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Y C Fung

Publications and source records attributed to Y C Fung.

At least 19 recordsLinked to original sources
PubMed1992

Strain distribution in small blood vessels with zero-stress state taken into consideration.

The active and passive deformation of a blood vessel is related to the stress in it. Any analysis of stress and strain must begin with the zero-stress state. Recent reports on large blood vessels such as the aorta, pulmonary arteries, and vena cava have shown that, at zero-stress state, blood vessels are not tubes, but opens sectors. This report presents data on the zero-stress state of small blood vessels with lumen diameters down to approximately 50 microns. Zero-stress state of a vessel was obtained by cutting the vessel into rings and then the rings into sectors; each sector is characterized by an opening angle, alpha. In rat ileal and plantar arterioles, the opening angles are in the order of 100-250 degrees; those in the venules are in the order of 50-100 degrees. The effect of norepinephrine on the opening angle alpha is minor; it decreases alpha of the superior mesenteric artery, and increases alpha of the ileocecocolic and ileal arteries. EDTA has little effect on alpha of arteries greater than 100 microns in diameter, but decreases alpha of arteries less than 100 microns. The physiological meaning of the opening angle is demonstrated in terms of the residual strains in a vessel at the no-load state and homeostatic strains at normal blood pressure. The strains in real vessels are compared with those in hypothetical vessels having an opening angle of zero. It is shown that ignoring the opening angle will cause a large error in strain evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Microscopic vs. macroscopic deformation of the pulmonary alveolar duct.

The stretch of the perimeters of alveolar ducts was measured at the surface of saline-filled specimens of human and dog lung parenchyma that were stretched biaxially. The microscopic stretch of these ducts was measured at several levels of isotropic biaxial macroscopic stretch of the parenchyma with stretch ratio (lambda x = lambda y) in the range of 1.20-1.40, which roughly corresponds to tidal breathing in humans and dogs. Alveolar walls were found to be load-carrying elements in the saline-filled lung, as seen by their straightness at all levels of stretch. Quantitatively, let l, A, L, and S denote, respectively, the duct perimeter length and area and the parenchymal target perimeter and area in the deformed state and lo, Ao, Lo, and So the corresponding variables in the undeformed state. The microscopic stretch ratio of the ducts (l/lo) was found to be approximately 4% larger than the macroscopic stretch ratio (L/Lo) in human lung and approximately 10% larger in dog lung. The microscopic area ratio of the ducts (A/Ao) was found to be approximately 10% larger than the macroscopic area ratio (S/So) in human lung and approximately 22% larger in dog lung. Ducts within human parenchyma were seen to be about twice as stiff as ducts within dog parenchyma over the range of macroscopic stretch studied. This correlates with the volume fractions of collagen and elastin being higher in the human lung than in dog lung. The observed nonuniformity in strain field at the microstructural level suggests the need to include a force balance between alveolar ducts and septal walls when modeling the mechanics of saline-filled parenchyma.

Animals↗
PubMed1992

Effect of temperature on the biaxial mechanics of excised lung parenchyma of the dog.

The influence of temperature on the mechanical properties of excised saline-filled lung parenchyma of the dog was studied at low lung volume. The motivation of this study was to determine whether lung tissue material without the influence of surface tension undergoes a phase transition in the 20-40 degrees C range, as does synthetic elastin studied by Urry in 1984-1986. Dynamic biaxial and uniaxial tensile tests were done, and strain vs. Lagrangian stress curves were recorded during slow cooling and heating between 40 and 10 degrees C. To emphasize the effects of elastin, strains (defined as stretch ratio minus one) were kept below 30%. A slight decrease in compliance occurred with cooling over the entire temperature range. This effect may be attributed to collagen. It was accompanied by a gradual increase in length as the tissue cooled, an effect that may be attributed to elastin. This process was partially reversible with reheating. However, this effect is in contrast with the sudden drastic change in mechanical properties of synthetic elastin described by Urry. Hysteresis, creep, and stress relaxation were small at these low strains. Possible causes of these effects are discussed.

