Evaluation Of Aortic Aneurysms Research Articles

A New and Practical Model of Human-Like Ascending Aorta Aneurysm in Rats

Introduction: Ascending aortic aneurysm is a serious health risk. In order to study ascending aortic aneurysms, elastase and calcium ion treatment for aneurysm formation are mainly used, but their aneurysm formation time is long and the aneurysm formation rate is low. Thus, this study aimed to construct a rat model of ascending aorta aneurysm with a short modeling time and high aneurysm formation rate, which may mimic the pathological processes of human ascending aorta aneurysm. Methods: Cushion needles with different pipe diameters (1.0, 1.2, 1.4, and 1.6 mm) were used to establish a human-like rat model of ascending aortic aneurysm by narrowing the ascending aorta of rats and increasing the force of blood flow on the vessel wall. The vascular diameters were evaluated using color Doppler ultrasonography after 2 weeks. The characteristics of ascending aortic aneurysm in rats were detected by Masson’s trichrome staining, Verhoeff’s Van Gieson staining, and hematoxylin and eosin staining, while real-time polymerase chain reaction was utilized to assess the total RNA of cytokine interleukin-1β, interleukin 6, transforming growth factor-beta 1, and metalloproteinase 2. Results: Two weeks after surgery, the ultrasound images and the statistical analysis demonstrated that the diameter of the ascending aorta in rats increased more than 1.5 times, similar to that in humans, indicating the success of animal modeling of ascending aortic aneurysm. Moreover, the optimal constriction diameter of the ascending aortic aneurysm model is 1.4 mm by the statistical analysis of the rate of ascending aortic aneurysm and mortality rate in rats with different constriction diameters. Conclusions: The human-like ascending aortic aneurysm model developed in this study can be used for the studies of the pathological processes and mechanisms of ascending aortic aneurysm in a more clinically relevant fashion.

A novel abdominal aortic aneurysm model produced by periarterial application of hydrochloric acid.

Previous abdominal aortic aneurysm (AAA) animal modeling methodologies were either expensive or complicated. Here, we developed a novel AAA model which was simple to set up and generated minimal calcification. Twenty-four rats were divided randomly into four groups. Groups 1, 2 and 3 underwent surgery in which 15% hydrochloric acid (HCl) was applied periarterially to the abdominal aorta for 5 min, followed by sacrifice 1 week (group 1), 2 weeks (group 2), and 4 weeks (group 3) after surgery. The maximum aortic diameter (MAD) was measured at surgery and before animal sacrifice. Rats in group 4 were sham-treated. The MADs in group 1, 2 and 3 showed significant dilation compared with group 4, with a mean dilation rate of 33.8% in the first week after surgery. Histopathological examination revealed infiltration of macrophages into the adventitia, obvious apoptosis of smooth muscle cells, and rupture and collapse of the elastic fibers. Furthermore, no calcification was observed in the dilated aorta. The mRNA expression levels of inflammatory factors were at least two-fold higher in group 1 than in group 4, indicating significant inflammatory response in the progression of AAA information. In conclusion, periarterial application of 15% HCl is a convenient and reliable model to create an abdominal aortic aneurysm in rats, and the potential development mechanism may be related to the proinflammatory effects of HCl.

Effect of anti-CIRP antibody on inflammatory response, tumor formation and abdominal aortic aneurysm in rats

Purpose: To investigate the effect of anti-cold induced RNA binding protein (CIRP) antibody on inflammation, tumor formation and abdominal aortic aneurysm in rats.Methods: Thirty healthy male Wistar rats were assigned to pseudo-operation, abdominal aortic aneurysm model, and anti-CIRP groups, with 10 in each group. The levels of CIRP, TNF- α, monocyte giant cytokine chemokine-1 (MCP-1), Toll-like receptor 4 (TLR4)) and nuclear factor kappaB (NF- κB)were determined compared among the groups.Results: At both 2 and 4 weeks, the expression of CIRP protein in the model group was significantly higher than that in the sham operation group (p < 0.05). At these two time-points, tumor formation and maximum diameter were higher in anti-CIRP and model control rats than in pseudo-operation rats. After 4 weeks of treatment, the protein expressions of TNF- α, MCP-1, TLR4 and NF-κB were higher in anti-CIRP and model control rats than in pseudo-operation rats, but were lower than model control values (p < 0.05).Conclusion: CIRP expression is significantly increased in abdominal aortic aneurysm tissue and serum, and is involved in the onset and progress of abdominal aortic aneurysm. Anti-CIRP antibody therapy effectively suppresses tumorigenesis, and inhibits tumor wall inflammatory reaction viaTLR4/NF-κB pathway. This finding provides a clue and new strategy for the clinical management of abdominal aortic aneurysm.
 Keywords: CIRP, Abdominal aortic tumor wall, Inflammatory reaction, Protein expression, Tumor body

