Browsing by Subject "Aorta"

Now showing 1 - 8 of 8
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    Age-related changes of aorta in Syrian hamsters of APA strain
    (Murcia : F. Hernández, 1995) Yamanouchi, J.; Sugawara, Y.; Itagaki, S.; Doi, K.
    Age related changes in thoracic aorta (TA) and abdominal aorta (AA) of male APA hamsters from 3 to 12 months of age were examined morphometrically and ultrastructurally. The nuclear density of smooth muscle cells (SMCs) was larger in AA than in TA, and it decreased with advancing age. In contrast, the collagen fibre density was larger in TA than in AA, and it increased correlatively with aging, especially in TA. Electron microscopic examinations revealed that subendothelial cystic spaces and aggregations of fragments of elastic and collagen fibres were found at 3 months of age and progressed with advancing age in TA, while they were not evident in AA even at 12 months of age. Irregularity of medial SMC contours and an amount of SMC-associated collagen fibres were more prominent in TA than in AA throughout the experimental period. Degenerative changes of endothelial cells and medial SMCs progressed with aging in both TA and AA, and degenerated SMCs were characterized by aggregations of swollen mitochondria.
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    Differential proliferation of rat aortic and mesenteric smooth muscle cells in culture
    (Murcia : F. Hernández, 1992) Waldbillig, David K.; Pang, Stephen C.
    Smooth muscle cells (SMC) from various arterial origins have been successfully maintained in culture. The present study evaluates the proliferative activity of aortic and mesenteric SMC in culture. Aortic and mesenteric SMC were obtained from male Wistar rats by explant and enzyme digestion techniques, respectively. Vascular SMC obtained by either method exhibited a characteristic hill-and-valley growth pattern in culture after confluence and were positively labelled with either anti-smooth muscle actin or myosin by an indirect immunofluorescent method. The rate of incorporation of thymidine into DNA and cell number counting were used as indices of proliferation in vitro. Vascular SMC from passages 4-33 were first synchronized with either Dullbecco's Modified Eagle's Medium (DME) or Ham's F-12 medium, supplemented with insulin-transfemngselenium (ITS), for 72 hours. SMC were then stimulated with 10% bovine serum for either 24 or 72 hours with the former processed for scintillation counting, the latter for cell number determination. The incorporation of tritiated thymidine into DNA following a 2 hour incubation was determined by scintillation counting after perchloric acid extraction. In terms of cell numbers, proliferative responses to bovine serum were determined by Coulter counting. Autoradiography was also carried out in some cultures to determine both thymidine and mitotic labelling indices. The rate of thymidine incorporation in aortic cells was 2-3 fold higher than in mesenteric cells. Aortic and mesenteric SMC lines exhibited similar cell cycle intervals in terms of total duration and individuals cycle parameters. However, the total thymidine index was higher in the aortic than mesenteric SMC. These results suggest that SMC from different arterial origins possess different rates of proliferation. Differences in the rate of in vitro proliferation in these cell lines are due to differences in growth fraction, the number of celis traversing the cell cycle. The mechanisms underlying these differential proliferative potentials remain to be determined.
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    Ecocardiografía transesofágica tridimensional en la evaluación de la estenosis valvular aórtica
    (2014-12-04) Saura Espín, Daniel R.; Morena Valenzuela, Gonzalo de la; Valdés Chávarri, Mariano; Facultad de Medicina
    Objetivos: Determinar la factibilidad de la medida del área valvular aórtica anatómica mediante la ecocardiografía transesofágica tridimensional en tiempo real en pacientes con estenosis valvular aórtica moderada y severa. Determinar los predictores de la factibilidad. Determinar la concordancia y las desviaciones sistemáticas de las técnicas tridimensionales para la cuantificación del área valvular aórtica respecto al método ecocardiográfico habitual si las hubiere. Describir la concordancia en los criterios de severidad de la estenosis aórtica entre el área anatómica medida mediante la planimetría en el ecocardiograma transesofágico tridimensional y los gradientes de presión transvalvular obtenidos por técnicas Doppler. Describir las características demográficas, clínicas y ecocardiográficas de los pacientes con estenosis aórtica severa confirmada con planimetría en ecocardiograma transesofágico tridimensional, y que presenten gradiente sistólico transvalvular bajo pese a fracción de eyección preservada. Describir la consistencia de la clasificación de la estenosis aórtica severa en función del flujo y el gradiente transvalvular, empleando la información anatómica proporcionada por el ecocardiograma transesofágico tridimensional. Explorar el valor pronóstico de los datos del ecocardiograma transesofágico tridimensional obtenidos en los pacientes con estenosis aórtica. Metodología: Para todos los objetivos salvo el último se llevó a cabo un estudio clínico de observación con diseño transversal que incluyó a 307 pacientes con estenosis valvular aórtica moderada o severa que fueron sometidos a ecocardiograma transtorácico convencional y asimismo a ecocardiograma transesofágico tridimensional en tiempo real para llevar a cabo la planimetría del área valvular aórtica. Se practicó análisis estadístico de concordancia y análisis de regresión multivariable. Para el último de los objetivos se empleó un diseño