Pathogenesis of Pulmonary Emphysema

Neutrophil1。研究了烟草烟雾中尼古丁对中性粒细胞存活的影响。中性粒细胞存活时间随尼古丁剂量的增加而延长。对提取的DNA进行透射电镜和电泳分析，发现尼古丁对中性粒细胞凋亡有抑制作用。研究了中性粒细胞暴露于烟草烟雾中的滤过性。中性粒细胞暴露于烟雾中表现出超微结构异常和滤过性下降。过滤性的降低是由于暴露在烟雾的气体成分中的氧化剂。尼古丁阻止了浓度依赖性的降低，尼古丁的作用是由于抗氧化作用。氧化剂致肺损伤1。烟酸和烟酰胺均能抑制氧化所致肺损伤。这些药物阻止了氧化暴露引起的NAD的减少。H202暴露对培养支气管上皮细胞的损伤呈浓度依赖性和时间依赖性。添加烟酸、烟酰胺、茶碱或DBcAMP可抑制H202诱导的上皮损伤。烟酸抑制了H202暴露引起的细胞内ATP的减少。

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.