scholarly journals Suprarenal Aorta

2020 ◽  
Author(s):  
Keyword(s):  
Suprarenal Aorta

Effects of long-term chloroquine administration on the natural history of aortic aneurysms in mice

2015 ◽  
Vol 93 (8) ◽  
pp. 641-648 ◽  
Author(s):  
Azza Ramadan ◽  
Mark D. Wheatcroft ◽  
Adrian Quan ◽  
Krishna K. Singh ◽  
Fina Lovren ◽  
...  
Keyword(s):  
Natural History ◽  
Thrombus Formation ◽  
Aortic Aneurysms ◽  
Ang Ii ◽  
Abdominal Aortic ◽  
Suprarenal Aorta ◽  
History Of ◽  
Categorical Distribution

Autophagy regulates cellular homeostasis and integrates the cellular pro-survival machinery. We investigated the role of autophagy in the natural history of murine abdominal aortic aneurysms (AAA). ApoE−/− mice were implanted with saline- or angiotensin II (Ang-II)-filled miniosmotic pumps then treated with either the autophagy inhibitor chloroquine (CQ; 50 mg·(kg body mass)–1·day–1, by intraperitoneal injection) or saline. Ang-II-elicited aneurysmal expansion of the suprarenal aorta coupled with thrombus formation were apparent 8 weeks later. CQ had no impact on the incidence (50% for Ang-II compared with 46.2% for Ang-II + CQ; P = NS) and categorical distribution of aneurysms. The markedly reduced survival rate observed with Ang-II (57.1% for Ang-II compared with 100% for saline; P < 0.05) was unaffected by CQ (61.5% for Ang-II + CQ; P = NS compared with Ang-II). CQ did not affect the mean maximum suprarenal aortic diameter (1.91 ± 0.19 mm for Ang-II compared with 1.97 ± 0.21 mm for Ang-II + CQ; P = NS). Elastin fragmentation, collagen accumulation, and smooth muscle attrition, which were higher in Ang-II-treated mice, were unaffected by CQ treatment. Long-term CQ administration does not affect the natural history and prognosis of experimental AAA, suggesting that global loss of autophagy is unlikely to be a causal factor in the development of aortic aneurysms. Manipulation of autophagy as a mechanism to reduce AAA may need re-evaluation.

The incidence of iliac aneurysms in patients with abdominal aortic aneurysms: Comparison of four centers in Europe and the USA

VASA ◽  
2004 ◽  
Vol 33 (2) ◽  
pp. 68-71 ◽  
Author(s):  
Eugster ◽  
Bolli ◽  
Pfeiffer ◽  
Sandmann ◽  
Chuter ◽  
...  
Keyword(s):  
External Iliac Artery ◽  
Aortic Aneurysms ◽  
Iliac Arteries ◽  
Maximal Diameter ◽  
Abdominal Aortic ◽  
Suprarenal Aorta ◽  
Significant Difference ◽  
The Usa ◽  
Preoperative Ct ◽  
Common Iliac Arteries

Background: The purpose of this study was to compare the anatomy of the aortoiliac vessels in patients scheduled for infrarenal abdominal aortic aneurysm (AAA) repair in four different countries. Material and methods: Consecutives series of 100 preoperative CT-scans were evaluated at each center. Diameters of the suprarenal aorta, maximal diameter of the aneurysm, right and left common and external iliac artery as well as the hypogastric arteries were recorded and compared between each center. Results: Configuration of the AAA above bifurcation was similar at each center. The dimensions of the aortic bifurcation and the common iliac arteries were different among the centers. Common iliac arteries with diameters over 25mm were significantly more common at center 1 (p < 0.001, p = 0.002 and p < 0.001). Among centers 2,3 and 4 there was no significant difference in common iliac diameters. Conclusions: Configuration of the iliac arteries in AAA was significantly different for Swiss patients compared to American, Austrian and German patients. Reasons for these differences are unclear, epidemiological or genetic factors may be responsible.

scholarly journals Kallikrein‐1 Blockade Inhibits Aortic Expansion in a Mouse Model and Reduces Prostaglandin E2 Secretion From Human Aortic Aneurysm Explants

