Blood flow and blood velocity measurement in vivo by electromagnetic induction

1982 ◽  
Vol 4 (2) ◽  
pp. 61-78 ◽  
Author(s):  
D.G. Wyatt
2007 ◽  
Vol 42 (4) ◽  
pp. 495-511 ◽  
Author(s):  
Peter Vennemann ◽  
Ralph Lindken ◽  
Jerry Westerweel

2017 ◽  
Author(s):  
Paul W. Sweeney ◽  
Simon Walker-Samuel ◽  
Rebecca J. Shipley

AbstractThe neurovascular mechanisms underpinning the local regulation of cerebral blood flow (CBF) and oxygen transport remain elusive. In this study we have combined novel in vivo imaging of cortical microvascular and mural cell architecture with mathematical modelling of blood flow and oxygen transport, to provide new insights into CBF regulation that would be inaccessible in a conventional experimental context. Our study implicates vasomotion of smooth muscle actin-covered vessels, rather than pericyte-covered capillaries, as the main mechanism for modulating tissue oxygenation. We also resolve seemingly paradoxical observations in the literature around reduced blood velocity in response to arteriolar constrictions and deduce the cause to be propagation of constrictions to upstream penetrating arterioles. We provide support for pericytes acting as signalling conduits for upstream smooth muscle activation, and erythrocyte deformation as a complementary regulatory mechanism. Finally, we caution against the use of blood velocity as a proxy measurement for flow. Our combined imaging-modelling platform complements conventional experimentation allowing cerebrovascular physiology to be probed in unprecedented detail.


2021 ◽  
Author(s):  
Sebastien Salles ◽  
Jami Shepherd ◽  
Hendrik J. Vos ◽  
Guillaume Renaud

Intraosseous blood circulation is thought to have a critical role in bone growth and remodeling, fracture healing, and bone disorders. However, it is rarely considered in clinical practice due to the absence of a suitable non-invasive in vivo measurement technique. In this work, we assessed blood perfusion in tibial cortical bone simultaneously with blood flow in the superficial femoral artery with ultrasound imaging in 5 healthy volunteers. After suppression of stationary signal with Singular-Value-Decomposition, pulsatile blood flow in cortical bone tissue is revealed, following the heart rate measured in the femoral artery. Using a method combining transverse oscillations and phase-based motion estimation, two-dimensional vector flow was obtained in the cortex of the tibia. After spatial averaging over the cortex, the peak blood velocity along the long axis of the tibia was measured four times larger than the peak blood velocity across the bone cortex. This suggests that blood flow in central (Haversian) canals is larger than in perforating (Volkmann's) canals, as expected from the intracortical vascular organization in humans. The peak blood velocity indicates a flow from the endosteum to the periosteum and from the heart to the foot for all subjects. Because aging and the development of bone disorders are thought to modify the direction and velocity of intra-cortical blood flow, their quantification is crucial. This work reports for the first time an in vivo quantification of the direction and velocity of blood flow in human cortical bone.


1996 ◽  
Vol 271 (2) ◽  
pp. H461-H468 ◽  
Author(s):  
C. J. Jones ◽  
L. Kuo ◽  
M. J. Davis ◽  
W. M. Chilian

The actions of nitroglycerin on the coronary microcirculation are controversial, with some laboratories reporting that coronary arterioles dilate to the drug and others reporting that they do not. Our goal was to reconcile these disparate observations. Specifically, we hypothesized that dilation of coronary arterioles by nitroglycerin is overwhelmed by intrinsic autoregulatory escape mechanisms. Accordingly, we projected that coronary arterioles would show transient, but not sustained, dilation to nitroglycerin in vivo. Furthermore, we hypothesized that isolated coronary arterioles would show sustained dilation to the drug, because intrinsic escape mechanisms would be absent under these conditions. To test these hypotheses, we measured diameter changes of canine coronary microvessels in vivo during continuous nitroglycerin administration (intracoronary infusion or epicardial suffusion) using intravital fluorescent microscopy (n = 17 dogs) at two time points: early (1-3 min), when coronary artery blood flow velocity was increased, and late (15-20 min), after blood flow velocity returned to control. Tb study responses of coronary arterioles in the absence of autoregulatory influences, we measured the diameter of isolated canine coronary arterioles to varying doses of nitroglycerin (n = 8 vessels, maximal diameter 81 +/- 4 microns). During the early phase of nitroglycerin infusion (1,3, and 10 micrograms.kg-1.min-1), coronary arterioles dilated by 4 +/- 1, 7 +/- 2, and 13 +/- 2% (all P < 0.05), whereas small arteries dilated by 1 +/- 2, 3 +/- 1, and 4 +/- 1%, respectively (P < 0.05 for the higher doses). Coronary artery blood velocity measured increased by 45 +/- 15% (3 micrograms.kg-1.min-1, P < 0.05). Suffusion of nitroglycerin (10(-5) M) dilated coronary arterioles, but not small arteries, by 17 +/- 5% (P < 0.05) between 1 and 3 min. After 15-20 min of nitroglycerin (3 micrograms.kg-1.min-1 by intracoronary infusion), diameters of coronary arterioles and coronary artery blood velocity returned to control, whereas dilation of small arteries remained significant at 4 +/- 1%. Coronary arteriolar dilation by epicardial suffusion of nitroglycerin also waned to control values by 15-20 min, whereas dilation of small arteries was observed: 5 +/- 2% (P < 0.05). In vitro, nitroglycerin caused dose-dependent dilation of coronary arterioles to their maximal diameter, which was sustained for 20 min. Thus nitroglycerin dilates coronary arterioles and small arteries. The dilation in vivo is transient for arterioles but sustained for arteries. In vitro, the dilation is sustained. Because microvessels in vitro are capable of sustaining dilation for 20 min, we conclude that the waning of arteriolar dilation in vivo is related to autoregulatory escape from dilation by nitroglycerin.