Discovery of novel biomarkers for atherosclerotic aortic aneurysm through proteomics-based assessment of disease progression

Since aortic aneurysms (AAs) are mostly asymptomatic, but they have a high mortality rate upon rupture, their detection and progression evaluation are clinically important issues. To discover diagnostic biomarkers for AA, we performed proteome analysis of aortic media from patients with thoracic atherosclerotic AA (TAAA), comparing protein levels between the aneurysm and normal tissue areas. After hierarchical clustering analysis of the proteome analysis data, tissue samples were classified into three groups, regardless of morphological features. This classification was shown to reflect disease progression stage identified by pathological examination. This proteomics-based staging system enabled us to identify more significantly altered proteins than the morphological classification system. In subsequent data analysis, Niemann-Pick disease type C2 protein (NPC2) and insulin-like growth factor-binding protein 7 (IGFBP7) were selected as novel biomarker candidates for AA and were compared with the previously reported biomarker, thrombospondin 1 (THBS1). Blood concentrations of NPC2 and IGFBP7 were significantly increased, while THBS1 levels were decreased in TAAA and abdominal atherosclerotic AA patients. Receiver operating characteristic analysis of AA patients and healthy controls showed that NPC2 and IGFBP7 have higher specificity and sensitivity than THBS1. Thus, NPC2 and IGFBP7 are promising biomarkers for the detection and progression evaluation of AA.

Targeted Gold Nanoparticles as an Indicator of Mechanical Damage in an Elastase Model of Aortic Aneurysm.

Elastin is a key structural protein and its pathological degradation deterministic in aortic aneurysm (AA) outcomes. Unfortunately, using current diagnostic and clinical surveillance techniques the integrity of the elastic fiber network can only be assessed invasively. To address this, we employed fragmented elastin-targeting gold nanoparticles (EL-AuNPs) as a diagnostic tool for the evaluation of unruptured AAs. Electron dense EL-AuNPs were visualized within AAs using micro-computed tomography (micro-CT) and the corresponding Gold-to-Tissue volume ratios quantified. The Gold-to-Tissue volume ratios correlated strongly with the concentration (0, 0.5, or 10U/mL) of infused porcine pancreatic elastase and therefore the degree of elastin damage. Hyperspectral mapping confirmed the spatial targeting of the EL-AuNPs to the sites ofdamaged elastin. Nonparametric Spearman's rank correlation indicated that the micro-CT-based Gold-to-Tissue volume ratios had a strong correlation with loaded (ρ = 0.867, p-val = 0.015) and unloaded (ρ = 0.830, p-val = 0.005) vessel diameter, percent dilation (ρ = 0.976, p-val = 0.015), circumferential stress (ρ = 0.673, p-val = 0.007), loaded (ρ = -0.673, p-val = 0.017) and unloaded (ρ = -0.697, p-val = 0.031) wall thicknesses, circumferential stretch (ρ = -0.7234, p-val = 0.018), and lumen area compliance (ρ = -0.831, p-val = 0.003). Likewise, in terms of axial force and axial stress vs. stretch, the post-elastase vessels were stiffer. Collectively, these findings suggest that, when combined with CT imaging, EL-AuNPs can be used as a powerful tool in the non-destructive estimation of mechanical and geometric features of AAs.

Excessive Methionine Supplementation Exacerbates the Development of Abdominal Aortic Aneurysm in Rats

Objective: The relationship between methionine (Met) and abdominal aortic aneurysm (AAA) has been previously demonstrated, but the mechanisms controlling this association remain unclear. This study investigated the potential contribution of hypermethioninemia (HMet) to the development of AAA. Methods: A model of AAA was induced by intraluminal porcine pancreatic elastase (PPE) infusion in 60 male Sprague-Dawley rats divided into 4 groups (n = 15 per group). Met was supplied by intragastric administration (1 g/kg body weight/day) from 1 week before surgery until 4 weeks after surgery. The aortic diameter was measured by ultrasound. Aortas were collected 4 weeks after surgery and subjected to biochemical analysis, histological assays, and transmission electron microscopy. Results: After 5 weeks of Met supplementation, HMet increased the dilation ratio of the HMet + PPE group, and hyperhomocysteinemia was also induced in HMet and HMet + PPE rats. Increased matrix metalloproteinase-2 (MMP-2), osteopontin, and interleukin-6 expression was detected in HMet + PPE rats. Furthermore, increased autophagy was detected in the HMet + PPE group. Conclusion: This study demonstrates that HMet may exacerbate the formation of AAA due to the increased dilation ratio partially via enhancing MMP-2 and inflammatory responses.