Animals↗
PubMed1992

Influence of STZ-induced diabetes on zero-stress states of rat pulmonary and systemic arteries.

Zero-stress states of the main pulmonary arteries and aorta and small systemic arteries were determined in 22 nondiabetic and 29 streptozocin (STZ)-induced diabetic rats. The zero-stress state of each vessel was obtained by cutting the vessel transversely into a series of short rings, then cutting each ring radially, which caused the ring to spring open into a sector. Each sector can be characterized by its opening angle. The opening angle has strong regional dependence. In some regions of rat arteries, the opening angle can be greater than 360 degrees. Rats were studied 5, 10, 20, 30, and 40 days after an injection of 75 mg/kg body wt i.v. STZ. During diabetes development, the opening angles in general increased and reached a plateau in approximately 30 days. The maximum change of opening angle over normal lies in the range of 18-105 degrees, depending on location. The pulmonary arteries were affected by diabetes as much as the systemic arteries. The course of change of the opening angle during diabetogenesis was different from those of the serum glucose level and blood pressure. Blood pressure in carotid, external iliac, and pulmonary arteries did not change significantly in diabetogenesis. To clarify the physiological meaning of the opening angle, we measured the circumferential strain in the blood vessel wall in homeostatic condition and the residual strain at the no-load state, with both strains referred to the zero-stress state. We calculated the corresponding stresses in the vessel wall. The circumferential stress in the vessel wall was greatly increased by diabetes; great errors will result if the opening angle is ignored.

Animals↗
PubMed1991

What are the residual stresses doing in our blood vessels?

We show that the residual strain and stress in the blood vessels are not zero, and that the zero-stress state of a blood vessel consists of open-sector segments whose opening angles vary along the longitudinal axis of the vessel. When the homeostatic state of the blood vessel is changed, e.g., by a sudden hypertension, the opening angle will change. The time constant of the opening angle change is a few hours (e.g., in the pulmonary artery) or a few days (e.g., in the aorta). From a kinematic point of view, a change of opening angle is a bending of the blood vessel wall, which is caused by a nonuniformly distributed residual strain. From a mechanics point of view, changes of blood pressure and residual strain cause change of stress in the blood vessel wall. Correlating the stress with the change of residual strain yields a fundamental biological law relating the rate of growth or resorption of tissue with the stress in the tissue. Thus, residual stresses are related to the remodeling of the blood vessel wall. Our blood vessel remodels itself when stress changes. The stress-growth law provides a biomechanical foundation for tissue engineering.

Animals↗
PubMed1991

Residual strains in porcine and canine trachea.

Residual strains exist in canine and porcine tracheas. They are revealed by cutting the trachea first perpendicular to its axis into rings, then radially into sectors. Each sector is characterized by an opening angle which is defined as the angle subtended between two radii joining the middle point of the inner wall to the tips of the inner wall. The trachea being non-axisymmetric, the opening angle depends on the position of the radial cut. The trachea being also nonuniform in the axial direction, the opening angle varies along the length of the trachea. In the dog, the opening angle of the trachea cut at the anterior position (cartilaginous) is about 100 degrees at the larynx; it increases fairly linearly to 180 degrees midway down the trachea; then increases slowly to about 200 degrees at the lower end where the trachea bifurcates into the main bronchi. Dog trachea cut in the posterior (muscular) position have an opening angle of about 50 degrees at the larynx, which increases to about 70 degrees three-quarters of the way down the trachea, then drops to 60 degrees at the lower end. In the pig, the opening angle of the trachea is much smaller, the values at anterior and posterior cuts are similar (without significant difference), and their mean value decreases from about 15 degrees at the laryngeal end to about 5 degrees at the lower end. These species and regional differences are discussed in relation to tracheal geometry and structure.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1991

The zero-stress state of rat veins and vena cava.