2016 ◽  
Vol 121 (4) ◽  
pp. 849-857 ◽  
Author(s):  
Crystal L. Coolbaugh ◽  
Emily C. Bush ◽  
Charles F. Caskey ◽  
Bruce M. Damon ◽  
Theodore F. Towse

Automated software improves the accuracy and reliability of blood velocity, vessel diameter, blood flow, and shear rate ultrasound measurements, but existing software offers limited flexibility to customize and validate analyses. We developed FloWave.US —open-source software to automate ultrasound blood flow analysis—and demonstrated the validity of its blood velocity (aggregate relative error, 4.32%) and vessel diameter (0.31%) measures with a skeletal muscle ultrasound flow phantom. Compared with a commercial, manual analysis software program, FloWave.US produced equivalent in vivo cardiac cycle time-averaged mean (TAMean) velocities at rest and following a 10-s muscle contraction (mean bias <1 pixel for both conditions). Automated analysis of ultrasound blood flow data was 9.8 times faster than the manual method. Finally, a case study of a lower extremity muscle contraction experiment highlighted the ability of FloWave.US to measure small fluctuations in TAMean velocity, vessel diameter, and mean blood flow at specific time points in the cardiac cycle. In summary, the collective features of our newly designed software—accuracy, reliability, reduced processing time, cost-effectiveness, and flexibility—offer advantages over existing proprietary options. Further, public distribution of FloWave.US allows researchers to easily access and customize code to adapt ultrasound blood flow analysis to a variety of vascular physiology applications.


2002 ◽  
Vol 24 (4) ◽  
pp. 193-214 ◽  
Author(s):  
Caterina M. Gallippi ◽  
Gregg E. Trahey

A method for adaptive clutter rejection via blind source separation (BSS) using principal and independent component analyses is presented in application to blood velocity measurement in the carotid artery. In particular, the filtering method's efficacy for eliminating clutter and preserving lateral blood flow signal components is presented. The performance of IIR filters is compromised by shorth data ensembles (10 to 20 temporal samples) as implemented for color-flow and high frame-rate imaging due to initialization requirements. Further, the ultrasonic imaging system's transfer function maps axial wall and lateral blood motion to overlapping spectra. As such, frequency domain-based approaches to wall filtering are ineffective for distinguishing wall from blood motion signals. Rather than operating in the frequency domain, BSS performs clutter rejection by decomposing the input data ensemble into N constitutive source signals in time, where N is the ensemble length. Source signal energy coupled with respective signal depth and time course profiles reveal which source signals correspond to blood, noise and clutter components. Clutter components may then be removed without disruption of lateral blood flow information needed for two-dimensional blood velocity measurement. A simplistic data simulation is employed to offer an intuitive understanding of BSS methods for signal separation. The adaptive BSS filter is further demonstrated using a Field II simulation of blood flow through the carotid artery including tissue motion. BSS clutter filter performance is compared to the performance of FIR, IIR and polynomial regression clutter filters. Finally, the filter is employed for clinical application using a Siemens Elegra scanner, carotid artery data with lateral blood flow collected from healthy volunteers, and Speckle Tracking; velocity magnitude and angle profiles are shown. Once again, the BSS clutter filter is contrasted to FIR, IIR and polynomial regression clutter filters using clinical examples. Velocities computed with Speckle Tracking after BSS wall filtering are highest in the center of the artery and diminish to low velocities near the vessel walls, with velocity magnitudes consistent with physiological expectations. These results demonstrate that the BSS adaptive filter sufficiently suppresses wall motion signal for clinical lateral blood velocity measurement using data ensembles suitable for color-flow and high frame-rate imaging.


Author(s):  
Enrico D.F. Motti ◽  
Hans-Georg Imhof ◽  
Gazi M. Yasargil

Physiologists have devoted most attention in the cerebrovascular tree to the arterial side of the circulation which has been subdivided in three levels: 1) major brain arteries which keep microcirculation constant despite changes in perfusion pressure; 2) pial arteries supposed to be effectors regulating microcirculation; 3) intracerebral arteries supposed to be deprived of active cerebral blood flow regulating devices.The morphological search for microvascular effectors in the cerebrovascular bed has been elusive. The opaque substance of the brain confines in vivo investigation to the superficial pial arteries. Most morphologists had to limit their observation to the random occurrence of a favorable site in the practically two-dimensional thickness of diaphanized histological sections. It is then not surprising most investigators of the cerebral microcirculation refer to an homogeneous network of microvessels interposed between arterioles and venules.We have taken advantage of the excellent depth of focus afforded by the scanning electron microscope (SEM) to investigate corrosion casts obtained injecting a range of experimental animals with a modified Batson's acrylic mixture.


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