Caffeic Acid Phenethyl Ester Inhibits the Progression of Elastase Induced Aortic Aneurysm in Rats

Caffeic Acid Phenethyl Ester Inhibits the Progression of Elastase Induced Aortic Aneurysm in Rats

Perivascular scaffolds loaded with adipose tissue-derived stromal cells attenuate development and progression of abdominal aortic aneurysm in rats.

Abdominal aortic aneurysm (AAA) is the pathological dilation and weakening of the abdominal aorta wall. Inflammation, degradation of the extracellular matrix (ECM) and loss of smooth muscle cells and skewing of their function are pivotal in AAA pathology. We developed a recombinant collagen-based patch (RCP) to provide structural integrity and deliver Adipose tissue-Derived Stromal Cells (ASC) for repair. Patches supported adhesion and function as well as proliferation of ASC. ASC-loaded RCPs or bare patches, applied around the aorta after AAA induction in rats, both maintained structural integrity of the aortic wall at time of explant (2w). However, wall thinning, accompanied by loss of elastin fibers and loss of medial SMC, was only attenuated in ASC-loaded RCP-treated AAA rats. Interestingly, this coincided with migration of ASC into the media and a reduced influx of macrophages. We hypothesize that the medially-migrated ASC dampened or skewed the adverse innate immunity and thus suppressed SMC apoptosis, phenotypic skewing and elastin degradation. We conclude that the periadventitial delivery of ASC with RCP suppresses development and progression of AAA, which is has an expected future clinical benefit in combination with an appropriate early screening program of patients at risk for aneurysms. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A:2494-2506, 2018.

Early growth response factor-1 DNA enzyme 1 inhibits the formation of abdominal aortic aneurysm in rats.

The aim of the present study was to characterize the effects of early growth response factor-1 DNA enzyme (EDRz) in a rat abdominal aortic aneurysm (AAA) model to determine the mechanism by which EDRz inhibits AAA and affects the formation of AAA by regulating the activity of matrix metalloproteinase (MMP)-2 and MMP-9. EDRz was transfected into the abdominal aorta of rats using the jetPRIME transfection reagent following infusion with elastase. Fluorescent microscopy, hematoxylin and eosin staining, ultrastructural analysis, reverse transcription-quantitative polymerase chain reaction, western blotting and immunohistochemical analysis were performed to characterize the response to EDRz. The EDRz group showed minimal aneurysm formation when compared with the control group, with significantly lower aortic diameter expansion (2.5±0.1 vs. 3.5±0.1 mm; P<0.05). Early growth response factor 1 (Egr-1) mRNA and protein levels were significantly decreased in the EDRz group, as expected. The decrease in Egr-1 was accompanied by decreases in the mRNA and protein levels of MMP-2 and MMP-9 (P<0.05). Transfection of the Egr-1 specific synthetic DNA enzyme EDRz significantly reduced AAA following elastase infusion in rats, at least in part due to the decreased expression of downstream MMP-2 and MMP-9.

The preventive and curative effects of melatonin against abdominal aortic aneurysm in rats

ObjectiveOxygen free radicals are important components involved in the histopathologic tissue alterations observed during abdominal aortic aneurysms (AAAs). This study examined whether melatonin has protective or therapeutic effects against AAAs. MethodsSprague-Dawley rats were divided into four groups. A CaCl2 model was used to induce AAA. Starting on the operation day (Mel+AAA+Mel group) or 4 weeks after the operation (AAA+Mel group), the rats received intraperitoneal melatonin (10 mg/kg/day) for 6 and 2 weeks, respectively. The control and AAA groups received vehicle for 2 weeks after the sham operation and AAA induction, respectively. Angiographic measurements were recorded at the beginning, week 4, and week 6 of the study. After decapitation, aorta tissues were taken for the measurement of malondialdehyde, 8-hydroxy-2′-deoxyguanosine, glutathione levels, and myeloperoxidase and caspase-3 activity. Matrix metalloproteinase (MMP)-2, MMP-9, tumor necrosis factor-α, and inducible nitric oxide synthase protein expressions were analyzed by Western blot technique. Aortic tissues were also examined by light microscopy. ResultsCaCl2 caused an inflammatory response and oxidative damage indicated by rises in malondialdehyde and 8-hydroxy-2′-deoxyguanosine levels. Myeloperoxidase and caspase-3 activities were increased, but glutathione levels were reduced. On the one hand, MMP-2, MMP-9, tumor necrosis factor-α, and inducible nitric oxide synthase protein expressions were increased in the vehicle-treated AAA group. On the other hand, melatonin treatment reversed all of these biochemical indices and histopathologic alterations. ConclusionsAccording to the data, although melatonin tended to reverse the biochemical parameters given on week 4, the preventive effect is more pronounced when given concomitantly with AAA induction because values were closer to the control levels.

