摘要
目的:探讨慢性阻塞性肺疾病(COPD)模型大鼠肺泡巨噬细胞延迟整流钾通道(KV)活性变化。方法:随机将大鼠分为COPD模型组和对照组,采用香烟烟雾吸入法复制大鼠COPD模型。应用全细胞电压或电流膜片钳的方法,观察和比较正常对照大鼠与COPD模型大鼠肺泡巨噬细胞(AM)KV电流活性、膜电位和电容的差异。结果:(1)COPD组支气管肺泡灌洗液(BALF)中单个核细胞总数及AM细胞数均显著高于对照组(P<0.01);(2)COPD大鼠BALF中AM细胞Kv电流幅度[(520.5±38.7)pA,+50mV,n=30]显著低于对照组[(713.6±44.4)pA,+50mV,n=30,P<0.01];(3)COPD组AM细胞电容[(101.6±7.6)pF,n=42]与对照组[(97.4±1.6)pF,n=67]无显著差异(P>0.05)。但模型组AM膜电位[(-24.6±4.5)mV,n=18]负值显著低于对照组[(-37.9±6.1)mV,n=34,P<0.01]。结论:COPD大鼠肺泡AM细胞KV功能下调,细胞膜电位负值降低,兴奋性升高。该机制可能与AM细胞促进COPD发病的形成机制有关。
AIM： To explore the change of delayed rectifier potassium channel （Kv） activity in alveolar lrkacrophages （AM） in chronic obstructive pulmonary clisease （COPD） rats. METHODS： COPD model was established by exposure of the animals to cigarette smoke. With whole - cell voltage - or current - clamp techniques, Kv activity, membrane capacitance and resting membrane potential （Em） in AM from COPD model and control rats were compared. RESULTS： （1） Significant increases in total mononuclear cells and AM in bronchoal aveolar lavage fluid （BALF） were found in COPD group compared with in control group. （2） The AM Kv current altitude in COPD group [ （520.5 ± 38.7）pA, ＋ 50 mV, n = 30] was significantly lower than that in control group [ （713.6 ± 44.4）pA, ＋ 50 mV, n = 30, P 〈 0.01 ]; （3） AM from COPD group had no significantly different capacitances （ P 〉 0.05）, but had more positive Em （ P 〈 0,01 ） compared with those from control group. CONCLUSION： Inhibition of Kv function, increase in excitability and more positive Em in AM from COPD rats may be involved in the AM contribution to the COPD development.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第9期1728-1730,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.39670338)
关键词
肺疾病
慢性阻塞性
膜电位
钾通道
巨噬细胞
Pulmonary, disease, chronic obstructive
Membrane potentials
Potassium channels
Macrophages
