scholarly journals Acute aortic rupture in a dog with spirocercosis following the administration of medetomidine : clinical communication

2005 ◽  
Vol 76 (3) ◽  
Author(s):  
K.E. Joubert ◽  
M.J. McReynolds ◽  
F. Strydom
Keyword(s):  
Aortic Wall ◽  
Aortic Rupture ◽  
Clinical Signs ◽  
Diagnostic Procedures ◽  
Definitive Diagnosis ◽  
Aortic Aneurysms ◽  
Post Mortem ◽  
Clinical Communication ◽  
Acute Rupture ◽  
Strong Suspicion

Spirocercosis is an emerging disease in veterinary medicine. A strong suspicion of spirocercosis is usually evident after a thorough clinical examination and radiography of the chest has been performed. Lesions seen on radiography include an oesophageal mass, spondylitis and oesophageal air. Unfortunately, radiography is not diagnostic and additional diagnostic procedures are required to confirm the diagnosis. Endoscopy is commonly performed to diagnose the condition. The dog presented in this study had radiographic and clinical signs consistent with spirocercosis and definitive diagnosis was required. Shortly after sedation with medetomidine, the dog went into cardiac arrest and failed to respond to resuscitative measures. On post mortem, the diagnosis of spirocercosis was confirmed and the cause of death was identified as acute aortic rupture. Aortic aneurysms are not an uncommon finding and cause of acute death in dogs with spirocercosis. The acute rupture of the aorta in this case is most probably the result of cardiovascular changes associated with the administration of medetomidine. Medetomidine causes an acute rise in systemic vascular resistance with hypertension. The increase in shear stress across the weakened aortic wall resulted in rupture. Caution with the use of medetomidine in patients with spirocercosis is advised.

Abstract 667: The Role of Aortic Wall-Nuclear Factor- kappa B (NF-kB) Signaling in Formation of Dissecting Aortic Aneurysms

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Talha Ijaz ◽  
Hong Sun ◽  
Adrian Recinos ◽  
Ronald G Tilton ◽  
Allan R Brasier
Keyword(s):  
Flow Cytometry ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Aortic Rupture ◽  
Aortic Aneurysms ◽  
Tunel Staining ◽  
Abdominal Aortic ◽  
Significant Difference

Introduction: Abdominal aortic aneurysm is a devastating disease since it can lead to aortic rupture and instantaneous death. We previously demonstrated that IL-6 secreted from the aortic wall is necessary for the development of abdominal aortic aneurysm and dissection (AAD). Since IL-6 is a NF-kB/RelA dependant gene, we investigated the role of aortic wall- NF-kB/RelA signaling in the development of AAD. Methods and Results: To test the role of aortic wall-RelA, we utilized Cre-Lox technology to delete RelA from aortic cells. Tamoxifen-inducible, Col1a2-promoter driven Cre mice (Col1a2-Cre) were crossed with mT/mG Cre-reporter mice to determine which aortic cells undergo genetic recombination after Cre activation. Flow cytometry analysis of the aortic wall indicated that 88% of the genetically recombined cells were SMCs and 8% were fibroblasts. Next, RelA floxed (RelA f/f) mice, generated in our lab, were crossed with Col1a2-Cre mice. RelA f/f Cre+ and RelA f/f Cre- were stimulated with tamoxifen for 10 days to generate aortic-RelA deficient (Ao-RelA-/-) or wild-type (Ao-RelA+/+) transgenics. Flow cytometry, qRT-PCR, and immunohistochemistry analysis suggested a depletion of aortic-RelA greater than 60%. To test the role of Ao-RelA in AAD, Ao-RelA -/- (n= 20) and Ao-RelA +/+ (n=14) mice were infused with angiotensin II for 7 days. Surprisingly, 20% of Ao-RelA-/- mice died from development of AAD and aortic rupture while no deaths were observed in Ao-RelA+/+ group. In addition, 40% of Ao-RelA-/- mice developed AAD compared to 14% of Ao-RelA+/+ mice. There was no significant difference in TUNEL staining or ERTR7+ fibroblast population between the two groups. Conclusion: Our studies suggest that aortic wall-RelA may be necessary for protection from AAD.