Systemic Delivery of Nanoparticles Loaded with Pentagalloyl Glucose Protects Elastic Lamina and Prevents Abdominal Aortic Aneurysm in Rats.

Degeneration of elastin plays a vital role in the pathology and progression of abdominal aortic aneurysm (AAA). Our previous study showed that pentagalloyl glucose (PGG), a core derivative of tannic acid, hinders the development of AAAs in a clinically relevant animal model when applied locally. In this study, we tested whether targeted nanoparticles (NPs) can deliver PGG to the site of an aneurysm and prevent aneurysmal growth by protecting elastin. PGG-loaded albumin NPs with a surface-conjugated elastin-specific antibody were prepared. Aneurysms were induced by calcium chloride-mediated injury to the abdominal aorta in rats. NPs were injected into the tail vein after 10days of CaCl2 injury. Rats were euthanized after 38days. PGG delivery led to reduction in macrophage recruitment, matrix metalloproteinase (MMP) activity, elastin degradation, calcification, and development of aortic aneurysm. Such NP delivery offers the potential for the development of effective and safe therapies for AAA.

Nanoparticles Effectively Target Rapamycin Delivery to Sites of Experimental Aortic Aneurysm in Rats.

Several drugs targeting the pathogenesis of aortic aneurysm have shown efficacy in model systems but not in clinical trials, potentially owing to the lack of targeted drug delivery. Here, we designed a novel drug delivery system using nanoparticles to target the disrupted aortic aneurysm micro-structure. We generated poly(ethylene glycol)-shelled nanoparticles incorporating rapamycin that exhibited uniform diameter and long-term stability. When injected intravenously into a rat model in which abdominal aortic aneurysm (AAA) had been induced by infusing elastase, labeled rapamycin nanoparticles specifically accumulated in the AAA. Microscopic analysis revealed that rapamycin nanoparticles were mainly distributed in the media and adventitia where the wall structures were damaged. Co-localization of rapamycin nanoparticles with macrophages was also noted. Rapamycin nanoparticles injected during the process of AAA formation evinced significant suppression of AAA formation and mural inflammation at 7 days after elastase infusion, as compared with rapamycin treatment alone. Correspondingly, the activities of matrix metalloproteinases and the expression of inflammatory cytokines were significantly suppressed by rapamycin nanoparticle treatment. Our findings suggest that the nanoparticle-based delivery system achieves specific delivery of rapamycin to the rat AAA and might contribute to establishing a drug therapy approach targeting aortic aneurysm.

Correlation of osteopontin and nuclear factor-κB expression with pathogenesis of abdominal aortic aneurysm in rats

Objective To establish rat model of abdominal aortic aneurysm (AAA),observe the expression of osteopontin (OPN) and nuclear factor-κB (NF-κB) and explore the molecular mechanism of AAA.Methods Thirty rats were divided into 3 groups (n =10 each).The rat AAA models were made by perfusing pancreatopeptidase E from hog pancreas into the aorta of rats for 30 min.Aortas were taken out two weeks after perfusion and the diameter of all aortas was measured.Hematoxylin and eosin (HE) staining was used to observe the structural change and elastase staining to observe how the area of elastase altered in the middle tuna of the aorta.Immunohistochemistry and Western blotting were used to detect the expression of OPN,NF-κB and matrix metalloproteinase-2 (MMP-2).Results Rat AAA model was successfully made.As compared with saline group and normal group,the infiltration of inflammatory cells was significantly increased and the quantity of elastase was significantly reduced in experimental group.Immunohistochemistry revealed that the expression of OPN was significantly increased in experimental group (P ＜ 0.05).Western blotting demonstrated that the expression of OPN was also obviously increased in experimental group (P ＜ 0.01).Conclusion OPN may increase the expression of MMP-2 through the NF-κB pathway in rat AAA model,thereby accelerating the degradation of extracellular matrix and eventually leading to occurrence of AAA. Key words: Abdominal aortic aneurysm; Osteopontin; Nuclear factor-κB; Matrix metallo-proteinase-2