longitudinal con seguimiento prospectivo del mismo grupo de pacientes, con estimación de las tasas de mortalidad y sus predictores con el método de Kaplan-Meier y regresión de Cox. Resultados y conclusiones: En una población que representa a la de la práctica clínica habitual con estenosis valvular aórtica moderada o severa en nuestro medio, el área valvular aórtica anatómica pudo ser cuantificada mediante planimetría a partir de las imágenes del ecocardiograma transesofágico tridimensional en el 92% de los casos. El grado de calcificación valvular aórtica fue el único predictor independiente del fracaso de la técnica de medida. La planimetría directa del área valvular aórtica tiene buena concordancia con el método transtorácico habitual, e infraestima levemente el valor del orificio valvular respecto al estándar clínico. Por otra parte, el cálculo del área valvular aórtica mediante la ecuación de continuidad empleando el área del tracto de salida del ventrículo izquierdo medida en el ecocardiograma transesofágico tridimensional tiene una buena concordancia con el método clínico habitual, pero sobreestima el valor del área respecto a éste. La determinación de la severidad de la estenosis valvular aórtica mediante el área planimetrada en el ecocardiograma transesofágico tridimensional muestra discordancias importantes con la severidad establecida según los gradientes transvalvulares. La inconsistencia de criterios en la valoración de la severidad de la estenosis valvular aórtica existe tanto en los pacientes con fracción de eyección del ventrículo izquierdo normal como deprimida. Los pacientes con estenosis aórtica severa confirmada con planimetría en el ecocardiograma transesofágico tridimensional y con gradiente bajo pese a fracción de eyección normal tienen mayores valores de área valvular aórtica dentro del rango severo y peor acoplamiento ventrículo-arterial. La clasificación de la estenosis aórtica severa en función del flujo y gradiente transvalvular valorada con ecocardiograma transesofágico tridimensional tiene una consistencia sólo moderada respecto al estándar clínico. El área valvular aórtica anatómica medida directamente mediante planimetría de las imágenes del ecocardiograma transesofágico tridimensional se relaciona de forma independiente con el riesgo de muerte en los pacientes con estenosis aórtica moderada o severa. Aims: To study the feasibility of planimetry of aortic valve area by means of real-time three-dimensional transesophageal echocardiography in patients with moderate and severe aortic stenosis. To determine the predictors of feasibility. To study the reliability and concordance of aortic valve planimetry by three-dimensional echocardiography in comparison with transthoracic echocardiography. To describe the consistency in the severity criteria of aortic stenosis by means of both three-dimensional planimetry and mean systolic gradient. To describe demographic, clinical and echocardiographic characteristics of patients with paradoxical low-gradient severe aortic stenosis as confirmed with planimetry. To describe the reliability of the new proposed classification of severe aortic stenosis regarding systolic flow and transvalvular gradient if anatomical assessment by real-time three-dimensional transesophageal echocardiography were performed. Least, to explore the prognostic value of the information obtained with tested technique. Methods: For all objectives but the last one, we performed a clinical observational study with cross-sectional design that included 307 patients with moderate or severe aortic stenosis who underwent both conventional transthoracic echocardiography and real-time three-dimensional transesophageal echocardiography. Planimetry of aortic valve area from three-dimensional datasets was carried out. Statistical analysis of concordance and multivariate regression analysis was performed. For the last of the objectives, a longitudinal prospective design was used to follow the same group of patients, with estimates of mortality and its predictors with the Kaplan-Meier and Cox regression methods. Results and conclusions: Aortic valve area planimetry by means of three-dimensional echocardiography was achieved in 92% of patients with moderate or severe aortic stenosis. The sample was obtained from actual clinical practice. Valvular calcification grade was the only single independent predictor of non-feasibility. Planimetry of aortic valve area shows good agreement with the transthoracic method, and it slightly underestimates the value in comparison with the diagnostic clinical standard. On the other hand, aortic valve area by means of continuity equation (but using the cross-sectional area o left ventricle outflow tract as obtained from three-dimensional datasets) has fair reliability as compared with the clinical standard, but it overestimates the measurement. Aortic stenosis severity grading by three-dimensional planimetry and transvalvular mean systolic gradient showed clinically significant discordances; such disagreement was found both in patients with normal and depressed systolic function. Patients with paradoxical low-gradient severe aortic stenosis (as confirmed by three-dimensional planimetry) show higher aortic valve area values (within severity range) and worse ventricular-arterial coupling parameters. The classification of severe aortic stenosis depending on both flow and transvalvular gradient assessed by three-dimensional transesophageal echocardiography shows only moderate consistency as compared with the clinical standard. The anatomic aortic valve area measured directly by planimetry of the images of three-dimensional transesophageal echocardiography is associated independently with the risk of death in patients with moderate or severe aortic stenosis.
