CAJ | 학술논문

目的观察高碳酸血症对兔急性肺损伤(ALI)模型是否具有保护作用,并观察其对ALI时氧自由基生成的影响,探讨高碳酸血症对ALI可能的作用机制.方法于中国医科大学药理学实验室将22只新西兰大白兔随机分为对照组(C组,n=6)、非高CO2通气组(N组,n=8)、高CO2(8%CO2)通气组(H组,n=8).将动物气管切开,进行机械通气.N组和H组通过静脉注射油酸(0.1 ml/kg)复制ALI模型.C组给予生理盐水(0.1 ml/kg).监测肺组织呼吸力学指标、血气分析指标的变化.继续机械通气至3 h,将动物处死,取出心肺,检测肺组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,测定肺组织湿质量/干质量比、肺通透指数等指标并观察肺组织病理学改变.结果 H组气道峰压显著低于N组,动态胸肺顺应性显著高于N组,动脉血氧分压H组明显高于N组(P＜0.05).肺组织中MDA含量H组明显低于N组(P＜O.05);SOD活性H组明显高于N组(P＜0.05);肺湿质量/干质量比及肺通透指数H组明显低于N组(P＜0.05).H组病理组织学改变较N组明显减轻.结论机械通气时吸入8%的CO2所致高碳酸血症对ALI动物模型有一定的保护作用,其机制可能与提高了肺组织中SOD活力,减轻了脂质过氧化有关.
목적 관찰고탄산혈증대토급성폐손상(ALI)모형시부구유보호작용,병관찰기대ALI시양자유기생성적영향,탐토고탄산혈증대ALI가능적작용궤제.방법 우중국의과대학약이학실험실장22지신서란대백토수궤분위대조조(C조,n=6)、비고CO2통기조(N조,n=8)、고CO2(8%CO2)통기조(H조,n=8).장동물기관절개,진행궤계통기.N조화H조통과정맥주사유산(0.1 ml/kg)복제ALI모형.C조급여생리염수(0.1 ml/kg).감측폐조직호흡역학지표、혈기분석지표적변화.계속궤계통기지3 h,장동물처사,취출심폐,검측폐조직중초양화물기화매(SOD)활성화병이철(MDA)함량,측정폐조직습질량/간질량비、폐통투지수등지표병관찰폐조직병이학개변.결과 H조기도봉압현저저우N조,동태흉폐순응성현저고우N조,동맥혈양분압H조명현고우N조(P＜0.05).폐조직중MDA함량H조명현저우N조(P＜O.05);SOD활성H조명현고우N조(P＜0.05);폐습질량/간질량비급폐통투지수H조명현저우N조(P＜0.05).H조병리조직학개변교N조명현감경.결론 궤계통기시흡입8%적CO2소치고탄산혈증대ALI동물모형유일정적보호작용,기궤제가능여제고료폐조직중SOD활력,감경료지질과양화유관.
Objective To investigate the protective effects of hypereapnia on acute lung injury(ALI)in an model of rabbits in vivo,and to observe its effect on oxygen free radicals in the lung tissue in order to uncover the potential mechanisms.Method In the laboratory of pharmacology,China Medical Univereity,twenty-two healthy New Zealand white rabbits were randomly assigned to control group(Group C,n=6)with the injection of normal saline(0.1 ml/kg),and sixteen rabbits were injected with oleic acid(0.1ml/kg)intravenously,and then were randomly dirided into normocapnia group(Group N,n=8)and hypercapnia group(Group H,n=8,FiCO2=8%).Then tracheostomy was performed,and the experimental animals were ventilated for 3 hours after oleic acid or sterile normal saline administration.Lung mechanics,hemodynamics,blood-gas analysis were monitored.The rabbits were exsangninated.and the lungs and heart were taken out from the thorax.The concentration of superoxide dismutase(SOD)and malondialdehyde(MDA)in the lung tissue were assayed.Lung tissue wet/dry ratio and pulmonary permeability index were measured and histologic damage was assessed after three hours'mechanical ventilation.Results Peak airway pressure in Group H was significantly lower than that in Group N and the dynamic lung comphance Was significantly higher than that in Group N(P＜0.05).PaO2 in Group H was significantly higher than that in Group N(P＜0.05).The concentration of MDA in the lung tissue in group H was significantly lower than that in Group N(P＜0.05),and SOD in group H was significantly higher than that in Group N(P＜O.05).Lung tissue wet/dry ratio and pulmonary permeability in group H were significantly lower than that in Group N(P＜0.05).Histological tissus damage in Group N wassignificantly severer than that in Group H.Conclusions Hypercapnia induced by inhalation of high concentration of carbon dioxide(8%)plays protective role in this in vivo model of ALI.The mechanisms may be associated with enhanced SOD activity and the attenuation of lipid peroxidation in the lung tissue.