The zero-stress state of a vein is, like that of an artery, not a closed cylindrical tube, but is a series of segments whose cross-sections are open sectors. An opening angle of each sector is defined as the angle subtended between two radii joining the midpoint of the inner wall to the tips of the inner wall. Data on the opening angles (mean +/- standard deviation) of the veins and vena cava of the rat are presented. For the superior vena cava and subclavian, jugular, facial, renal, common iliac, saphenous, and plantar veins, the opening angle varies in the range of 25 to 75 deg. The inferior vena cava (below the heart), however, has noncircular, nonaxisymmetric cross-sections, a curved axis, and a rapid longitudinal variation of its "diameter"; its zero-stress state is not circular sectors; but the opening angle is still a useful characterization. The mean opening angle of the interior vena cava varies in the range of 40 to 150 deg in the thoracic portion, and 75 to 130 deg in the abdominal portion, with the larger values occurring about the middle of each portion. There are considerable length, diameter reductions, and wall thickening of the vena cava from the homeostatic state to the no-load state in vitro. Physically, the zero-stress state is the basis of the stress analysis of blood vessels. The change of opening angle is a convenient parameter to characterize any nonuniform remodeling of the vessel wall due to changes in physical stress or chemical environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Species dependence of the zero-stress state of aorta: pig versus rat.

The zero-stress state of an aorta can be characterized by the angle with which each segment of the vessel opens up when it is cut radially. The opening angle varies with the region of the aorta: significantly with respect to the axial location, less significantly with respect to polar angle of the radial cut. Both pig and rat aortas have large opening angles in the neighborhood of 130 deg in the aortic arch region. In the thoracic region, the species difference is evident. The opening angle of the pig aorta in the middle thoracic region is rather constant in the neighborhood of 60 deg. The opening angle of the rat aorta in the thoracic region varies considerably, decreasing to 10 deg at the lower end of the thoracic region. In the abdominal region the opening angle of the pig increases from 60 to about 80 deg, that of the rat increases from about 10 to 90 deg. The potassium ion has effect on vascular smooth muscle, but has little effect on the opening angle. This suggests that the opening angle is not sensitive to smooth muscle contraction, similar to a previously known result that the opening angle is not affected by papaverine. The vessel wall thickness and vessel diameter were measured. It is shown that the ratio of the wall thickness to diameter of the pig is considerably larger than that of the rat throughout the aorta.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Changes of zero-stress state of rat pulmonary arteries in hypoxic hypertension.

Zero-stress state of the main pulmonary arteries, from the main trunk to a vessel with a lumen diameter approximately 60 microns, was determined in 25 normal control and 38 hypoxic pulmonary hypertensive rats. Pulmonary hypertension was induced by placing the rats in a hypoxic chamber with 10% O2-90% N2 at atmospheric pressure. The zero-stress state of each vessel was obtained by first cutting the vessel transversely into a series of rings and then cutting each ring radially, whereupon the ring opened into a sector, which is characterized by an opening angle defined as the angle subtended between two lines originating from the midpoint of the inner wall (endothelium) to the tips of the inner wall. Whereas the pulmonary blood pressure increased monotonically during the development of pulmonary hypertension, the opening angle followed a different course; e.g., the values (means +/- SD) of the opening angle at the pulmonary trunk at times 0 (control) and 2, 12, 28, 96, 144, 240, 480, and 720 h after exposure to hypoxia are, respectively, 294 +/- 30 degrees, 378 +/- 24 degrees, 385 +/- 12 degrees, 374 +/- 11 degrees, 246 +/- 63 degrees, 267 +/- 49 degrees, 193 +/- 19 degrees, 195 +/- 83 degrees, and 239 +/- 38 degrees. Trends at other places on the artery are similar, but the magnitudes differ. In this period of time, intimal edema and thickening were found. The intima media thickened rapidly from 48 to 240 h and then more slowly from 240 to 720 h. Adventitia thickened later; its thickness exceeded that of the intima media at approximately 96 h. Thus the changes of zero-stress state of the pulmonary arteries are seen to be related to the nonuniform remodeling of the vessel wall as revealed by the edema, blebs, and thickening of different layers.

Animals↗
PubMed1990

Residual strain in rat left ventricle.

