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动脉瘤或闭塞性疾病——决定肾下腹主动脉粥样硬化临床病程的因素。

Aneurysm or occlusive disease--factors determining the clinical course of atherosclerosis of the infrarenal aorta.

作者信息

McGee G S, Baxter B T, Shively V P, Chisholm R, McCarthy W J, Flinn W R, Yao J S, Pearce W H

机构信息

Department of Surgery, Feinberg Cardiovascular Institute, Chicago, Ill.

出版信息

Surgery. 1991 Aug;110(2):370-5; discussion 375-6.

PMID:1858045
Abstract

Atherosclerosis of the infrarenal aorta results in distinct clinical entities--aortoiliac occlusive disease (AOD) and abdominal aortic aneurysm (AAA). Although loss of collagen has been implicated in AAA, collagen accumulation plays a role in AOD. In vivo collagen-gene expression can be assessed using complementary DNA for collagen types I and III alpha-chains. The purpose of this study is to compare total collagen (type I + III) and collagen types I and III messenger RNA in AAA, AOD and normal aorta. Specimens were collected from the infrarenal aorta during operation for AOD (n = 7), AAA (n = 7), autopsy, or organ procurement (normal; n = 7). Northern transfer analysis of total RNA was used to compare mRNA levels for type I and III collagen. After preliminary extraction, specimens were hydrolyzed for hydroxyproline analysis used to calculate total collagen (type I + III). Relative levels of type I (pro-a1[1]) mRNA were greater in both AOD (0.77 +/- 0.35) and AAA tissue (0.94 +/- 0.24; p = 0.6) than in normal aorta (0.02 +/- 0.03). Type III (pro-a1[III]) mRNA levels were also greater in AOD (2.52 +/- 0.19; p = 0.09) and AAA tissue (3.15 +/- 1.3) than in normals (0.97 +/- 0.47). Total collagen concentration was increased in AOD (45.6% +/- 3.1% dry weight; p less than 0.05) but not AAA tissue (27.8% +/- 4%) when compared to normal aorta (34.7% +/- 2.3%). Collagen type I and III gene expression is greater in older, diseased aorta, yet collagen accumulated only in AOD. This implies a similar synthetic response in both AOD and AAA. Thus, proteolytic degradation in AAA appears to determine collagen content and possibly the clinical course of the atherosclerotic process.

摘要

肾下腹主动脉粥样硬化会导致不同的临床病症——主髂动脉闭塞性疾病(AOD)和腹主动脉瘤(AAA)。虽然胶原蛋白的流失与腹主动脉瘤有关,但胶原蛋白的积累在主髂动脉闭塞性疾病中起作用。可以使用I型和III型胶原蛋白α链的互补DNA来评估体内胶原蛋白基因的表达。本研究的目的是比较腹主动脉瘤、主髂动脉闭塞性疾病和正常主动脉中总胶原蛋白(I型+III型)以及I型和III型胶原蛋白信使核糖核酸的情况。在因主髂动脉闭塞性疾病进行手术期间(n = 7)、腹主动脉瘤手术期间(n = 7)、尸检或器官获取时(正常;n = 7)从肾下腹主动脉采集标本。使用总RNA的Northern印迹分析来比较I型和III型胶原蛋白的信使核糖核酸水平。在初步提取后,将标本水解用于羟脯氨酸分析,以计算总胶原蛋白(I型+III型)。I型(pro-α1[I])信使核糖核酸的相对水平在主髂动脉闭塞性疾病组织(0.77±0.35)和腹主动脉瘤组织(0.94±0.24;p = 0.6)中均高于正常主动脉(0.02±0.03)。III型(pro-α1[III])信使核糖核酸水平在主髂动脉闭塞性疾病组织(2.52±0.19;p = 0.09)和腹主动脉瘤组织(3.15±1.3)中也高于正常组织(0.97±0.47)。与正常主动脉(34.7%±2.3%)相比,主髂动脉闭塞性疾病组织中的总胶原蛋白浓度增加(45.6%±3.1%干重;p<0.05),而腹主动脉瘤组织中则没有增加(27.8%±4%)。在病变的老年主动脉中,I型和III型胶原蛋白基因表达更高,但胶原蛋白仅在主髂动脉闭塞性疾病中积累。这意味着主髂动脉闭塞性疾病和腹主动脉瘤中存在类似的合成反应。因此,腹主动脉瘤中的蛋白水解降解似乎决定了胶原蛋白含量以及动脉粥样硬化过程的临床进程。

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