2021 ◽  
Vol 10 (5) ◽  
Author(s):  
Corey S. Moran ◽  
Erik Biros ◽  
Smriti M. Krishna ◽  
Susan K. Morton ◽  
Daniel J. Sexton ◽  
...  
Keyword(s):  
Aortic Aneurysm ◽  
Mouse Model ◽  
Matrix Metalloproteinase ◽  
Cyclooxygenase 2 ◽  
Matrix Metalloproteinase 2 ◽  
Prostaglandin E ◽  
Blocking Antibody ◽  
Active Matrix ◽  
Suprarenal Aorta ◽  
Metalloproteinase 9

Background Abdominal aortic aneurysm (AAA) is an important cause of mortality in older adults. The kinin B2 receptor agonist, bradykinin, has been implicated in AAA pathogenesis through promoting inflammation. Bradykinin is generated from high‐ and low‐molecular‐weight kininogen by the serine protease kallikrein‐1. The aims of this study were first to examine the effect of neutralizing kallikrein‐1 on AAA development in a mouse model and second to test how blocking kallikrein‐1 affected cyclooxygenase‐2 and prostaglandin E 2 in human AAA explants. Methods and Results Neutralization of kallikrein‐1 in apolipoprotein E‐deficient ( ApoE −/− ) mice via administration of a blocking antibody inhibited suprarenal aorta expansion in response to angiotensin (Ang) II infusion. Kallikrein‐1 neutralization decreased suprarenal aorta concentrations of bradykinin and prostaglandin E 2 and reduced cyclooxygenase‐2 activity. Kallikrein‐1 neutralization also decreased protein kinase B and extracellular signal‐regulated kinase 1/2 phosphorylation and reduced levels of active matrix metalloproteinase 2 and matrix metalloproteinase 9. Kallikrein‐1 blocking antibody reduced levels of cyclooxygenase‐2 and secretion of prostaglandin E 2 and active matrix metalloproteinase 2 and matrix metalloproteinase 9 from human AAA explants and vascular smooth muscle cells exposed to activated neutrophils. Conclusions These findings suggest that kallikrein‐1 neutralization could be a treatment target for AAA.

Abstract 101: Dipeptidylpeptidase-iv Inhibition Using MK626 Attenuates BAPB/AT2 Induced Murine Aneurysm

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
John S Byrne ◽  
Emily Chen ◽  
Mansoor Husain ◽  
Maral Ouzounian ◽  
Clint Robbins ◽  
...  
Keyword(s):  
Cross Sections ◽  
Elastic Fibre ◽  
Wild Type ◽  
Aneurysmal Dilatation ◽  
Descending Aorta ◽  
Dipeptidylpeptidase Iv ◽  
Matrix Deposition ◽  
Suprarenal Aorta ◽  
Recent Addition ◽  
Glucagon Like Peptide 1

The dearth of effective treatments to diminish aneurysm progression is a recognized clinical challenge. Modulation of the glucagon-like peptide-1 (GLP-1) pathway is a recent addition to anti-diabetic management regimes, and has pleiotropic effects to inhibit arterial wall macrophage infiltration, a key pathological event in aneurysmal disease. We therefore hypothesized that inhibition of endogenous breakdown of GLP-1, using the dipeptidylpeptidase-IV inhibitor MK626, would attenuate BAPN/AT2 induced murine aneurysm. Eight-week-old C57/Bl6 mice received two weeks of oral beta-aminopropriononitrile (BAPN) and four weeks of angiotensin-2 (AT2) via mini-osmotic pump. MK626 3mg/kg in methylcellulose vehicle was administered daily and compared to control methylcellulose vehicle. At four weeks, whole aortas were dissected and photomicrographed. Cross sections of aorta were stained using H&E and EVG. Compared to wild-type, BAPN/AT2 caused dilatation of the aorta from the ascending to the suprarenal segment (p<0.002) with infrarenal sparing (p=0.77). Focal aneurysmal dilatation reproducibly occurred in the suprarenal aorta (wild-type diameter 0.93±0.03mm, n=8; BAPN/AT2 diameter 2.26±0.12, n=8; p<0.0001). Treatment with MK626 attenuated dilatation of the descending aorta compared to controls (BAPN/AT2 control 1.26±0.05mm, n=8; MK626 1.07±0.05mm, n=10; p=0.03). The focal suprarenal aneurysmal dilatation was significantly reduced by treatment with MK626 (BAPN AT2 control 2.26±0.34mm, n=8; MK626 1.66±0.32mm, n=10; p=0.0001). BAPN/AT2 induced aortic aneurysm was associated with excess matrix deposition, increased medial thickness, and elastic fibre fragmentation. Modulation of the GLP pathway using the dipeptidylpeptidase-IV inhibitor MK626 attenuates aneurysm in a BAPN/AT2 induced murine model.