Residual stress in an organ is defined as the stress that remains when all external loads are removed. Residual stress has generally been ignored in published papers on left ventricular wall stress. To take residual stress into account in the analysis of stress distributions in a beating heart, one must first measure the residual strain in the no-load state of the heart. Residual strains in equatorial cross-sectional rings (2-3 mm thick) of five potassium-arrested rat left ventricles were measured. The effects of friction and external loading were reduced by submersing the specimen in fluid, and a hypothermic, hyperkalemic arresting solution containing nifedipine and EGTA was used to delay the onset of ischemic contracture. Stainless steel microspheres (60-100 microns) were lightly imbedded on the surface of the slices, and the coordinates of the microspheres were digitized from photographs taken before and after a radial cut was made through the left ventricular free wall. Two-dimensional strains computed from the deformation of a slice after one radial cut were defined as the residual strains in that slice. It was found that the distributions of the principal residual stretch ratios were asymmetric with respect to the radial cut: in areas where substantial transmural strain gradients existed, the distributions of strain components were different on the two sides of the radial cut. A second radial cut produced deformations significantly smaller than those produced from the first radial cut. Hence, a slice with one radial cut may be considered stress free.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Persistence of asymmetry in nonaxisymmetric entry flow in a circular cylindrical tube and its relevance to arterial pulse wave diagnosis.

In an experiment motivated by the study of arterial blood flow along the lines suggested by the traditional Chinese medicine, the flow in a pipe whose lumen was blocked by a semi-circular plug two tube-diameters long was visualized by suspended particles, recorded by cinematography, and analyzed digitally. The Reynolds number was in the range of 100 to 450 based on the pipe diameter, similar to that of blood flow in the radial artery in the arms of man. The blockage was found to have a profound effect on the velocity profile of the flow in the wake, but it had little influence on the symmetry of the velocity profile upstream of the block, except in its immediate neighborhood. When the end conditions far away from the block were steady, the flow in the wake was steady. The asymmetry of the flow in the wake can be judged by the deviation of the location of the maximum axial velocity from the center line of the pipe as seen in the plane of symmetry of the blockage. Our results show that the deviation can be described as the sum of two components. The first is a strong one which decays exponentially in an entry length which is about twice as long as the classical Boussinesq entry length of axisymmetric flow. The second is a weaker component which is wavy spatially and persists far downstream (many times the entry length). The separated flow and vortex system behind the blockage are sensitive to the flow rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1989

Relationship between hypertension, hypertrophy, and opening angle of zero-stress state of arteries following aortic constriction.

Examination of changes occurring in the zero-stress state of an organ provides a way to study cellular growth in the organ due to change of physical stresses. The zero-stress state of the aorta is not a tube. It is a sector with an opening angle that varies with the location on the aorta and changes with cellular remodeling. Blood vessel remodeling can be induced by imposing a constriction on the abdominal aorta by a metal clip (aortic banding), which causes an increase of blood pressure, hypertrophy of the aortic wall, and large change of opening angle. The correlation of the opening angle with the blood vessel wall thickness and blood pressure changes in rat's aorta due to aortic banding is presented in this report. The opening angle changes daily following the aortic banding. Blood pressure rises in vessels of the upper body, but that in the lower body decreases at first and then rises to an asymptotic value. Blood vessel wall thickness increases in rough proportion to blood pressure. Vessel diameter changes also. But the most dramatic is the course of change of the zero-stress state. Typically, the time to reach 50 percent of asymptotic hypertrophy of blood vessel wall thickness is about 3-5 days. The corresponding time for blood pressure is about 7 days. The opening angle of the zero-stress state, however, increases rapidly at first, reaches a peak in about 2 to 4 days, then decreases gradually to a reduced asymptote. The exact values of the time constants depend on the location along the aortic tree. In general, the course of change of residual strain is very different from those of the blood pressure and the blood vessel wall thickness.

Animals↗
PubMed1989

Change of residual strains in arteries due to hypertrophy caused by aortic constriction.