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    Expression of CCL2 signaling pathway genes in patients with periodontitis and atherosclerosis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Zhao, Yuxia; Wang, Lianqun; Dong, Rui; Cheng, Xuejun; Jia, Liqun; Qu, Dan; Zhang, Lin
    Objective. Periodontitis and atherosclerosis are chronic inflammatory diseases characterized by leukocyte infiltration. We investigated the expression of CCL4, CCR5, c-Jun, c-Fos, NF-κB, and CCL2 as well as the possible mechanism involved in the regulation of CCL2 in human periodontitis tissues and atherosclerotic aorta based on previous research on the CCL4/CCR5/c-Jun and c-Fos/CCL2 pathway leading to CCL2 expression in collagen-induced arthritis (CIA) rat. Methods. Sixty-five volunteers were recruited and the condition of their gingiva and coronary arteries were assessed. The subjects were divided into four groups: healthy control, chronic periodontitis (CP), coronary artery diseases (CAD), and noncoronary artery diseases (non-CAD). Total RNA was isolated from gingiva in periodontitis patients and control populations and from the aorta in patients with and without CAD. PCR was used to examine CCL4, CCR5, c-Jun, c-Fos, NF-κB, and CCL2 levels. The production of CCL2 in the gingiva and aorta was analyzed by immunostaining. Results. PCR revealed that CCL4, CCR5, and CCL2 mRNA levels were increased in CP patients' gingivae and aortas from coronary artery bypass grafting (CABG) patients. Marked c-Jun, c-Fos, and NF-κB gene productions were detected in CP patients’ gingivae but did not show statistical differences between the CAD and non-CAD groups. Stronger immunoreactivity against CCL2 was observed in periodontitis gingiva and aorta from CABG patients. Conclusions. Our findings suggest that the CCL4/CCR5/c-Jun and c-Fos/CCL2 pathways may be involved in CCL2 expression in periodontitis. CCL4, CCR5, and CCL2 might act as possible nodes to link the presence of periodontitis and atherosclerosis.
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    The association of medial collagenous tissue with atheroma formation in the aging human aorta as revealed by a special technique
    (Murcia : F. Hernández, 1986) Greenberg, Stephen R.
    A new technique which brilliantly colors collagen fibers in a field of polarized light reveals that during mid-life the smooth muscle cells in the tunica media of the human aorta begin to disappear. The connective tissue is divided between two regions; one below the subintimal layer and the other under the adventitia. Fine collagen fibers extend upward from the former into the subintima and beyond into the intima and the overlying atheromatous plaques of the aging aorta. Thus, the source of fibrous thickening of the vessel is not confined solely to the intimal layer; at least, a portion of the total collagen content arises deep within the aortic wall.
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    The toxic effects of bis (tributyltin) oxide on the rat thoracic aorta
    (Murcia : F. Hernández, 1992) Yoshizuka, M.; Hara, K.; Doi, K.; Mori, Naoki; Yokoyama, M.; Ono, Eizo; Fujimoto, Sunao
    The toxic effects of bis (tributyltin) oxide (TBTO) on the ultrastructure and permeability of rat thoracic aorta were studied electron microscopically and the accumulation sites of tin were determined with an X-ray microanalyzer. Male Wistar rats received O.O5ml/kg of TBTO as an emulsion in 1 m1 of distilled water througb a stomach tube. After time intervals of 2, 4, 6, 8, 10, 12 h after intubation, thoracic aortae were isolated and prepared for electron microscopy. Marked swelling of mitochondria in the aortic endothelial cells appeared at 4 h after TBTO treatment. By x-ray microanalysis, tin L-a peaks (3.44 keV) were obtained from these swollen mitochondria. Subendothelial edema progressed between 6 and 8 h after TBTO treatment. By tracer experiment, it was seen that large amounts of peroxidase reaction products filled the expanded subendothelial space. At 12 h after TBTO treatment, degenerative changes of the endothelial cells were prominent. These results indicated that orally administered TBTO accumulated in the mitochondria of the endothelial cells of thoracic aorta. The direct toxic effects of TBTO on mitochondria might induce severe damage to the endothelial cells and cause disturbance of the permeability barrier function of the endothelial layer and subendothelial edema.