scholarly journals Significance of Hemodynamics Biomarkers, Tissue Biomechanics and Numerical Simulations in the Pathogenesis of Ascending Thoracic Aortic Aneurysms

2020 ◽  
Vol 26 ◽  
Author(s):  
Salvatore Campisi ◽  
Raja Jayendiran ◽  
Francesca Condemi ◽  
Magalie Viallon ◽  
Pierre Croisille ◽  
...  
Keyword(s):  
Aortic Wall ◽  
Aortic Rupture ◽  
Scientific Evidence ◽  
Aortic Disease ◽  
Aortic Aneurysms ◽  
Imaging Biomarkers ◽  
Aortic Tissue ◽  
Thoracic Aortic Aneurysms ◽  
Non Invasive ◽  
Valve Function

Abstract:: Guidelines for the treatment of aortic wall diseases are based on measurements of maximum aortic diameter. However aortic rupture or dissections do occur for small aortic diameters. Growing scientific evidence underlines the importance of biomechanics and hemodynamics in aortic disease development and progression. Wall shear stress (WWS) is an important hemodynamics marker which depends on aortic wall morphology and on the aortic valve function. WSS could be helpful to interpret aortic wall remodeling and define personalized risk criteria. The complementarity of Computational Fluid Dynamics and 4D Magnetic Resonance Imaging as tools for WSS assessment is a promising reality. The potentiality of these innovative technologies will provide maps or atlases of hemodynamics biomarkers to predict aortic tissue dysfunction. Ongoing efforts should focus on the correlation between these non-invasive imaging biomarkers and clinico-pathologic situations for the implementation of personalized medicine in current clinical practice.

Abstract 1428: Cyclophilin a Promotes Vascular Oxidative Stress and Accelerates Development of Angiotensin II-Induced Aortic Aneurysms

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Kimio Satoh ◽  
Patrizia Nigro ◽  
Tetsuya Matoba ◽  
Michael R O’Dell ◽  
Zhaoqiang Cui ◽  
...  
Keyword(s):  
Cell Migration ◽  
Angiotensin Ii ◽  
Rhode Island ◽  
Inflammatory Cell ◽  
Aortic Wall ◽  
Bone Marrow Cells ◽  
Aortic Rupture ◽  
Gelatin Zymography ◽  
Cyclophilin A ◽  
Aortic Aneurysms

Cyclophilin A (CyPA) is a chaperone protein secreted from vascular smooth muscle cells (VSMC) in response to reactive oxygen species (ROS), that stimulates VSMC migration and inflammatory cell migration in vitro. Abdominal aortic aneurysm (AAA) formation involves inflammatory cytokine release, leukocyte recruitment, aortic wall degradation, and neovascularization. We hypothesized that VSMC-derived CyPA contributes to AAA pathogenesis due to its proinflammatory properties. To determine the role of CyPA in AAA formation, ApoE −/− and ApoE −/− CyPA −/− mice were infused with angiotensin II (AngII, 1000 ng/min/kg) for 4 weeks. There were no differences in blood pressure and cholesterol between ApoE −/− and ApoE −/− CyPA −/− mice before and after Ang II treatment. AngII-induced AAA formation and aortic rupture was frequently observed in ApoE −/− mice (89% and 40%). In contrast, ApoE −/− CyPA −/− mice were completely protected from AngII-induced AAA formation and aortic rupture (0% and 0%). ApoE −/− CyPA −/− mice showed decreased levels of monocyte chemoattractant protein (MCP)-1 in the aorta and lacked elastic lamina degradation, microvessel formation, and aortic expansion. In response to AngII, recruitment of leukocytes to the aortic wall was markedly impaired in ApoE −/− CyPA −/− mice compared with ApoE −/− mice (counts/area; 8.6±4.3 vs. 60.0±13.8, P <0.01). The incidence of AAA was 63% in CyPA +/+ marrow-transplanted ApoE −/− mice, while the incidence of AAA in ApoE −/− CyPA −/− mice remained 0% after transplantation of CyPA +/+ bone marrow cells. In situ and gelatin zymography demonstrated that CyPA was required for matrix metalloproteinase (MMP) activation in aortic wall. Treatment of mouse aortic wild-type VSMC with AngII augmented MMP activity, which was significantly less in CyPA −/− VSMC. Treatment of VSMC with 100 nM CyPA augmented MMP activity, suggesting the importance of extracellular CyPA as well as intracellular CyPA. Finally, VSMC-specific CyPA overexpressing mice revealed augmented AngII-induced MMP activity in the vascular wall. Vascular-derived CyPA contributes to AAA pathogenesis in mice by increasing proinflammatory cytokine expression, inflammatory cell migration, and MMP activation. This research has received full or partial funding support from the American Heart Association, AHA Founders Affiliate (Connecticut, Maine, Massachusetts, New Hampshire, New Jersey, New York, Rhode Island, Vermont).

