and reperfusion. Thereafter, blood samples and lung tissue samples were obtained for blood gas and biochemical analyses, including the measurements of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT). The lung wet/dry weight ratio and histopathological changes were also assessed. Results Compared to S and CS group, partial pressure of oxygen (P()2) values in IR and CIR groups significantly decreased (P〈0.05). In contrast, the alveolar-arterial oxygen gradient (A-aDOz), lung wet/dry weight ratio increased in IR and CIR groups (P〈0.05). Capsaiein pretreatment in CIR group increased lung wet/dry weight ratio and lung pathologic lesions, along with higher level of MDA and lower activity of SOD and CAT (P〈0.05, vs. IR). Conclusion Denervation of CapsCF aggravated lung ischemia- reperfusion injury of rabbits, which seems to be closely related to the excerbation of oxidative stress.
出处
《四川大学学报(医学版)》
CAS
CSCD
北大核心
2014年第2期245-248,253,共5页
Journal of Sichuan University(Medical Sciences)
基金
国家自然科学基金(No.81170077)资助