CAJ | 학술논문

目的评价胆绿素对脑死亡致大鼠肺损伤的影响.方法成年雄性清洁级Wistar大鼠23只,体重250～300 g,随机分为3组,假手术组(S组,n=7)仅向大鼠颅内置入Fogarty导管;脑死亡组(BD组,n=8)和胆绿素组(B组,n=8)向大鼠颅内置入Fogarty导管,通过膨胀球囊诱导脑死亡,膨胀球囊后30 min确认脑死亡情况,发生脑死亡后分别腹腔注射生理盐水1 ml或胆绿素35 mg/kg.分别于给予胆绿素前、后间断采集动脉血样,进行血气分析,计算PaO2/FiO2,并测定血浆胆红素浓度.给予胆绿素后1.5 h处死大鼠,取肺组织,测定MDA含量、SOD活性、总抗氧化能力、肺组织细胞凋亡情况及胆绿素还原酶的表达水平,对细胞凋亡情况进行免疫组化评分.结果与S组比较,BD组PaO2/FiO2、SOD活性和总抗氧化能力降低,MDA含量和凋亡细胞免疫组化评分升高(P＜0.05);与BD组比较,B组PaO2/FiO2、胆红素浓度、SOD活性、总抗氧化能力和胆绿素还原酶表达水平升高,MDA含量和凋亡细胞免疫组化评分降低(P＜0.05).结论外源性给予胆绿素可减轻脑死亡致大鼠肺损伤,其机制与抑制肺组织氧化应激反应和细胞凋亡有关.
목적 평개담록소대뇌사망치대서폐손상적영향.방법 성년웅성청길급Wistar대서23지,체중250～300 g,수궤분위3조,가수술조(S조,n=7)부향대서로내치입Fogarty도관;뇌사망조(BD조,n=8)화담록소조(B조,n=8)향대서로내치입Fogarty도관,통과팽창구낭유도뇌사망,팽창구낭후30 min학인뇌사망정황,발생뇌사망후분별복강주사생리염수1 ml혹담록소35 mg/kg.분별우급여담록소전、후간단채집동맥혈양,진행혈기분석,계산PaO2/FiO2,병측정혈장담홍소농도.급여담록소후1.5 h처사대서,취폐조직,측정MDA함량、SOD활성、총항양화능력、폐조직세포조망정황급담록소환원매적표체수평,대세포조망정황진행면역조화평분.결과 여S조비교,BD조PaO2/FiO2、SOD활성화총항양화능력강저,MDA함량화조망세포면역조화평분승고(P＜0.05);여BD조비교,B조PaO2/FiO2、담홍소농도、SOD활성、총항양화능력화담록소환원매표체수평승고,MDA함량화조망세포면역조화평분강저(P＜0.05).결론 외원성급여담록소가감경뇌사망치대서폐손상,기궤제여억제폐조직양화응격반응화세포조망유관.
Objective To investigate the effects of exogenous biliverdin on lung injury induced by brain death (BD) in rats. Methods Twenty-three adult male Wistar rats in which Fogarty balloon catheter was successfully inserted into cranial cavity were randomly divided into 3 groups: group Ⅰ sham operation (group S,n = 7); group Ⅱ brain death (group BD, n = 8) and group Ⅲ biliverdin + BD (group B, n = 8). The animals were anesthetized, intubated and mechanically ventilated. Femoral artery and vein were cannulated for MAP monitoring and drug and fluid administration. Brain death was induced by injecting slowly normal saline into the balloon in group Ⅱ and Ⅲ. BD was confirmed by dilated and fixed pupils, apnea, transient hypertension and EEG changes. In group Ⅲ biliverdin 35 mg/kg was injected intraperitoneally as soon as BD was confirmed. The animals were mechanically ventilated for another 1.5 h during which MAP was maintained at 80-120 mm Hg by iv norepinephrine infusion. Arterial blood samples were obtained before anesthesia, immediately before and at 5, 30,60, 90 min after intraperitoneal biliverdin for blood gas analysis and determination of plasma bilirubin concentration. PaO2/FiO2 was calculated. The animals were sacrificed at 1.5 h after biliverdin administration. The left lung was removed for detection of MDA content, SOD activity, total antioxidant capacity, cell apoptosis and biliverdin reductase expression in lung tissue. Results Brain death significantly decreased PaO2/FiO2, lung SOD activity and total antioxidant capacity and increased lung MDA content and apoptosis as compared with sham operation group. IP biliverdin significantly attenuated BD-induced lung injury in group B as compared with group BD. The plasma bilirubin concentration and biliverdin reductase expression were significantly higher in group B than group BD. Conclusion Exogenous biliverdin can attenuate BD-induced lung injury by inhibiting pulmonary oxidative stress response and apoptosis.