Hypertension Accelerates the Growth of Experimental Aortic Aneurysms

Gadowski, Gregory R.; Ricci, Michael A.; Hendley, Edith D.; Pilcher, David B.

doi:10.1006/jsre.1993.1068

Cited by 37 publications

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“…They found that aneurysms in the hypertensive animals were significantly larger on day 7 and day 14 than the normotensive group. Overall, the mean growth rate was nearly twice as high in the hypertensive group (Gadowski 1993). This is in keeping with observational studies which have reported an increased rate o f rupture (which in turn is associated with greater diameter and rate of expansion) amongst hypertensive patients , Brown 1999.…”

supporting

confidence: 85%

The role of the CCR5 Δ32 polymorphism in abdominal aortic aneurysms

Sandford¹,

Bown²,

London³

et al. 2009

Int J Immunogenetics

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All rights reserved INFORMATION TO ALL U SE R S The quality of this reproduction is d ep endent upon the quality of the copy submitted.In the unlikely event that the author did not sen d a com plete manuscript and there are m issing p a g es, th e se will be noted. Also, if material had to be removed, a note will indicate the deletion. Dissertation Publishing UMI U 526187Published by ProQ uest LLC 2013. Copyright in the Dissertation held by the Author. Microform Edition © ProQ uest LLC. All rights reserved. This work is protected against unauthorized copying under Title 17, United States C ode. ProQ uest LLC 789 East Eisenhow er Parkway P.O. Box 1346 Ann Arbor, Ml 48106-1346 ST A TEM EN T O F O R IG IN A LIT YI hereby declare that the work contained in this thesis is entirely my own, except where acknowledged, and has not been submitted for a degree to this or any other University. R.M.Sandford A B ST R A C T The Role o f the CCR5 A 32 Polymorphism in Abdominal Aortic Aneurysms By R.M.SandfordC-C Chemokine receptor 5 (CCR5) is involved in the regulation o f the inflammatory response. Abdominal aortic aneurysms (AAA) may arise as the result o f a chronic inflammatory process which is influenced by a genetic predisposition. The CCR5 gene harbours a 32 base pair deletion (the A32 polymorphism, rs333). The aim o f this study was to investigate the role o f the CCR5 A32 polymorphism in the development of AAA.A case control study was conducted including 285 patients with AAA and 273 control subjects. A blood sample was taken from each individual and DNA extracted. CCR5 genotype was determined using the polymerase chain reaction (PCR). Flow cytometry was used to investigate the biological activity o f the A32 polymorphism.There was no significant difference between the AAA and the control group in relation to the A32 allele frequency (AAA group 10%, control group 12%, P=0.82, chi squared analysis). There was also no significant difference in CCR5 genotype between groups (wild type homozygotes 82% in AAA group vs 77% in control group, heterozygotes 16% in AAA group vs 21% in control group, and A32 homozygotes 2% in both groups, P=0.33, chi squared analysis). The polymorphism was shown to be biologically active with the number o f A32 alleles correlating with cell expression of CCR5 as detected with flow cytometry (P=<0.05).This study demonstrates that the CCR5 A32 is a biologically active genetic polymorphism, however, there is no association between this polymorphism and AAA. Firstly, to Professor Rob Sayers for allowing me the opportunity to undertake this research and also for his supervision and support throughout the project. P U B L IC A T IO N S A R IS IN G FROM T H IS T H E S ISSandford DM Diabetes Mellitus DNAAlso, to Mr M iff Bown for his friendship, patience and encouragement in addition to providing statistical and scientific support. Demographic data 103 Table 7.2: Patient and control subject co-morbidity 105 Table 7.3: Patient and control group medication 106 Table 7.4: Univariate analysis of demog...

