Enzymatic production of experimental emphysema in the dog. Route of exposure.
Enzymatic production of experimental emphysema in the dog. Route of exposure.
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狗实验性肺气肿的酶促产生。
DOI：
10.1164/arrd.1974.109.3.351
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发表时间：
1974
期刊：
影响因子：
--
通讯作者：
P. Kimbel
中科院分区：
文献类型：
--
作者：
G. Weinbaum;V. Marco;T. Ikeda;B. Mass;D. Meranze;P. Kimbel
这些研究表明，犬的实验性肺气肿是通过空气-肺界面而不是通过血管内途径引发的。在体内实验中，通过导管将木瓜蛋白酶或多形核白细胞匀浆（PMN）滴入一侧肺中，仅在直接接受木瓜蛋白酶或PMN的肺中发生肺气肿，表明活性物质没有吸收或体液传递到对侧肺。此外，1只犬静脉注射1，500 mg木瓜蛋白酶后，两肺均未出现病变。在体外研究中，只有当木瓜蛋白酶、PMN或弹性蛋白酶滴入支气管时，切除的肺叶才会产生肺气肿，而当肺叶通过肺动脉灌注这些物质时，则不会产生肺气肿。看来气肺界面是实验性肺气肿破坏性变化的起始部位。
These studies showed that experimental emphysema in the dog is initiated via the air-lung interface and not via the intravascular route. In in vivo experiments, in which papain or polymorphonuclear leukocyte homogenates (PMN) were instilled via a catheter into 1 lung, emphysema developed only in the lung directly receiving the papain or PMN, suggesting that there was no absorption or humoral transmission of an active substance to the opposite lung. In addition, 1,500 mg of papain administered intravenously to 1 dog did not produce lesions in either lung. In in vitro studies, emphysema was produced in excised lobes only when papain, PMN, or elastase was instilled into the bronchus and not when the lobes were perfused with these substances through the pulmonary artery. It appears that the air-lung interface is the site of initiation of the destructive changes of emphysema produced experimentally.