Direction of blood flow in a vein.
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ABSTRACT:
SUBMITTER: Bhaskar ME
PROVIDER: S-EPMC2665972 | biostudies-literature | 2009 Apr
REPOSITORIES: biostudies-literature
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Project description:Endothelial cell (EC) sensing of fluid shear stress direction is a critical determinant of vascular health and disease. Unidirectional flow induces EC alignment and vascular homeostasis, whereas bidirectional flow has pathophysiological effects. ECs express several mechanoreceptors that respond to flow, but the mechanism for sensing shear stress direction is poorly understood. We determined, by using in vitro flow systems and magnetic tweezers, that β1 integrin is a key sensor of force direction because it is activated by unidirectional, but not bidirectional, shearing forces. β1 integrin activation by unidirectional force was amplified in ECs that were pre-sheared in the same direction, indicating that alignment and β1 integrin activity has a feedforward interaction, which is a hallmark of system stability. En face staining and EC-specific genetic deletion studies in the murine aorta revealed that β1 integrin is activated and is essential for EC alignment at sites of unidirectional flow but is not activated at sites of bidirectional flow. In summary, β1 integrin sensing of unidirectional force is a key mechanism for decoding blood flow mechanics to promote vascular homeostasis.This article has an associated First Person interview with the first author of the paper.
| S-EPMC6589088 | biostudies-literature
Project description: Not available
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Project description:The essential function of the circulatory system is to continuously and efficiently supply the O2 and nutrients necessary to meet the metabolic demands of every cell in the body, a function in which vast capillary networks play a key role. Capillary networks serve an additional important function in the central nervous system: acting as a sensory network, they detect neuronal activity in the form of elevated extracellular K+ and initiate a retrograde, propagating, hyperpolarizing signal that dilates upstream arterioles to rapidly increase local blood flow. Yet, little is known about how blood entering this network is distributed on a branch-to-branch basis to reach specific neurons in need. Here, we demonstrate that capillary-enwrapping projections of junctional, contractile pericytes within a postarteriole transitional region differentially constrict to structurally and dynamically determine the morphology of capillary junctions and thereby regulate branch-specific blood flow. We further found that these contractile pericytes are capable of receiving propagating K+-induced hyperpolarizing signals propagating through the capillary network and dynamically channeling red blood cells toward the initiating signal. By controlling blood flow at junctions, contractile pericytes within a functionally distinct postarteriole transitional region maintain the efficiency and effectiveness of the capillary network, enabling optimal perfusion of the brain.
| S-EPMC7604512 | biostudies-literature
Project description:Hemodynamic shear stresses cause endothelial cells (ECs) to polarize in the plane of the flow. Paradoxically, under strong shear flows, ECs disassemble their primary cilia, common sensors of shear, and thus must use an alternative mechanism of sensing the strength and direction of flow. In our experiments in microfluidic perfusion chambers, confluent ECs developed planar cell polarity at a rate proportional to the shear stress. The location of Golgi apparatus and microtubule organizing center was biased to the upstream side of the nucleus, i.e. the ECs polarized against the flow. These in vitro results agreed with observations in murine blood vessels, where EC polarization against the flow was stronger in high flow arteries than in veins. Once established, flow-induced polarization persisted over long time intervals without external shear. Transient destabilization of acto-myosin cytoskeleton by inhibition of myosin II or depolymerization of actin promoted polarization of EC against the flow, indicating that an intact acto-myosin cytoskeleton resists flow-induced polarization. These results suggested that polarization was induced by mechanical displacement of EC nuclei downstream under the hydrodynamic drag. This hypothesis was confirmed by the observation that acute application of a large hydrodynamic force to ECs resulted in an immediate downstream displacement of nuclei and was sufficient to induce persistent polarization. Taken together, our data indicate that ECs can sense the direction and strength of blood flow through the hydrodynamic drag applied to their nuclei.
| S-EPMC3798183 | biostudies-literature
Project description:The accumulation of small strokes has been linked to cognitive dysfunction. Although most animal models have focused on the impact of arteriole occlusions, clinical evidence indicates that venule occlusions may also be important. We used two-photon excited fluorescence microscopy to quantify changes in blood flow and vessel diameter in capillaries after occlusion of single ascending or surface cortical venules as a function of the connectivity between the measured capillary and the occluded venule. Clotting was induced by injuring the target vessel wall with femtosecond laser pulses. After an ascending venule (AV) occlusion, upstream capillaries showed decreases in blood flow speed, high rates of reversal in flow direction, and increases in vessel diameter. Surface venule occlusions produced similar effects, unless a collateral venule provided a new drain. Finally, we showed that AVs and penetrating arterioles have different nearest-neighbor spacing but capillaries branching from them have similar topology, which together predicted the severity and spatial extent of blood flow reduction after occlusion of either one. These results provide detailed insights into the widespread hemodynamic changes produced by cortical venule occlusions and may help elucidate the role of venule occlusions in the development of cognitive disorders and other brain diseases.
