Biorheology - Volume 42, issue 6

Authors: Sato, Masaaki | Ohashi, Toshiro

Article Type: Research Article

Abstract: Vascular endothelial cells are located at the innermost layer of the blood vessel wall and are always exposed to three different mechanical forces: shear stress due to blood flow, hydrostatic pressure due to blood pressure and cyclic stretch due to vessel deformation. It is well known that endothelial cells respond to these mechanical forces and change their shapes, cytoskeletal structures and functions. In this review, we would like to mainly focus on the effects of shear stress and hydrostatic pressure on endothelial cell morphology. After applying fluid shear stress, cultured endothelial cells show marked elongation and orientation in the flow …direction. In addition, thick stress fibers of actin filaments appear and align along the cell long axis. Thus, endothelial cell morphology is closely related to the cytoskeletal structure. Further, the dynamic course of the morphological changes is shown and the related events such as changes in mechanical stiffness and functions are also summarized. When endothelial cells were exposed to hydrostatic pressure, they exhibited a marked elongation and orientation in a random direction, together with development of centrally located, thick stress fibers. Pressured endothelial cells also exhibited a multilayered structure with less expression of VE-cadherin unlike under control conditions. Simultaneous loading of hydrostatic pressure and shear stress inhibited endothelial cell multilayering and induced elongation and orientation of endothelial cells with well-developed VE-cadherin in a monolayer, which suggests that for a better understanding of vascular endothelial cell responses one has to take into consideration the combination of the different mechanical forces such as exist under in vivo mechanical conditions. Show more

Citation: Biorheology, vol. 42, no. 6, pp. 421-441, 2005

Authors: Zhu, Cheng | Lou, Jizhong | McEver, Rodger P.

Article Type: Research Article

Abstract: Force can shorten the lifetimes of macromolecular complexes (e.g., receptor–ligand bonds) by accelerating their dissociation. Perhaps paradoxical at first glance, bond lifetimes can also be prolonged by force. This counterintuitive behavior was named catch bonds, which is in contrast to the ordinary slip bonds that describe the intuitive behavior of lifetimes being shortened by force. Fifteen years after their theoretical proposal, catch bonds have finally been observed. In this article we review recently published data that have demonstrated catch bonds in the selectin system and suggested catch bonds in other systems, the theoretical models for their explanations, possible structural bases, …their relation to flow-enhanced adhesion, and the potential biorheological relevance. Show more

Keywords: Kinetics, force, flow, shear

Citation: Biorheology, vol. 42, no. 6, pp. 443-462, 2005

Authors: Zhao, Ke-Seng

Article Type: Research Article

Abstract: Persistent low perfusion and low blood pressure are the two major events in the pathogenesis of irreversible shock. This review is focused on our recent study on the mechanism of, and a new therapeutic approach to the two events in IS. One of the main causes of persistent low perfusion are leukocyte adhesion on venule walls and plugging in capillaries which comes from the low wall shear stress or shear rate, and high leukocyte–endothelial adhesion force in IS. However, blockade of leukocyte adhesion by monoclonal antibodies against the adhesion molecules can only attenuate the number of sticking WBC in venules, …but cannot make an appreciable improvement in capillary reflow and survival rate in IS, because it is difficult for the agents to flow into an obstructed capillary. We have shown that the administration of Polydatin, a crystalline product isolated from a traditional Chinese medicine, can restore the pulse pressure with high survival rate in irreversible shock. With an increase in pulse pressure, and the highly dispersive force resulting from pulsatile blood flow, the stationary blood cells can be pushed away from the obstructed capillary and thus promote capillary reflow. Therefore, enhancement of pulse pressure is a key factor for the treatment of low perfusion in irreversible shock. Hyperpolarization of arteriolar smooth muscle cells occurs in irreversible shock, which inhibits the potential-operated calcium channel and the influx of Ca2+ in arteriolar smooth muscle cells stimulated by norepinephrine, and finally leads to low vascular contractile responsiveness with refractory hypotension in irreversible shock. Activation of the potassium channels KATP and BKCa is involved in arteriolar smooth muscle cells hyperpolarization. In irreversible shock, ATP depletion, intracellular acidosis, ONOO− formation, and enhancement of a calcium spark results in activation of KATP and BKCa and consequent arteriolar smooth muscle cell hyperpolarization. Therefore, a new therapeutic strategy for refractory hypotension was suggested, including blockade of potassium channel activation to reconstitute vasoreactivity and the administration of vasopressors to elevate blood pressure in the treatment of irreversible shock. Show more

Keywords: Leukocyte plugging, capillary no-reflow, low vasoreactivity, refractory hypotension, shock

Citation: Biorheology, vol. 42, no. 6, pp. 463-477, 2005

Authors: Koutsiaris, Aristotle G.