Ultrastructural investigation of an adenoma of the pituitary post mortem

1987 ◽  
Vol 45 ◽  
pp. 622-623
Author(s):  
Shirley Siew ◽  
W. C. deMendonca
Keyword(s):  
Deleterious Effect ◽  
Anterior Lobe ◽  
Definitive Diagnosis ◽  
Pars Intermedia ◽  
Post Mortem ◽  
Close Apposition ◽  
Autopsy Material ◽  
Progressive Loss ◽  
Transmission Electron ◽  
Means Of Transmission

The deleterious effect of post mortem degeneration results in a progressive loss of ultrastructural detail. This had led to reluctance (if not refusal) to examine autopsy material by means of transmission electron microscopy. Nevertheless, Johannesen has drawn attention to the fact that a sufficient amount of significant features may be preserved in order to enable the establishment of a definitive diagnosis, even on “graveyard” tissue.Routine histopathology of the autopsy organs of a woman of 78 showed the presence of a well circumscribed adenoma in the anterior lobe of the pituitary. The lesion came into close apposition to the pars intermedia. Its architecture was more compact and less vascular than that of the anterior lobe. However, there was some grouping of the cells in relation to blood vessels. The cells tended to be smaller, with a higher nucleocytoplasmic ratio. The cytoplasm showed a paucity of granules. In some of the cells, it was eosinophilic.

scholarly journals A life-threatening spontaneous ascending aortic rupture due to a small penetrating aortic ulcer

2021 ◽  
Vol 9 ◽  
pp. 2050313X2110377
Author(s):  
Yasuhito Nakamura ◽  
Kiyoshi Doi ◽  
Syojiro Yamaguchi ◽  
Etsuji Umeda ◽  
Osamu Sakai ◽  
...  
Keyword(s):  
Rare Case ◽  
Aortic Wall ◽  
Aortic Rupture ◽  
Ascending Aorta ◽  
Bleeding Site ◽  
Penetrating Aortic Ulcer ◽  
Postoperative Course ◽  
Life Threatening ◽  
Aortic Dissections

We reported a rare case of spontaneous frank rupture of a small (4 mm) penetrating aortic ulcer in the ascending aorta resulted in catastrophic bleeding. The ulcer only created a pinhole wound in the adventitia without saccular aneurysms, intramural hematomas, or aortic dissections. Notably, the wound could be directly closed because the aortic wall was intact only 5 mm away from the bleeding site. The postoperative course was uneventful, and the patient was discharged on the 11th postoperative day. After 8 months, follow-up computed tomography showed no abnormality of the aortic wall at the repair site.

scholarly journals WALL STRESS IN ASCENDING AORTA ANEURYSMS AS A PREDICTIVE FACTOR OF BREAKAGE

2021 ◽  
Vol 108 (Supplement_3) ◽  
Author(s):  
R J Burgos Lázaro ◽  
N Burgos Frías ◽  
S Serrano-Fiz García ◽  
V Ospina Mosquera ◽  
F Rojo Pérez ◽  
...  
Keyword(s):  
Aortic Wall ◽  
Wall Stress ◽  
Middle Layer ◽  
Ascending Aorta ◽  
Aortic Aneurysms ◽  
Maximum Diameter ◽  
Resistance Factors ◽  
Risk Of Rupture ◽  
Traction Test