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    Visualizing TGF-ß and BMP signaling in human atherosclerosis: a histological evaluation based on Smad activation
    (F. Hernandez y JuanF. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología., 2012) van Dijk, R.A.; Engels, C.C; Schaapherder, A.F; Mulder-Stapel, A.; ten Dijke, P.; Hamming, J.F; Lindeman, J.H.N.
    Background: The TGF-ß superfamily members Transforming Growth Factor-ß (TGF-ß/Activin) and Bone Morphogenetic Proteins (BMP) have been implicated in the pathogenesis of atherosclerosis. However, their role in human disease remains controversial. In this study we used Smad phosphorylation as a read out for TGF-ß and BMP signaling during the initiation, progression and (de)stabilization of human atherosclerotic disease. Material and methods: A systematic analysis was performed in 114 peri-renal aortic patches (stained with Movat Pentachrome, H&E, pSmad2, pSmad1,5,8 and PAI-1) covering the entire atherosclerotic spectrum (van Dijk, 2010). Immunostaining against T-cells (CD3) and monocytes and macrophages (CD68) was used to explore a putative association between TGF-ß and BMP signaling and vascular inflammation. Results: Smad phosphorylation was present within the normal arterial wall in approximately 10% of the endothelial cells and intimal smooth muscle cells. A significant increase in pSmad2 and pSmad1,5,8 positivity was found in non-progressive lesions (>50% positivity). No further increase or decrease was found in the progressive atherosclerotic lesions, vulnerable and stabilized lesions. No association was found between TGF-ß and BMP signaling and CD3 and CD68 expression, nor cap thickness. Conclusion: Activation of the TGF-ß and BMP pathways is an early event in atherosclerotic lesion formation. No significant relationships were found between Smad phosphorylation and vessel wall inflammation or plaque vulnerability.
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    Watanabe rabbits with heritable hypercholesterolaemia: a model of atherosclerosis
    (Murcia : F. Hernández, 1998) Aliev, G.; Burnstock, G.
    Many factors play important roles in the development of atherosclerotic lesions. The leading risk factor for atherosclerosis is familial hypercholesterolaemia (FH). FH is a genetic disease characterized by a deficiency of receptors for low density lipoprotein (LDL) on the plasmalemma of endothelial cells, a high level of serum LDL, and early development of atherosclerosis and skin xanthoma. Watanabe and colleagues have developed a line of rabbits with unprovoked hypercholesterolaemia, increased blood level of LDL, pronounced atherosclerosis and skin xanthoma. These Watanabe Heritable Hyperlipidaemic (WHHL) rabbits possess an inheritable mutation of one gene, similar to that in human FH. The morphogenesis of atherosclerosis in patients with FH is characterized by multifocal deposit of lipids in the stromal cells of thymus, spleen, skin, interstitial and parenchymatous cells of kidneys and the presence of some single foam cells in aorta. The manifestation of atherosclerotic lesions in WHHL rabbits increases progressively with age but the presence of atherosclerotic lesions in newborn WHHL rabbits suggest that the process may commence in ulero. Moreover, the main mass of plasma cholesterol in WHHL rabbits is first found in LDL and to a lesser degree in lipoproteins of intermediate density. This is contrary to diet-induced atherosclerosis in rabbits where the main mass of serum cholesterol is found in very low density p-lipoproteins. Thus the distribution of cholesterol among lipoprotein fractions differs from that in WHHL rabbits. Atherosclerotic damage of arteries in WHHL rabbits goes through several stages. During the progression of intimal damage, lipid and foam cell deposits are found in the internal surface together with developing plaques and increased content of lipids in the tunica media. Calcification often follows this process. The main factors initiating atherosclerosis in WHHL rabbits are adhesion of leukocytes and platelets to endothelial cells and the accumulation of lipids in the aortic wall. The deposits of lipids in macrophages and intimal smooth muscle cells in WHHL rabbits occurs mostly at the expense of cytoplasmic neutral lipid particles with some accumulation in lysosomes. Hypertension as a risk factor increases the area of atherosclerotic damage in all arterial vessels in WHHL rabbits, particularly in the thoracic and abdominal aorta. Morphogenesis of the development of atherosclerosis in WHHL and diet-induced atherosclerosis in rabbits was similar, but differs from rats with heritable hypercholesterolaemia. Damage or loss of endothelial cells can predispose the atherosclerotic vessels to vasospasm and can leave vessels unprotected against vasoconstrictor stimuli. The development of the WHHL model has not only given insight into the mechanisms of development of familial hypercholesterolaemia but has also provided a model for assessing various therapeutic approaches for the prevention and treatment of atherosclerosis.