Abstract: ? Forinvestigatingthepathogenesisofchronicobstructivepulmonarydisease (COPD) ,theanimalmodel ofemphysemawasreproducedbyporcinepancreaticelastaseintratrachealinstillationoradditionalcigarette smokinginham sters.Morphologyoflungtissue,pulmonaryarterialpressure (PAP) ,malondialldehyde (MDA)contentandangiotensin convertingenzyme (ACE)activityinserumaswellasprostanoids(PGE2 ,TXB2 ,6 keto PGF1α)contentsinlungtissuewere measuredafter 1and 3months.Accordingtoourexperiment,apparentemphysemawasobservedinlungtissueafter 1 month.PAP ,MDA ,PGE2 ,andTXB2 increasedsignificantly (P <0 0 5～ 0 .0 1 ) ,butACE、6 keto PGF1αobviouslyde creased .RatioofTXB2 to 6 keto PGF1αsignificantlyincreased.ExceptMDA ,6 keto PGF1αandTXB2 /6 keto PGF1αgroups (P <0 0 5～ 0 .0 1 ) ,whenthreemonthemphysemagroupcomparedwithonemonthgroup,otherparameterswerenotsig nificantlydifferent.MDA ,6 keto PGF1αandTXB2 /6 keto PGF1αweresignificantlydifferent(P <0 0 5～ 0 .0 1 ) ,butACE activityobviouslyincreasedbetweenemphysemaandadditionalcigarette smokinggroup .Imbalancebetweenelastaseand antielastase,whichwascausedbyintratrachealinstillationelastasewasakeylinkwithpathogenesisofCOPD .Superquality cigarette smokingwasnotanimportantfactor.Itcouldbeconcludedthatporcinepancreaticelastaseintratrachealinstillation wasthekeyfactor,whichcausedemphysema.

Key words: Emphysema Pancreatic elastase Cigarette smoking Hamster.

摘要： 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

关键词: 肺气肿, 胰弹性蛋白酶, 烟雾吸入, 地鼠