Abstract INTRODUCTION The surgical indication for ascending aortic aneurysms (AAA) is established when the maximum diameter &gt; 50 mm; It responds to Laplace's Law (T wall = P × r / 2e). The aim of the study is to define wall stress in AAA. MATERIAL AND METHODS 218 ascending aortic walls have been studied: 96 from organ donors, and 122 from AAA: Marfán 58 (47.5%), bicuspid aortic valve 26 (21.4%), and atherosclerosis 38 (31.1%). The samples were studied "in vitro", according to the model Young's (relationship between stress and deformed area), by means of the mechanical traction test (Tension = Force / Area). The analysis was performed with the stress-elongation curve (d Tension / d Elongation). RESULTS The stress of the aortic wall, classified from highest to lowest according to pathology and age was: cystic necrosis of the middle layer, arteriosclerosis, age &gt; 60 years, between 35 and 59, and &lt; 34 years. The stress of “control aortas” wall increased directly in relation to the age of the donors. CONCLUSIONS The maximum diameter of the ascending aorta, the patient's type of pathology and age are factors that affect the maximum tension of the aortic wall and resistance, factors that allow differentiation and prediction of the risk of rupture of the AAA. The validation of the results obtained through numerical simulation was significant and the uniaxial analysis has modeled the response of the vessels to their internal pressure.

scholarly journals Association between clinical respiratory signs, lung lesions detected by thoracic ultrasonography and growth performance in pre‐weaned dairy calves

2021 ◽  
Vol 74 (1) ◽  
Author(s):  
Inmaculada Cuevas-Gómez ◽  
Mark McGee ◽  
José María Sánchez ◽  
Edward O’Riordan ◽  
Nicky Byrne ◽  
...  
Keyword(s):  
Respiratory Disease ◽  
Rectal Temperature ◽  
Clinical Signs ◽  
Live Weight ◽  
Dairy Calves ◽  
Post Mortem ◽  
Lung Lesions ◽  
Lung Lobe ◽  
Lung Consolidation ◽  
Severe Lung

Abstract Background Bovine respiratory disease (BRD) is the main cause of mortality among 1-to-5 month old calves in Ireland, accounting for approximately one-third of deaths. Despite widespread use of clinical respiratory signs for diagnosing BRD, lung lesions are detected, using thoracic ultrasonography (TUS) or following post-mortem, in calves showing no clinical signs. This highlights the limitation of clinical respiratory signs as a method of detecting sub-clinical BRD. Using 53 purchased artificially-reared male dairy calves, the objectives of this study were to: (i) characterise the BRD incidence detected by clinical respiratory signs and/or TUS, (ii) investigate the association between clinical respiratory signs and lung lesions detected by TUS, and (iii) assess the effect of BRD on pre-weaning growth. Results Clinical BRD (based on Wisconsin clinical respiratory score and/or rectal temperature > 39.6 ºC) was detected in 43 % and sonographic changes (lung lesions) were detected in 64 % of calves from purchase (23 (SD; 6.2) days of age) until weaning, 53 days post-arrival. Calves with clinical BRD were treated. Sixty-one per cent calves affected with clinical BRD had lung lesions 10.5 days (median) before detection of clinical signs. Moderate correlations (rsp 0.70; P < 0.05) were found between cough and severe lung lesions on arrival day, and between rectal temperature > 39.6 ºC and lung lesions ≥ 2 cm2 on day 7 (rsp 0.40; P < 0.05) post-arrival. Mean average daily live weight gain (ADG) of calves from purchase to weaning was 0.75 (SD; 0.10) kg; calves with or without clinical BRD did not differ in ADG (P > 0.05), whereas ADG of those with severe lung lesions (lung lobe completely consolidated or pulmonary emphysema) was 0.12 kg/d less (P < 0.05) than calves without lung lesions. Conclusions Thoracic ultrasonography detected lung consolidation in calves that did not show signs of respiratory disease. The presence of severe lung lesions was associated with reduced pre-weaning growth. These findings emphasise the importance of using TUS in addition to clinical respiratory scoring of calves for an early and accurate detection of clinical and sub-clinical BRD.