The stress and strain that remain in an organ when the external load is removed are called residual stress and strain. They can be revealed by cutting up the organ in such a way as to reveal the zero-stress configuration. The function of the organ depends on the residual strain. For a blood vessel, the zero-stress configuration is very different from that of the no-load condition, and it changes over time when the physical stress acting on the vessel is changed. Data on rat aorta are presented. Physical changes were obtained by constricting the aorta at the celiac trunk level with a band of metal. Banding causes an increase of blood pressure and hypertrophy of the vessel in the upper body and a transient decrease of blood pressure in the lower body. If the aorta is cut transversely into rings and each ring is cut radially, it will open up into a noncircular arc, which may be characterized by its opening angle. It is shown that the opening angle varies systematically along the aorta and that it changes significantly together with changes of blood pressure and hypertrophy. In the ascending aorta, the opening angle increased from 171 degrees and to 214 degrees in 4 days after banding, then decreased gradually to an asymptotic value of 126 degrees in 40 days. At other sections, the swing of opening angle is smaller. The implications are discussed.

Animals↗
PubMed1989

Connecting incremental shear modulus and Poisson's ratio of lung tissue with morphology and rheology of microstructure.

The width and curvature of the collagen and elastin fiber bundles in the human pulmonary interalveolar septa and alveolar mouths are measured. The data, together with the known mechanical properties of collagen and elastin fibers, are used to derive the incremental elastic moduli of the lung tissue. The constitutive equation for small incremental stress and strain superposed on a homeostatic inflated lung is linear and isotropic, and characterized by two material constants.

Collagen↗
PubMed1988

Trauma of lung due to impact load.

A quantitative evaluation of lung injury due to impact loading is of general interest. Hemorrhage and edema are the usual sequelae to traumatic pulmonary impact. To gain some quantitative understanding of the phenomena, we perfused excised rabbit lung with Macrodex at isogravimetric condition and monitored lung weight continuously after impact. It is shown that a factor of importance is the rigidity of the surface on which the lung rests. The rate of lung weight increase is smaller if the lung was 'freely' supported on a soft cloth, more if it was supported on a rigid plate. This suggests the influence of stress wave reflection. The critical condition correlates with the initial velocity of impact at the surface of the lung, or with the maximum deflection. For a freely supported lung, the rate of lung weight increase was 22% of the initial total lung weight per h after impact when the impact velocity was 11.5 ms-1, 30% when the velocity was 13.2 ms-1, several 100% at 13.5 ms-1, signaling massive lung injury. Since the velocity of sound in rabbit lung is 33.3 ms-1 when the inflation (transpulmonary) pressure is 10 cm H2O, the critical velocity of 13.5 ms-1 corresponds to a Mach number of 0.4. The maximum surface displacement of the lung is almost linearly proportional to the initial velocity of impact. The exact cause of edema and hemorrhage is unknown; we hypothesize that it is due to tensile stress in the alveolar wall caused by the impact.

Animals↗
PubMed1988

A hypothesis on the mechanism of trauma of lung tissue subjected to impact load.

When a compressive impact load is applied on the chest, as in automobile crash or bomb explosion, the lung may be injured and show evidences of edema and hemorrhage. Since soft tissues have good strength in compression, why does a compression wave cause edema? Our hypothesis is that tensile and shear stresses are induced in the alveolar wall on rebound from compression, and that the maximum principal stress (tensile) may exceed critical values for increased permeability of the epithelium to small solutes, or even fracture. Furthermore, small airways may collapse and trap gas in alveoli at a critical strain, causing traumatic atelectasis. The collapsed airways reopen at a higher strain after the wave passes, during which the expansion of the trapped gas will induce additional tension in the alveolar wall. To test this hypothesis, we made three new experiments: (1), measuring the effect of transient overstretch of the alveolar membrane on the rate of lung weight increase; (2) determining the critical pressure for reopening collapsed airways of rabbit lung subjected to cyclic compression and expansion; (3) cyclic compression of lung with trachea closed. We found that in isolated rabbit lung overstretching increases the rate of edema fluid formation, that the critical strain for airway reopening is higher than that for closing, and that these critical strains are strain-rate dependent, but independent of the state of the trachea, whether it is open or closed. Furthermore, a theoretical analysis is presented to show that the maximum principal (tensile) stress is of the same order of magnitude as the maximum initial compressive stress at certain localities of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