| S-EPMC3210348 | biostudies-literature
Project description:ObjectiveAtherosclerosis-prone regions of arteries are characterized by complex flow patterns where the magnitude of shear stress is low and direction rapidly changes, termed disturbed flow. How endothelial cells sense flow direction and how it impacts inflammatory effects of disturbed flow are unknown. We therefore aimed to understand how endothelial cells respond to changes in flow direction.Approach and resultsUsing a recently developed flow system capable of changing flow direction to any angle, we show that responses of aligned endothelial cells are determined by flow direction relative to their morphological and cytoskeletal axis. Activation of the atheroprotective endothelial nitric oxide synthase pathway is maximal at 180° and undetectable at 90°, whereas activation of proinflammatory nuclear factor-κB is maximal at 90° and undetectable at 180°. Similar effects were observed in randomly oriented cells in naive monolayers subjected to onset of shear. Cells aligned on micropatterned substrates subjected to oscillatory flow were also examined. In this system, parallel flow preferentially activated endothelial nitric oxide synthase and production of nitric oxide, whereas perpendicular flow preferentially activated reactive oxygen production and nuclear factor-κB.ConclusionsThese data show that the angle between flow and the cell axis defined by their shape and cytoskeleton determines endothelial cell responses. The data also strongly suggest that the inability of cells to align in low and oscillatory flow is a key determinant of the resultant inflammatory activation.
| S-EPMC3812824 | biostudies-literature
Project description:Background/aimIn patients with acute central retinal vein occlusion (CRVO), dynamic angiography may reveal the presence of pulsatile flow (termed here pulsatile venular outflow, PVO) within first order veins (that is, the large veins). The main goal of this study was to investigate the mechanism underlying PVO.Methods10 patients with CRVO and PVO were included. Quantitative and qualitative analysis of venous flow on dynamic angiograms allowed the correlation, temporally, of second and first order vein flow on the one hand, and venous flow and systolic cycle on the other.ResultsAnalysis of the time-velocity curve showed that (1) the onset of arterial systole preceded the onset of PVO by less than 0.08 seconds (n = 5); (2) PVO onset was simultaneous to the time of onset of minimal flow (Vmin) in first order veins (n = 10); (3) the time of onset of maximal flow (Vmax) in first order veins occurred 0.20-0.44 seconds after the onset of PVO (n = 6).ConclusionsDuring CRVO with severe reduction in blood flow, the presence of PVO is the result of the existence of a distinct haemodynamic regimen in first and second order veins. These data support the hypothesis that second order veins flow is synchronous with the arterial flow, while the delayed peak flow in first order veins may reflect the consequences of the delayed IOP curve and/or of intermittent venous compression.
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Project description:ObjectivesA thrombus can occur in the stump of the pulmonary vein after left upper lobectomy, potentially causing postoperative cerebral infarction. This study aimed to verify the hypothesis that stagnation of blood flow inside the pulmonary vein stump causes thrombus formation.MethodsThe three-dimensional geometry of the pulmonary vein stump after left upper lobectomy was recreated using contrast-enhanced computed tomography. Blood flow velocity and wall shear stress (WSS) inside the pulmonary vein stump were analysed using the computational fluid dynamics (CFD) method and compared between the two groups (those with or without thrombus).ResultsThe volumes of average flow velocity per heartbeat < 10 mm/s, 3 mm/s, 1 mm/s (p-values 0.0096, 0.0016, 0.0014, respectively) and the volumes where flow velocity was always below the three cut-off values (p-values 0.019, 0.015, 0.017, respectively) were significantly larger in patients with a thrombus than in those without thrombus. The areas of average WSS per heartbeat < 0.1 Pa, 0.03 Pa, 0.01 Pa (p-values 0.0002, < 0.0001, 0.0002, respectively), and the areas where WSS was always below the three cut-off values (p-values 0.0088, 0.0041, 0.0014, respectively) were significantly larger in patients with thrombus than in those without thrombus.ConclusionsThe area of blood flow stagnation in the stump calculated by CFD method was significantly larger in patients with than in those without thrombus. This result elucidates that stagnation of blood flow promotes thrombus formation in the pulmonary vein stump in patients who undergo left upper lobectomy.
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