Pathogenesis of Pulmonary Emphysema

中性粒细胞1。研究了烟草烟雾中尼古丁对中性粒细胞存活的影响。尼古丁以剂量相关方式延长中性粒细胞存活期。结果：1.提取的DNA经透射电子显微镜和电泳法分析表明，尼古丁可抑制中性粒细胞的凋亡。研究了烟草烟雾对中性粒细胞的滤过性。暴露在烟雾中的中性粒细胞出现超微结构异常，滤过性降低。过滤能力的下降是由于暴露在烟雾的气体成分中的氧化剂。尼古丁对小鼠肺损伤的抑制作用呈浓度依赖关系，尼古丁的作用机制可能是通过抗氧化作用实现的。烟酸或烟酰胺可抑制氧化剂所致的肺损伤。这些药剂阻止了因接触氧化剂而引起的NAD的下降。H202暴露对培养的支气管上皮细胞具有浓度和时间依赖性的损伤作用。烟酸、烟酰胺、茶碱或DBcAMP可抑制H202所致的细胞损伤。烟酸可抑制H202所致的细胞内ATP的降低。

Neutrophil1. Effects of nicotine in the tabacco smoke on neutrophil survival were investigated. Neutrophil survival prolonged with nicotine in dose related fashion. A transmission electron microscopy and electrophoresis of the exracted DNA revealed that nicotine inhibits neutrophil apoptosis.2. Filtrability of neutrophils exposed to tabacco smoke was investigated. Neutrophils exposed to the smoke showed ultrastructural abnormalities and a decreased filtrability. The decrease in filtrability was due to exposure of oxidants in the gas components of the smoke. Nicotine prevented the decrease in concentration dependent fashion and the effect of nicotine was due to antioxidant effects.Lung injury induced by oxidant1. Lung injury induced by oxidant was inhibited by niacin or nicotinamide. These agents prevented a decrease in NAD which was induced by oxidant exposure.2. Cultured bronchial epithelial cells were damaged by H202 exposure in concentration- and time-dependent fashion. The epithelial damage induced by H202 was inhibited by an addition of niacin, nicotinamide, theophilline, or DBcAMP.Niacin inhibited a decrease in intracellular ATP which was brought about by H202 exposure.