CORRELATION OF INFLAMMATORY INFILTRATE WITH THE ENLARGEMENT OF EXPERIMENTAL AORTIC-ANEURYSMS
CORRELATION OF INFLAMMATORY INFILTRATE WITH THE ENLARGEMENT OF EXPERIMENTAL AORTIC-ANEURYSMS
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DOI：
10.1016/0741-5214(92)90101-d
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发表时间：
1992-08-01
影响因子：
4.3
通讯作者：
CHEJFEC, G
中科院分区：
文献类型：
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作者：
ANIDJAR, S;DOBRIN, PB;CHEJFEC, G
炎性细胞经常出现在人类主动脉瘤的壁中，但其意义尚不确定。为了研究它们的作用，在大鼠中建立了动脉瘤的体内模型。在26只大鼠的离体腹主动脉内注入15个单位的猪胰弹性蛋白酶2小时。在体内测量血管，并在选定的时间间隔切除用于常规组织学和免疫组织学研究。在未处理的对照大鼠中，主动脉的直径为1.04 +/- 0.02 mm。输注弹性蛋白酶后，主动脉立即扩张26%至1.31 +/- 0.02 mm（p = NS），无组织学可证实的剩余弹性膜。输注后2.5天，主动脉扩张近300%至3.09 +/- 0.08 mm（p < 0.05）。输注后3天和4天，血管分别扩张388%至4.04 +/- 0.09 mm和367%至3.82 +/- 0.31 mm。这些血管还在中膜中显示出大量炎性细胞。输注后6天，血管扩大421%至4.38 +/- 0.03 mm（p < 0.05），浸润物持续存在巨噬细胞、多形中性粒细胞和T淋巴细胞的免疫组织学染色。输注后12天，动脉瘤仍然增大，但稳定在4.23 +/- 0.14 mm（p = NS）。此时，炎性细胞的数量恢复到对照水平。炎性浸润和血管瘤增大之间的时间相关性表明炎性细胞可能参与血管瘤血管壁的破坏，从而促进进行性增大。为了进一步检验这一假设，另外16只大鼠的睾丸被注入巯基乙酸盐加纤溶酶。这些试剂是免疫系统的非特异性激活剂。输注后5天，未处理的主动脉扩大213%至2.21 +/- 0.23 mm（p < 0.05），弹性膜碎裂，壁中有大量活化的巨噬细胞。输注后9天，炎症反应持续存在，动脉扩张288%至3.00 +/- 0.28 mm（p < 0.05）。这些发现与炎症细胞可能参与动脉瘤进行性或“继发性”扩大的假设一致。
Inflammatory cells often are seen in the walls of human aortic aneurysms, but their significance is uncertain. To investigate their actions an in vivo model of arterial aneurysms was developed in the rat. Fifteen units of hog pancreatic elastase were infused for 2 hours into the isolated abdominal aorta in 26 rats. The vessels were measured in vivo and were excised for conventional histologic and immunohistologic study at selected intervals. In untreated control rats the diameter of the aorta was 1.04 +/- 0.02 mm. Immediately after infusion with elastase the aorta dilated 26% to 1.31 +/- 0.02 mm (p = NS), with no histologically demonstrable remaining elastic lamellae. Two and one half days after infusion the aorta dilated nearly 300% to 3.09 +/- 0.08 mm (p < 0.05).These vessels exhibited large numbers of activated macrophages and T cells in the media. Three and 4 days after infusion the vessels dilated 388% to 4.04 +/- 0.09 mm and 367% to 3.82 +/- 0.31 mm, respectively. These vessels also exhibited numerous inflammatory cells in the media. Six days after infusion the vessels enlarged 421% to 4.38 +/- 0.03 mm (p < 0.05), and the infiltrate persisted staining immunohistologically for macrophages, polymorphic neutrophils, and T lymphocytes. Twelve days after infusion the aneurysms remained enlarged but stable at 4.23 +/- 0.14 mm (p = NS). At this time the number of inflammatory cells regressed to control levels. The temporal correlation between inflammatory infiltrate and aneurysmal enlargement suggests that inflammatory cells may participate in the destruction of the aneurysmal vessel wall thereby promoting progressive enlargement. To further examine this hypothesis, the aortas in 16 additional rats were infused with thioglycolate plus plasmin. These agents are nonspecific activators of the immune system. Five days after infusion the untreated aorta enlarged 213% to 2.21 +/- 0.23 mm (p < 0.05), with fragmentation of elastic lamellae and numerous activated macrophages in the wall. Nine days after infusion the inflammatory response persisted, and the aortas dilated 288% to 3.00 +/- 0.28 mm (p < 0.05). These findings are consistent with the hypothesis that inflammatory cells may participate in the progressive or "secondary" enlargement of aneurysms.