Binder R, Stone P J, Calore J D, Dunn D M, Snider G L, Franzblau C, Valeri C R
Respiration. 1985;47(4):267-77. doi: 10.1159/000194782.
In order to assess blood factors which might explain why some cigarette smokers develop airflow obstruction while others do not, we compared two groups of PiM phenotype volunteers matched for age, sex and total pack-years of cigarette smoking; one group had airflow obstruction and the other did not. Functional levels of alpha-2-macroglobulin (alpha-2-M) and alpha-1-protease inhibitor (alpha-1-PI) were separately assessed by a protease binding procedure. Neutrophils were isolated from blood by counterflow centrifugation, and their elastase content was assayed with 3H-elastin-SDS (sodium dodecyl sulfate). The obstructed and nonobstructed groups were not different with respect to functional or immunoreactive levels of alpha-1-PI and alpha-2-M or elastase levels in their neutrophils. We do not find imbalances of circulating elastase or antielastase levels in PiM phenotype smokers with airflow obstruction.
为了评估可能解释为何一些吸烟者会出现气流阻塞而另一些人不会的血液因素，我们比较了两组在年龄、性别和吸烟总包年数上匹配的PiM表型志愿者；一组有气流阻塞，另一组没有。通过蛋白酶结合程序分别评估α-2-巨球蛋白（α-2-M）和α-1-蛋白酶抑制剂（α-1-PI）的功能水平。通过逆流离心从血液中分离出中性粒细胞，并用3H-弹性蛋白-十二烷基硫酸钠（SDS）测定其弹性蛋白酶含量。气流阻塞组和非气流阻塞组在α-1-PI和α-2-M的功能或免疫反应水平以及中性粒细胞中的弹性蛋白酶水平方面没有差异。我们未发现在有气流阻塞的PiM表型吸烟者中循环弹性蛋白酶或抗弹性蛋白酶水平失衡。
