The regulation of effective circulating blood volume.
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Neutrophils play a role in the development of pulmonary edema in many models of the adult respiratory distress syndrome, but the mechanism of their action is not completely understood. We asked whether two neutrophil secretory products, human neutrophil cationic protein (NCP) and human neutrophil elastase (HNE), would nonenzymatically alter the movement of albumin across a cultured endothelial monolayer. Both enzymes were inactivated by heating before use. HNE was additionally enzymatically inactivated with a chloromethylketone oligopeptide (CMK) inhibitor and with alpha 1-proteinase inhibitor (alpha 1-PI). Heated NCP, heated HNE, and CMK-complexed HNE all increased transendothelial albumin transfer. The cation protamine also increased albumin transfer across the endothelium and this increase was blocked by heparin. Alpha 1-PI and fetal bovine serum also prevented the cationic proteins from increasing albumin transfer. Using the release of lactate dehydrogenase as a marker of cytotoxicity, heated HNE was toxic to endothelial cells, heated NCP had only minimal toxicity, and protamine had no toxicity. Changes in endothelial cell shape with gap formation was seen after exposure to both heated HNE and heated NCP. Both the cytotoxicity associated with heated HNE and the cell shape changes associated with heated NCP and heated HNE could be blocked by heparin. These results suggest that in addition to neutrophil proteases and reactive O2 molecules, neutrophil-derived cationic proteins can directly and nonenzymatically contribute to edema formation during acute inflammation.
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BACKGROUND AND AIM OF THE STUDY: The dynamics of the mitral valve result from the synergy of left heart geometry, local blood flow and tissue integrity. Herein is presented the first coupled fluid-structure computational model of the mitral valve in which valvular kinematics result from the interaction of local blood flow and a continuum representation of valvular microstructure. METHODS: The diastolic geometry of the mitral valve was assembled from previously published experimental data. Anterior and posterior leaflets were modeled as networks of entangled collagen fibers, embedded in an isotropic matrix. The resulting non-linear continuum description of mitral tissue was implemented in a three-dimensional membrane formulation. Chordal tension-only behavior was defined from experimental tensile tests. The computational model considered the valve immersed in a domain of Newtonian blood, with an experimentally determined viscosity corresponding to a shear rate of 180 s(-1) at 37 degrees C. Ventricular and atrial pressure curves were applied to ventricular and atrial surfaces of the blood domain. RESULTS: Peak closing flow and volume were 51 ml/s and 1.17 ml, respectively. Papillary muscle force ranged dynamically between 0.0 and 2.6 N. Acoustic pressure (RMS) was found to be 3.3 Pa, with a peak frequency of 72 Hz at 0.064 s from the onset of systole. Model predictions showed excellent agreement with available transmitral flow, papillary force and first heart sound (S1) acoustic data. CONCLUSION: The addition of blood flow and an experimentally driven microstructural description of mitral tissue represent a significant advance in computational studies of the mitral valve. This model will be the foundation for future computational studies on the effect of pathophysiological tissue alterations on mitral valve competence.
Viscosity and shear dependent changes in electrical resistance (delta R) were measured simultaneously in blood perfused capillaries (I.D. = 0.58 mm, 1 = 300 mm, TW = 0.04 to 0.5 Pa). It appears that delta R is primarily caused by the development of a low resistant cell free marginal layer. Red cell aggregation strongly supports the development of delta R, while in non-aggregating blood the shear induced change in conductivity is rather small. Theoretical and experimental data become closely correlated if the calculated width of the marginal layer, being 1 to 5% of the capillary radius, is inserted into a modified form of Poiseuille's law. It is concluded that under the conditions of plug flow the non-Newtonian flow behavior of EDTA blood almost exclusively depends upon the width of the marginal layer, being a function of shear stress and hematocrit.
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Recently it has been shown experimentally that transport of heat and gas (specifically oxygen and helium) are augmented in the laminar flow of aqueous suspensions of polystyrene spheres 50 and 150 micrometer in diameter. In this report, data on heat and gas transport are correlated. Application of this correlation to flowing blood leads to the following conclucions. There is no significant augmentation of oxygen and heat transport in flowing blood even at shear rates much higher than physiological shear rates; an observation which is in accord with the experimental results. The augmentation of the diffusion coefficient of plasma proteins in flowing blood, though not very high, appears to be measurable. Of the total measured augmentation of about 6000--30 000% in platelet diffusivity in flowing blood, quoted from the literature, about 500% is attributable from this correlation to fluid mechanical forces, and the balance is hypothetically attributed to other forces (electrical or biochemical) present in blood.
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The problem of dissolution of a bubble in the bloodstream is examined. The bubble is assumed to be filled with a mixture of a sparingly water-soluble gas (osmotic agent) and air. The dissolution of the bubble has three definite stages. In Stage 1, the bubble quickly swells in air. The swelling ratio depends on the surface tension, blood pressure, level of oxygen metabolism and initial mole fraction of osmotic agent in the bubble. In Stage 2, the osmotic agent slowly diffuses out of the bubble. The squared radius decreases nearly linearly with time, at a rate proportional to the Ostwald coefficient and diffusivity of the osmotic agent. In Stage 3, the partial pressure of the osmotic agent becomes so high that it condenses into a liquid. In order to prolong the lifetime of 5-micron bubbles in the bloodstream from < 1 s (as found with pure air), the osmotic agent must have a low Ostwald coefficient (< or = 10(-4)) and a relatively high saturated vapor pressure at body temperature (> or = 0.3 atm = 3 x 10(4) Pa).
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In hyperthermia treatment planning vessels with a diameter larger than 0.5 mm must be treated individually. Such vessels can be described as 3D curves with associated diameters. The temperature profile along the vessel is discretized one dimensionally. Separately the tissue is discretized three dimensionally on a regular grid of voxels. The vessel as well as the tissue are positioned in one global space. Methods are supplied to describe the tissue-vessel interaction, the shift of the blood temperature profile describing the flow of blood along the vessel and the calculation of the vessel wall temperature. The calculation of the interaction is based on tissue temperature samples and the blood temperature together with the distance between the centre of the vessel and the tissue temperature sample. An analytical expression for a vessel inside a coaxial tissue cylinder is then used for the calculation of the heat flow rate across the vessel wall. The basic test system is a vessel segment embedded inside a coaxial tissue cylinder. All the tests use this setup while the following simulation parameters are varied: position and orientation of the vessel relative to the tissue grid, vessel radius, sample density of the blood temperature and power deposition inside the tissue cylinder. The blood temperature profile is examined by calculation of the local estimate of the equilibration length. All tests show excellent agreement with the theory.
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The historical development of the mechanics of blood flow can be traced from ancient times, to Leonardo da Vinci and Leonhard Euler and up to the present times with increasing biological knowledge and mathematical analysis. In the last two decades, quantitative and numerical methods have steadily given more complete and precise understanding. In the arterial system wave propagation computations based on nonlinear one-dimensional modeling have given the best representation of pulse wave propagation. In the veins, the theory of unsteady flow in collapsible tubes has recently been extensively developed. In the last decade, progress has been made in describing the blood flow at junctions, through stenoses, in bends and in capillary blood vessels. The rheological behavior of individual red blood cells has been explored. A working model consists of an elastic membrane filled with viscous fluid. This model forms a basis for understanding the viscous and viscoelastic behavior of blood.