Acute Occlusion of Abdominal Aorta: Unusual Embolization Site for a Cardiac Tumor Mass

2002 ◽  
Vol 88 (5) ◽  
pp. 417-419 ◽  
Author(s):  
Pierfrancesco Veroux ◽  
Carmelo Mignosa ◽  
Massimiliano Veroux ◽  
Giovanni Bartoloni ◽  
Maria Giovanna Bonanno ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Abdominal Aorta ◽  
Young Patients ◽  
Mortality Rates ◽  
Atrial Myxoma ◽  
Thoracic Pain ◽  
Total Occlusion ◽  
Left Atrial Myxoma ◽  
Suprarenal Aorta

We report a rare case of complete embolization of a left atrial myxoma resulting in total occlusion of the suprarenal abdominal aorta. A 54-year-old man was admitted to hospital because of acute thoracic pain with paraplegia and acute renal failure. Abdominal computed tomography and angiography showed evidence of total occlusion of the suprarenal aorta. Intraoperatively, the aorta was found to be occluded by a hard neoformation, histologically defined as atrial myxoma. A diagnosis of atrial myxoma should be suspected in young patients suffering from acute thoracic pain and affected by paraplegia and acute renal failure. Early diagnosis may significantly abate the morbidity and mortality rates associated with this condition.

scholarly journals Early Morphofunctional Changes in AngII-Infused Mice Contribute to Regional Onset of Aortic Aneurysm and Dissection

2020 ◽  
Vol 57 (6) ◽  
pp. 367-375
Author(s):  
Lydia Aslanidou ◽  
Bram Trachet ◽  
Linda Sasset ◽  
Goran Lovric ◽  
Nikolaos Stergiopulos ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Abdominal Aorta ◽  
Vascular Reactivity ◽  
Ex Vivo ◽  
Aortic Aneurysms ◽  
Microstructural Damage ◽  
Suprarenal Aorta ◽  
Aortic Aneurysm And Dissection

Aortic aneurysms and dissections are silent and lethal conditions, whose pathogenesis remains incompletely understood. Although angiotensin II (AngII)-infused ApoE−/− mice have been widely used to study aortic aneurysm and dissection, early morphofunctional alterations preceding the onset of these conditions remain unknown. The goal of this study was to unveil early morphofunctional changes underlying the onset of aneurysm and dissection. At 3 days post-AngII infusion, suprarenal abdominal aorta presented significant volumetric dilatation and microstructural damage. Ex vivo assessment of vascular reactivity of the suprarenal dissection-prone aorta and its side branches, showed an endothelial and contractile dysfunctions that were severe in the suprarenal aorta, moderate distally, and absent in the side branches, mirroring the susceptibility to dissection of these different vascular segments. Early and specific morphofunctional changes of the suprarenal aorta may contribute to the regional onset of aortic aneurysm and dissection by exacerbating the biomechanical burden arising from its side branches.