Free-radical scavenger edaravone inhibits both formation and development of abdominal aortic aneurysm in rats

An ideal pharmaceutical treatment for abdominal aortic aneurysm (AAA) is to prevent aneurysm formation and development (further dilatation of pre-existing aneurysm). Recent studies have reported that oxidative stress with reactive oxygen species (ROS) is crucial in aneurysm formation. We hypothesized that edaravone, a free-radical scavenger, would attenuate vascular oxidative stress and inhibit AAA formation and development. An AAA model induced with intraluminal elastase and extraluminal calcium chloride was created in 42 rats. Thirty-six rats were divided three groups: a low-dose (group LD; 1 mg/kg/d), high-dose (group HD; 5 mg/kg/d), and control (group C, saline). Edaravone or saline was intraperitoneally injected twice daily, starting 30 minutes before aneurysm preparation. The remaining six rats (group DA) received a delayed edaravone injection (5 mg/kg/d) intraperitoneally, starting 7 days after aneurysm preparation to 28 days. AAA dilatation ratio was calculated. Pathologic examination was performed. ROS expression was semi-quantified by dihydroethidium staining and the oxidative product of DNA induced by ROS, 8-hydroxydeoxyguanosine (8-OHdG), by immunohistochemical staining. At day 7, ROS expression and 8-OHdG-positive cells in aneurysm walls were decreased by edaravone treatment (ROS expression: 3.0 ± 0.5 in group LD, 1.7 ± 0.3 in group HD, and 4.8 ± 0.7 in group C; 8-OHdG-positive cells: 106.2 ± 7.8 cells in group LD, 64.5 ± 7.7 cells in group HD, and 136.6 ± 7.4 cells in group C; P < .0001), compared with group C. Edaravone treatment significantly reduced messenger RNA expressions of cytokines and matrix metalloproteinases (MMPs) in aneurysm walls (MMP-2: 1.1 ± 0.5 in group LD, 0.6 ± 0.1 in group HD, and 2.3 ± 0.4 in group C; P < .001; MMP-9: 1.2 ± 0.1 in group LD, 0.2 ± 0.6 in group HD, and 2.4 ± 0.2 in group C; P < .001). At day 28, aortic walls in groups LD and HD were less dilated, with increased wall thickness and elastin content than those in group C (dilatation ratio: 204.7% ± 16.0% in group C, 156.5% ± 6.6% in group LD, 136.7% ± 2.0% in group HD; P < .0001). Delayed edaravone administration significantly prevented further aneurysm dilatation, with increased elastin content (155.2% ± 2.9% at day 7, 153.1% ± 11.6% at day 28; not significant). Edaravone inhibition of ROS can prevent aneurysm formation and expansion in the rat AAA model. Free-radical scavenger edaravone might be an effective pharmaceutical agent for AAA in clinical practice.

Elastic fibers reconstructed using adenovirus-mediated expression of tropoelastin and tested in the elastase model of abdominal aortic aneurysm in rats

An adenoviral vector carrying a recombinant tropoelastin (TE) gene with a Green Fluorescent Protein (GFP) tag adenoviral tropoelastin green fluorescent protein (AdTE-GFP) was transferred to aortic vascular smooth muscle cells (VSMCs) for studying the expression of recombinant elastin in vitro and the reconstruction of elastic fibers in vivo in experimental abdominal aortic aneurysm (AAA). The AAAs were induced in rats by perfusing the arteries with porcine pancreatic elastase, and after AAA formation, adenoviral vectors were perfused directly into the aneurysmal lumen. VSMCs transfected with AdTE-GFP in vitro and in vivo were detected by fluorescence microscopy. The TE mRNA levels and the level of recombinant elastin expression of AdTE-GFP transfected VSMCs in vitro (at 1, 3, and 5 days) and in vivo (at 2 and 4 weeks) were compared by real-time reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. The aortic diameters (AD) of the aneurysms were measured at three time points (immediately, 2 weeks, and 4 weeks post-perfusion) and comparisons were made among the AdTE-GFP transfected group, an empty adenovirus (AdNull) transfected group, and a phosphate buffered saline (PBS) perfused group. Formation of new elastic fibers in vivo was assessed by histologic analysis. AdTE-GFP transfection reversed AAA formation (mean +/- standard error), with the controls showing increased ADs (a 48.50 +/- 16.55% increase for the PBS perfusion group and a 39.84 +/- 15.59% increase for the AdNull treated group) and the AdTE-GFP transfected group showing a decreased AD (23.04 +/- 14.49%, P < .01). Histological studies showed that the AdTE-GFP transfected group also had reconstructed elastic fibers in the aneurysmal wall. Real-time PCR for TE mRNA demonstrated a significant increase upon transfection of AdTE-GFP in vitro and in vivo. Western blot analysis for GFP demonstrated elastin-GFP expression only upon transfection of AdTE-GFP, although the amount of elastin-GFP protein tended to be lower in vivo than in vitro. Elastin von-Giesson stain combined with GFP antibody immunohistochemistry demonstrated new elastic fibers in the transfected aneurysmal VSMCs. VSMCs were transfected efficiently with a special AdTE-GFP vector, enabling recombinant elastin to be produced in these VSMCs in vitro and in vivo. This expression of a recombinant elastin and the related reconstruction of elastic fibers within the aneurysmal tissue appeared to prevent or reverse the aneurysm dilatation.

