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      Inflammatory Aspects of Experimental Aneurysms. : Effect of Methylprednisolone and Cyclosporine

      , , , ,

      Annals of the New York Academy of Sciences

      Wiley

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          Most cited references 22

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          Elastase-induced experimental aneurysms in rats.

          An experimental in vivo model of aortic aneurysm was established by perfusing an isolated segment of rat abdominal aorta with pancreatic elastase. Ten rats were used in each protocol. Saline-perfused aortas developed no aneurysmal dilations. Elastase-perfused aortas contained aneurysms in the perfused area and a total loss of elastic tissue. Control aortas contained no elastic tissue lesions. There was a quantitative relation between the amount of elastase perfused and aneurysm formation: 1-2 units induced neither macroscopic nor microscopic lesions; 3-6 units induced microscopic elastic tissue damage without macroscopic aneurysm; and more than 6 units produced aneurysmal dilation in all cases. In situ elastase secretion by macrophages was induced by perfusing rat aortas with thioglycollate-activated macrophages or with thioglycollate alone. There was aortitis without true aneurysm and a total loss of elastic tissue in the vicinity of activated macrophages within the aortic media. Perfusion of infra-aneurysmal amount of elastase (1 or 2 units) or thioglycollate plus plasmin (2 units) always induced a large aneurysm, whereas plasmin alone induced neither macroscopic nor microscopic lesions. These morphological results were supported by the significantly elevated elastolytic activity within the aortic wall of animals perfused with thioglycollate plus plasmin 9 days, after perfusion (207.6 +/- 54.8 micrograms elastin-rhodamine lysed/18 hr; control rats, 25.43 +/- 11.13). The results suggest that the presence of elastase within the aortic media leads to aneurysm formation. Activated macrophages within the aortic media may be responsible for elastase secretion and elastic tissue destruction. Plasmin may enhance elastase activity and aggravate the aneurysmal lesion.
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            The role of inflammation in nonspecific abdominal aortic aneurysm disease.

            The predominant pathologic feature of abdominal aortic aneurysm is elastin destruction, and elastin destruction may be mediated by inflammation. In this investigation serial sections of abdominal aortic aneurysm specimens were selectively stained to study the relationship between inflammation and elastin degradation. In addition, soluble aortic extracts were examined for the presence of immunoglobulins. An inflammatory infiltrate was present in 8 of 10 of the abdominal aortic aneurysm specimens examined. The infiltrate was mononuclear, commonly located at the junction of the media and adventitia; it did not codistribute with loss of elastin. The presence of an inflammatory component in abdominal aortic aneurysm was associated with a large amount of immunoglobulin in soluble extracts from aneurysmal tissue compared to atherosclerotic and normal control extracts. This study further characterizes the microscopic pathology of abdominal aortic aneurysm and describes the presence of immunoglobulin in soluble tissue extracts. In addition, the possible role of inflammation in abdominal aortic aneurysm as it relates to protease expression is detailed.
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              Correlation of inflammatory infiltrate with the enlargement of experimental aortic aneurysms.

              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 less than 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)
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                Author and article information

                Journal
                Annals of the New York Academy of Sciences
                Ann NY Acad Sci
                Wiley
                0077-8923
                1749-6632
                November 1996
                November 1996
                : 800
                : 1 The Abdominal
                : 74-88
                Article
                10.1111/j.1749-6632.1996.tb33300.x
                © 1996

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