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为了进一步探讨慢性阻塞性肺疾患 (COPD)的发病机制 ,复制地鼠胰弹性蛋白酶性肺气肿动物模型及附加烟雾吸入。观察 1个月及 3个月时肺组织形态 ,肺动脉压 (PAP) ,血清丙二醛 (MDA)含量 ;血清血管紧张素转换酶 (ACE)活性及肺组织中前列腺素类 (PGE2 、TXB2 、6 keto PGF1α)物质含量的变化。结果发现单纯肺气肿组动物 1个月 ,已经形成中度肺气肿 ,PAP、MDA、PGE2 、TXB2 均有显著增加 (均P <0 0 1 )。而ACE、6 keto PGF1α显著降低 (分别P <0 0 1和P <0 0 5)。TXB2 / 6 keto PGF1α比值有显著增加 (P <0 0 1 )。肺气肿 3个月组较 1个月 ,除MDA、6 keto PGF1α及TXB2 / 6 keto PGF1α有进一步变化外 (P <0 0 5、P <0 0 1 ) ,其它指标无进一步变化。附加烟雾吸入较单纯肺气肿组 ,仅 1个月时MDA、3个月时 6 keto PGF1α及 1个月时TXB2 / 6 keto PGF1α有进一步变化 (P <0 0 5) ,而ACE的下降反而回升 (P <0 0 5、P <0 0 1 )外 ,其它指标无明显改变。提示 :气道内滴注胰弹性蛋白酶致使弹性蛋白酶与抗弹性蛋白酶之间失平衡是导致COPD的关键发病学环节。附加优质烟烟雾吸入在其发病学中仅占次要地位
In order to further explore the pathogenesis of chronic obstructive pulmonary disease (COPD), reproductive animal models of hamster pancreas elastase-induced emphysema and additional smoke inhalation. Pulmonary tissue morphology, pulmonary arterial pressure (PAP) and serum malondialdehyde (MDA) levels were observed at 1 month and 3 months. Serum levels of angiotensin converting enzyme (ACE) and prostaglandins (PGE2, TXB2, 6 keto PGF1α) content changes. The results showed that the animals in simple emphysema group had moderate emphysema for 1 month, and the levels of PAP, MDA, PGE2 and TXB2 were significantly increased (all P <0.01). ACE and 6 keto PGF1α were significantly decreased (P <0.01 and P <0.05, respectively). TXB2 / 6 keto PGF1α ratio increased significantly (P <0.01). There was no further change in the other indexes except the further changes of MDA, 6 keto PGF1α and TXB2 / 6 keto PGF1α (P <0 05, P 0 01) in the 3 months group with emphysema for 3 months. Compared with simple emphysema group, there was a further change in MDA, 6 keto PGF1α at 3 months and TXB2 / 6 keto PGF1α at 1 month (P <0 05), while the decline of ACE was reversed (P <0 05, P <0 0 1), the other indicators no significant change. Tip: Intratracheal instillation of pancreatic elastase resulting in the loss of balance between elastase and anti-elastase is the key pathogenesis of COPD. Additional good-quality smoke smoke inhalation only plays a secondary role in its pathogenesis