A three-dimensional computational fluid dynamics (CFD) simulation of the physiological pulsatile blood flow in the human aortic arch and its three branches has been conducted by using commercial software StarCD. The b...A three-dimensional computational fluid dynamics (CFD) simulation of the physiological pulsatile blood flow in the human aortic arch and its three branches has been conducted by using commercial software StarCD. The blood flow, of a peak Reynolds number of 3289 and a Womersley parameter of 16.44, was simulated in a rigid aorta geometry that was built by computer aided design (CAD) reconstruction method based on autopsy data of a female adult. The purpose of this work is to further the understanding of the complex nature of aorta flow, therefore it mainly focuses on analysis of the spatial and temporal distributions of velocities and wall shear stresses. The results, illustrated by 3D visualization pictures and 2D graphs of the primary velocity profiles, wall shear stress and pressure distributions, as well as the secondary flow patterns, are in good agreement with those of other experimental and computational works. The distributions of pressure and wall shear stress support the correlation between high and low shear stresses and pressures and the atherosclerotic lesions.展开更多
Background： Endothelial cell damage is an important pathophysiological step of restenosis after angioplasty and stenting. Cell transplantation has great therapeutic potential for endothelial recovery. We investigated...Background： Endothelial cell damage is an important pathophysiological step of restenosis after angioplasty and stenting. Cell transplantation has great therapeutic potential for endothelial recovery. We investigated the effect of transplanting endothelial progenitor cells （EPCs） derived from human early fetal aortas in rat injured arteries. Methods： The carotid arterial endothelium of Sprague-Dawley rats was damaged by dilatation with a 1.5 F balloon catheter, and then EPCs derived from human early fetal aortas （〈14 weeks） were injected into the lumen of the injured artery in transplanted rats, with an equal volume of normal saline injected into control rats. Rats were sacrificed at 2 and 4 weeks after treatment and transplanted cells were identified by immunohistochemical staining with anti-human CD31 and anti-human mitochondria antibodies. Arterial cross-sections were analyzed by pathology, immunohistochemistry, and morphometry. Results： Green fluorescence-labeled EPCs could be seen in the endovascular surface of balloon-injured vessels after transplantation. The intimal area and intimal/medial area ratio were significantly smaller in the transplanted group than in the control （P 〈 0.05） and the residual lumen area was larger （P 〈 0.05）. After EPC transplantation, a complete vascular endothelial layer was formed, which was positive for human yon Willebrand factor after immunohistochemical staining, and immunohistochemical staining revealed many CD31- and mitochondria-positive cells in the re-endothelialized endothelium with EPC transplantation but not control treatment. Conclusion： EPCs derived from human early fetal aorta were successfully transplanted into injured vessels and might inhibit neointimal hyperplasia after vascular injury.展开更多
文摘A three-dimensional computational fluid dynamics (CFD) simulation of the physiological pulsatile blood flow in the human aortic arch and its three branches has been conducted by using commercial software StarCD. The blood flow, of a peak Reynolds number of 3289 and a Womersley parameter of 16.44, was simulated in a rigid aorta geometry that was built by computer aided design (CAD) reconstruction method based on autopsy data of a female adult. The purpose of this work is to further the understanding of the complex nature of aorta flow, therefore it mainly focuses on analysis of the spatial and temporal distributions of velocities and wall shear stresses. The results, illustrated by 3D visualization pictures and 2D graphs of the primary velocity profiles, wall shear stress and pressure distributions, as well as the secondary flow patterns, are in good agreement with those of other experimental and computational works. The distributions of pressure and wall shear stress support the correlation between high and low shear stresses and pressures and the atherosclerotic lesions.
文摘Background： Endothelial cell damage is an important pathophysiological step of restenosis after angioplasty and stenting. Cell transplantation has great therapeutic potential for endothelial recovery. We investigated the effect of transplanting endothelial progenitor cells （EPCs） derived from human early fetal aortas in rat injured arteries. Methods： The carotid arterial endothelium of Sprague-Dawley rats was damaged by dilatation with a 1.5 F balloon catheter, and then EPCs derived from human early fetal aortas （〈14 weeks） were injected into the lumen of the injured artery in transplanted rats, with an equal volume of normal saline injected into control rats. Rats were sacrificed at 2 and 4 weeks after treatment and transplanted cells were identified by immunohistochemical staining with anti-human CD31 and anti-human mitochondria antibodies. Arterial cross-sections were analyzed by pathology, immunohistochemistry, and morphometry. Results： Green fluorescence-labeled EPCs could be seen in the endovascular surface of balloon-injured vessels after transplantation. The intimal area and intimal/medial area ratio were significantly smaller in the transplanted group than in the control （P 〈 0.05） and the residual lumen area was larger （P 〈 0.05）. After EPC transplantation, a complete vascular endothelial layer was formed, which was positive for human yon Willebrand factor after immunohistochemical staining, and immunohistochemical staining revealed many CD31- and mitochondria-positive cells in the re-endothelialized endothelium with EPC transplantation but not control treatment. Conclusion： EPCs derived from human early fetal aorta were successfully transplanted into injured vessels and might inhibit neointimal hyperplasia after vascular injury.