Article Type: Research Article

Abstract: Volume flow was estimated from axial erythrocyte velocity measurements in 30 mesenteric microvessels of 6 rabbits and was compared to Murray's law predictions. The diameters of capillaries and precapillary arterioles ranged between 5.6 and 12 μm. The significant pulsating flow component existing in these microvessels was taken into account by measuring instantaneous axial blood velocity throughout the course of a cardiac cycle and then averaging over the period. In addition, the effect of the velocity profile variation with diameter was taken into account, for the first time, by using a profile factor function. According to Murray's law, the relation between …blood volume flow and diameter is governed by a ‘cube’ law. Curve fitting to volume flow and diameter data pairs for rabbits, showed a dependence of volume flow on diameter raised to the 4th power (with a correlation coefficient equal to 0.97). The above result supports the hypothesis that, in the precapillary part of microvasculature, the principle of constant longitudinal pressure gradient rather than the principle of minimum work may be valid. Show more

Keywords: Microvessels, pulsating flow, velocity profile, Murray's law

Citation: Biorheology, vol. 42, no. 6, pp. 479-491, 2005

Authors: Choi, Hyo Won | Barakat, Abdul I.

Article Type: Research Article

Abstract: Endothelial cell (EC) responsiveness to shear stress is essential for vasoregulation and plays a role in atherogenesis. Although blood is a non-Newtonian fluid, EC flow studies in vitro are typically performed using Newtonian fluids. The goal of the present study was to determine the impact of non-Newtonian behavior on the flow field within a model flow chamber capable of producing flow disturbance and whose dimensions permit Reynolds and Womersley numbers comparable to those present in vivo. We performed two-dimensional computational fluid dynamic simulations of steady and pulsatile laminar flow of Newtonian and non-Newtonian fluids over a backward facing step. In …the non-Newtonian simulations, the fluid was modeled as a shear-thinning Carreau fluid. Steady flow results demonstrate that for Re in the range 50–400, the flow recirculation zone downstream of the step is 22–63% larger for the Newtonian fluid than for the non-Newtonian fluid, while spatial gradients of shear stress are larger for the non-Newtonian fluid. In pulsatile flow, the temporal gradients of shear stress within the flow recirculation zone are significantly larger for the Newtonian fluid than for the non-Newtonian fluid. These findings raise the possibility that in regions of flow disturbance, EC mechanotransduction pathways stimulated by Newtonian and non-Newtonian fluids may be different. Show more

Keywords: Endothelial cells, disturbed flow, mechanotransduction, shear stress, atherosclerosis

Citation: Biorheology, vol. 42, no. 6, pp. 493-509, 2005

Authors: Yalcin, Ozlem | Meiselman, Herbert J. | Armstrong, Jonathan K. | Baskurt, Oguz K.

Article Type: Research Article

Abstract: The role of red blood cell (RBC) aggregation as a determinant of in vivo blood flow is still unclear. This study was designed to investigate the influence of a well-controlled enhancement of RBC aggregation on blood flow resistance in an isolated-perfused heart preparation. Guinea pig hearts were perfused through a catheter inserted into the root of the aorta using a pressure servo-controlled pump system that maintained perfusion pressures of 30 to 100 mmHg. The hearts were beating at their intrinsic rates and pumping against the perfusion pressure. RBC aggregation was increased by Pluronic (F98) coating of RBC at a concentration …0.025 mg/ml, corresponding to about a 100% increment in RBC aggregation as measured by erythrocyte sedimentation rate. Isolated heart preparations were perfused with 0.40 l/l hematocrit unmodified guinea pig blood and with Pluronic-coated RBC suspensions in autologous plasma. At high perfusion pressures there were no significant differences between the flow resistance values for the two perfusates, with differences in flow resistance only becoming significant at lower perfusion pressures. These results can be interpreted to reflect the shear dependence of RBC aggregation: higher shear forces associated with higher perfusion pressures should have dispersed RBC aggregates resulting in blood flow resistances similar to control values. Experiments repeated in preparations in which the smooth muscle tone was inhibited by pre-treatment with papaverine indicated that significant effects of enhanced RBC aggregation could be detected at higher perfusion pressures, underlining the compensatory role of vasomotor control mechanisms. Show more

Citation: Biorheology, vol. 42, no. 6, pp. 511-520, 2005

Article Type: Other

Citation: Biorheology, vol. 42, no. 6, pp. 521-523, 2005