Serum cobalamin concentrations and small intestinal ultrasound changes in 75 cats with clinical signs of gastrointestinal disease: a retrospective study

2016 ◽  
Vol 19 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Maria C Jugan ◽  
John R August
Keyword(s):  
Small Intestine ◽  
Gastrointestinal Disease ◽  
Clinical Signs ◽  
Small Animal ◽  
Abdominal Ultrasound ◽  
Wall Layer ◽  
Normal Serum ◽  
Definitive Diagnosis ◽  
Albumin Concentration ◽  
Small Intestinal

Objectives The aim of the study was to evaluate ultrasonographic changes in the small intestine of cats with clinical signs of gastrointestinal disease and low or low–normal serum cobalamin concentrations. Methods Records for client-owned cats presenting to the small animal hospital with signs of gastrointestinal disease and in which serum cobalamin concentrations were measured from 2000–2013 were reviewed. Inclusion criteria were cobalamin concentrations <500 ng/l, abdominal ultrasound within 1 month of cobalamin testing and definitive diagnosis. Results Of 751 serum cobalamin measurements, hypocobalaminemia or low–normal cobalamin was identified in 270 cats, abdominal ultrasound was performed in 207 of those cats and a diagnosis was available for 75 of them. Small intestinal ultrasound changes were detected in 49/75 (65%) cats. Abnormalities included thickening, loss of wall layer definition, echogenicity alterations and discrete masses. Serum cobalamin concentrations <500 ng/l were observed with diagnoses of inflammatory disease, neoplasia, infectious disease and normal histopathology. Cobalamin concentration was significantly lower in cats with lymphoma or inflammatory bowel disease compared with other gastrointestinal neoplasia ( P = 0.031). No difference was found between cobalamin concentration and the presence of ultrasound abnormalities, specific ultrasound changes or albumin concentration. Conclusions and relevance One-third of symptomatic cats with hypocobalaminemia or low–normal cobalamin concentrations may have an ultrasonographically normal small intestine. For the majority of cats in this study, histopathologic abnormalities were observed in the small intestine, regardless of ultrasound changes. These findings suggest gastrointestinal disease should not be excluded based on low–normal cobalamin concentrations, even with a concurrent normal ultrasound examination. Additional studies are needed in cats with low–normal serum cobalamin concentrations, as a definitive diagnosis was not pursued consistently in those cats. However, data from this study suggest that careful monitoring, histopathologic evaluation and future cobalamin supplementation may be warranted.

scholarly journals Rapid diagnosis and management of parainfluenza I virus infection in common marmosets (Callithrix jacchus)

1986 ◽  
Vol 20 (2) ◽  
pp. 121-126 ◽  
Author(s):  
S. D. Sutherland ◽  
J. D. Almeida ◽  
P. S. Gardner ◽  
M. Skarpa ◽  
J. Stanton
Keyword(s):  
Clinical Signs ◽  
High Titre ◽  
Rapid Diagnosis ◽  
Parainfluenza Virus ◽  
Type I ◽  
Post Mortem ◽  
Laboratory Studies ◽  
Common Marmosets ◽  
Nasal Swabs ◽  
Immunofluorescence Studies

During 1983 a severe episode of respiratory infection occurred in a marmoset colony at these laboratories. Of 91 marmosets, 69 showed clinical signs of disease, one died and nine were so ill that euthanasia was necessary. Eight were examined post mortem and all showed consolidation of the lungs. Laboratory studies were carried out in an attempt to establish the cause of the outbreak and an interstitial pneumonia was found in seven animals which were examined histologically. Direct electron microscopy of nasal swabs and lung samples revealed the presence of a high titre of a paramyxovirus, and subsequent immunofluorescence studies established that the particular paramyxovirus involved was parainfluenza virus type I. Subsequent studies showed that surviving affected animals had seroconverted to parainfluenza I virus while animals that had not been implicated in the outbreak had not.

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