COX-2 in Cardiovascular Disease

Prostanoids are a large family of lipid mediators derived from the arachidonic acid metabolites of the cyclooxygenase (COX) enzymes. Therapeutically, COX is the target of the nonsteroid antiinflammatory drugs (NSAIDs), a chemically diverse group that includes ibuprofen, naproxen, and diclofenac, among dozens of others. Inhibition of prostanoid production by traditional NSAIDs accounts for all their major therapeutic effects, such as the dampening down of inflammation and the reduction of fever, and their potentially severe adverse side effects, most commonly within the gastrointestinal tract.1,2 See page 1137 Since the early 1990’s it has been clear there are two distinct enzymes responsible for the production of prostanoids: a constitutive COX-1 found in all tissues and an inflammation-associated enzyme COX-2.1,2 COX-2 is constitutively expressed in only a few sites, such as parts of the kidney and central nervous system, but is highly upregulated and active at sites of inflammation. These findings led to the hypothesis that selective COX-2 inhibitors could be antiinflammatory without the major side effects associated with traditional NSAIDs. Against this background several COX-2–selective inhibitors have been produced and brought to market, the first two being celecoxib (Celebrex) and rofecoxib (Vioxx). Preclinical studies of these COX-2–selective inhibitors were extremely promising. In animal models, for example, they were demonstrated to be as efficacious as traditional NSAIDs but to be lacking their toxic actions on the gastrointestinal tract. Clinical trials have, however, been marred by controversy. The CLASS trial for celecoxib, a 12-month osteoarthritis study of celecoxib, demonstrated celecoxib to have improved safety relative to ibuprofen but not …

Aortic Aneurysm and Dissection : Evaluation with Spiral CT Angiography

The study was undertaken for aortic evaluation and to see its usefulness for assessing aortic aneurysm, aortic dissection and pseudoaneurysm by spiral CT angiography (CTA). A total of 28 patients with aortic aneurysm (n=19), aortic dissection (n=5) and aortic pseudoaneurysm (n=4) were included. CTA findings were compared with ultrasonography in 14, digital subtraction angiography (DSA) in 14, MRI in 9; and surgical findings in 12 patients. CTA was an excellent imaging modality for comprehensive evaluation of aortic aneurysm, dissection and pseudoaneurysm combining the advantage of conventional contrast enhanced CT axial images and those of angiography in the form of 3D reformatted images.

Angiolathyrism: III. Vasa vasorum in experimental dissecting aortic aneurysm

In order to study the pathogenesis of dissecting aortic aneurysm, an attempt was made to demonstrate aortic medial vasa vasorum by infusion of India ink into 25 weanling rats that had been administered β-aminopropionitrile fumarate for as long as 30 days. More than half of the rats developed gross or microscopic dissecting aneurysms of the aorta, with the frequent occurrence of hemothorax due to rupture. India ink was present in the dissected lumen of the aortic wall but not within intact portions of the media. Capillary networks containing India ink were noted in periadventitial and adventitial layers and in periadventitial granulation tissue covering dissection, but were not found within the media. Infusion of India ink in 18 normal rats showed abundant capillary networks in periadventitial and adventitial layers but failed to reveal capillary vascular structure within the media of aorta. The results of this study indicate that in experimental dissecting aortic aneurysm in rats induced by β-aminopropionitrile fumarate the vasa vasorum do not play a role in its pathogenesis.