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Y C Fung

Publications and source records attributed to Y C Fung.

148 records · Page 9Linked to original sources
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Analysis of pig's coronary arterial blood flow with detailed anatomical data.

Blood flow to perfuse the muscle cells of the heart is distributed by the capillary blood vessels via the coronary arterial tree. Because the branching pattern and vascular geometry of the coronary vessels in the ventricles and atria are nonuniform, the flow in all of the coronary capillary blood vessels is not the same. This nonuniformity of perfusion has obvious physiological meaning, and must depend on the anatomy and branching pattern of the arterial tree. In this study, the statistical distribution of blood pressure, blood flow, and blood volume in all branches of the coronary arterial tree is determined based on the anatomical branching pattern of the coronary arterial tree and the statistical data on the lengths and diameters of the blood vessels. Spatial nonuniformity of the flow field is represented by dispersions of various quantities (SD/mean) that are determined as functions of the order numbers of the blood vessels. In the determination, we used a new, complete set of statistical data on the branching pattern and vascular geometry of the coronary arterial trees. We wrote hemodynamic equations for flow in every vessel and every node of a circuit, and solved them numerically. The results of two circuits are compared: one asymmetric model satisfies all anatomical data (including the mean connectivity matrix) and the other, a symmetric model, satisfies all mean anatomical data except the connectivity matrix. It was found that the mean longitudinal pressure drop profile as functions of the vessel order numbers are similar in both models, but the asymmetric model yields interesting dispersion profiles of blood pressure and blood flow. Mathematical modeling of the anatomy and hemodynamics is illustrated with discussions on its accuracy.

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Changes in the organization of the smooth muscle cells in rat vein grafts.

Mechanical tensile stress in vein grafts increases suddenly under the influence of arterial blood pressure. In this study, we examined the influence of increased tensile stress on the organization of the smooth muscle cells (SMCs) in the neointima and media of the rat vein grafts. An autogenous jugular vein was grafted into the abdominal aorta of the rat, and changes in the organization of the vein graft SMCs were studied by observing the distribution of SMC actin filaments and nuclei at 3 min and 1, 5, 10, and 30 days after surgery. In a normal jugular vein, the average wall circumferential tensile stress was approximately 3 kPa at an internal pressure of 3 mm Hg. The SMCs, that contained long, slender actin filamentous bundles, were oriented mainly in the circumferential direction of the vessel, and constituted a 2- to 3-cell-thick medial layer underneath the endothelium. In a vein graft, the wall circumferential tensile stress suddenly increased by approximately 140 times compared with the control level. In response to this suddenly increased stress, the SMC layer was stretched into a structure with scattered pores and disrupted SMC actin filamentous bundles within 3 min. This initial change was followed by a rapid reduction in the density of the SMC nuclei and actin filaments within 1 day and progressive SMC proliferation, that was associated with medial thickening and a change in the SMC orientation from 5 to 30 days. Further studies showed that a local inflation of normal jugular veins to 120 mm Hg for 3 min induced a similar change as found in the vein grafts, whereas the organization of the SMCs was not significantly changed in vein-vein grafts, that did not experience a change in tensile stress. These results suggested that increased tensile stress contributed to the initial damage of the SMCs and played a role in the regulation of medial SMC remodeling in vein grafts.

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Changes in the rheological properties of blood vessel tissue remodeling in the course of development of diabetes.

Rheological properties of blood vessels are expected to change in disease process if the structure of the vessel wall changes. This is illustrated in diabetes, which can be induced in rat by a single injection of Streptozocin. One of the rheological properties of the blood vessel is the stress-strain relationship. The nonlinear stress-strain relationship of arteries is best expressed as derivations of a strain-energy function. In this paper, the stress-strain relations are measured and the coefficients in the strain energy function of arteries are determined for diabetic and control rats. The meaning of these coefficients are explained. The influence of diabetes on the elastic property of the arteries is expressed by the changes of these coefficients. A point of departure of the present paper from all other blood vessel papers published so far is that all strains used here are referred to the zero-stress state of the arteries, whereas all other papers refer strains to the no-load state. The existence of a large difference between the zero-stress state and no-load state of arteries is one of our recent findings. We have explained that the use of zero-stress state as a basis of strain measurements reveals that the in vivo circumferential stress distribution is quite uniform in the vessel wall at the homeostatic condition. It also makes the strain energy function much more accurate than those in which the residual stress is ignored. Using these new results, the stress and strain distribution in normal and diabetic arteries are presented.

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