Role of renal interstitial hydrostatic pressure in natriuresis of systemic nitric oxide inhibition

1993 ◽  
Vol 264 (3) ◽  
pp. F411-F414 ◽  
Author(s):  
J. A. Haas ◽  
A. A. Khraibi ◽  
M. A. Perrella ◽  
F. G. Knox
Keyword(s):  
Nitric Oxide ◽  
Hydrostatic Pressure ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Significant Rise ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Suprarenal Aorta ◽  
Fractional Excretion Of Sodium

Systemic inhibition of nitric oxide synthesis with NG-monomethyl-L-arginine (L-NMMA) increases renal perfusion pressure (RPP) and urinary sodium excretion. Increased RPP has been proposed as one of the mechanisms for the natriuresis caused by intravenous infusion of L-NMMA. We tested the hypothesis that increases in renal interstitial hydrostatic pressure (RIHP) are required for the natriuresis of L-NMMA infusion. Experiments were performed in four groups of Sprague-Dawley rats in which partial aortic clamping and/or bilateral renal decapsulation was performed to control RPP and RIHP. Infusion of L-NMMA (15 mg/kg bolus + 500 micrograms.kg-1 x min-1 continuous infusion) increased RPP (delta+ 14 +/- 1 mmHg), RIHP (delta+ 3.6 +/- 0.7 mmHg), and fractional excretion of sodium (FENa; delta 2.4 +/- 0.6%, P < 0.005). When RPP was prevented from increasing by controlling RPP with an adjustable clamp around the suprarenal aorta, RIHP and FENa did not significantly change. When only RIHP was held constant by bilateral renal decapsulation, FENa was not significantly increased (delta+ 0.68 +/- 0.36%, not significant), despite a significant rise in RPP (delta+ 18 +/- 2 mmHg, P < 0.001). Control of both RPP and RIHP prevented the increase in FENa. Thus, when renal interstitial pressure was controlled, the infusion of L-NMMA did not result in an increase in FENa. These results demonstrate that an increase in RIHP is a necessary component in the natriuresis due to systemic infusion of L-NMMA.

Impaired control of renal hemodynamics and renin release during hyperkalemia in rabbits

1988 ◽  
Vol 254 (5) ◽  
pp. F704-F710 ◽  
Author(s):  
H. B. Lin ◽  
D. B. Young
Keyword(s):  
Perfusion Pressure ◽  
Plasma Potassium ◽  
Renal Perfusion ◽  
Renal Hemodynamics ◽  
Renin Release ◽  
Control Group ◽  
Rabbit Plasma ◽  
Suprarenal Aorta ◽  
Impaired Control ◽  
Significant Impairment

We analyzed the changes in control of renal hemodynamics and renin release resulting from hyperkalemia in the rabbit. Plasma potassium activity was maintained at a controlled elevated level by intravenous infusion of KCl. The potassium activity of the control group (n = 23) averaged 3.20 +/- 0.06 meq/l and that of the hyperkalemic group (n = 13) averaged 5.80 +/- 0.13 meq/l. Renal blood flow (RBF), glomerular filtration rate (GFR), and renin release were measured over a range of renal perfusion pressures achieved by constriction of the suprarenal aorta. The control group's RBF and GFR exhibited excellent autoregulatory capability from 100 to 80 mmHg. However, significant impairment of autoregulation was apparent in the hyperkalemic group. At 100 mmHg, RBF and GFR in the hyperkalemic group averaged 33 and 34% greater, respectively, than those of the control group (P less than 0.005); both variables in the hyperkalemic group were greater than the values of the control group over the autoregulatory range (100-80 mmHg). The renin release values for the two groups were not different at the 100-mmHg pressure level, although renin release of the hyperkalemic group increased to higher levels than those of the control group as perfusion pressure was reduced. At the 70- and 60-mmHg levels renin release from the hyperkalemic group averaged approximately 300% greater than that of the control group (P less than 0.05). However, when expressed as percentage change, the stimulatory effect of hyperkalemia was not apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals “Coral reef” atherosclerosis of the suprarenal aorta: A unique clinical entity

1984 ◽  
Vol 1 (6) ◽  
pp. 903-909 ◽  
Author(s):  
Peter G. Qvarfordt ◽  
Linda M. Reilly ◽  
Marc M. Sedwitz ◽  
William K. Ehrenfeld ◽  
Ronald J. Stoney
Keyword(s):  
Coral Reef ◽  
Clinical Entity ◽  
Suprarenal Aorta
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