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confidence: 85%

The role of the CCR5 Δ32 polymorphism in abdominal aortic aneurysms

Sandford¹,

Bown²,

London³

et al. 2009

Int J Immunogenetics

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“…Since this experimental model exhibits several similarities to human abdominal aortic aneurysms, 14 a variety of laboratories have used it to investigate the pathogenesis and prevention of aneurysm growth. 10,12,13,[15][16][17][18][19][21][22][23][24] In this study, we used a modification of the model that we recently described. 25 An inflammatory response is a critical step in this model.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] These inflammatory cells include neutrophils, monocyte-macrophages, and lymphocytes. 11,13,14,17,18 The interactions of these cells with one another modify their functions at the sites of inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…8 An elastase-induced rat aneurysm model is commonly used to investigate the pathogenesis and prevention of abdominal aortic aneurysms. [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] In this model, inflammatory cell infiltration of the aortic wall occurs in temporal relation to an increase in the aortic diameter. 9,11,13,14 Inflammatory cell infiltration is considered to be a critical step in the development of aortic aneurysms in these rats.…”

Section: Introductionmentioning

confidence: 99%

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The Effect of Immunosuppression on Aortic Dilatation in a Rat Aneurysm Model

et al. 2000

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This study was conducted to investigate whether systemic immunosuppression attenuated aortic dilatation in a rat aneurysm model. Sprague-Dawley rats were subjected to elastase infusion of the infrarenal aorta and divided into two groups of 12 rats each. The immunosuppression group (group 1) was given subcutaneous injections of cyclosporine A (5 mg/kg per day), azathioprine (2 mg/kg per day), and methylprednisolone (2 mg/kg per day) from the operative day until postoperative day (POD) 6. An additional subcutaneus injection of cyclophosphamide 30 mg/kg was also given on the operative day. The control group (group 2) was given subcutaneous injections of saline. Relaparotomy was performed on POD 7. After measurement of the aortic diameter, aortography and ultrasonography were performed in three rats from each group, following which the aortas were excised for histologic examination. The aortic diameter was significantly smaller in group 1 (2.58 +/- 0.37 mm) than in group 2 (6.21 +/- 1.74 mm) (P < 0.01) and the aortic lumen was slightly dilated in group 1, whereas it was spherically dilated in group 2. Total loss of elastic tissue was seen in both groups. Inflammatory cell infiltration and collagen fiber fragmentation were noted in group 2, whereas very little inflammatory cell infiltration and well-preserved collagen fibers were seen in group 1. These findings showed that immunosuppression attenuates aortic dilatation, partly by preserving the collagen fibers, in this rat aneurysm model.

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“…The model proposed by Anidjar et al [3], in which pancreatic elastase is infused directly into a crossclamped segment of the rat abdominal aorta, most closely duplicates the human AAA. In their model, aneurysms expanded with time, and sometimes ruptured in hypertensive animals [4]. There have been many studies using this model [5][6][7][8].…”

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A Rabbit Model of Abdominal Aortic Aneurysm Associated with Intimal Thickening

Matsushita

Kobayashi²,

Oda³

et al. 1999

Eur Surg Res

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A model of abdominal aortic aneurysm with intimal thickening was developed in the rabbit. A segment of the abdominal aorta just proximal to the bifurcation (1 or 2 cm in length) was dissected and isolated with clamps. This segment was perfused by injecting physiologic saline or 100 U/ml of hog pancreatic elastase from the lumen. Perfusion was performed manually for 5 min and the peak pressure in the segment was between 300 and 400 mm Hg in order to cause aortic wall injury. After 4 weeks, animals that had received perfusion with elastase had aneurysms in the perfused segment on arteriography. None of the other animals developed aortic aneurysms. Histologically, the segments of aorta perfused with saline exhibited intimal hyperplasia. In addition to the intimal hyperplasia, the segments of aorta perfused with elastase solution showed lysis of the elastic lamellae in the media that resulted in aneurysm formation.

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Hypertension Accelerates the Growth of Experimental Aortic Aneurysms

Cited by 37 publications

References 0 publications

The role of the CCR5 Δ32 polymorphism in abdominal aortic aneurysms

The role of the CCR5 Δ32 polymorphism in abdominal aortic aneurysms

The Effect of Immunosuppression on Aortic Dilatation in a Rat Aneurysm Model

A Rabbit Model of Abdominal Aortic Aneurysm Associated with Intimal Thickening

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