Structural remodeling of mouse gracilis artery after chronic alteration in blood supply

2005 ◽  
Vol 288 (5) ◽  
pp. H2047-H2054 ◽  
Author(s):  
Gabriel Gruionu ◽  
James B. Hoying ◽  
Axel R. Pries ◽  
Timothy W. Secomb

The goals of this study were to determine the time course and spatial dependence of structural diameter changes in the mouse gracilis artery after a redistribution of blood flow and to compare the observations with predictions of computational models for structural adaptation. Diameters were measured 1, 2, 7, 14, 21, 28, and 56 days after resection of one of the two blood supplies to the artery. Overall average diameter, normalized with respect to diameters in untreated vessels, increased slightly during the first 7 days, then increased more rapidly, reaching a peak around day 21, and then decreased. This transient increase in diameter was spatially nonuniform, being largest toward the point of resection. A previously developed theoretical model, in which diameter varies in response to stimuli derived from local metabolic and hemodynamic conditions, was extended to include effects of time-delayed remodeling stimuli in regions of reduced perfusion. Predictions of this model were consistent with observed diameter changes, including the transient increase in diameters near the point of resection, when a remodeling stimulus with a time delay of ∼7 days was included. The results suggest that delayed stimuli significantly influence the dynamic characteristics of vascular remodeling resulting from reduced blood supply.

Author(s):  
Philippe Bonnin ◽  
Nathalie Kubis ◽  
Christiane Charriaut-Marlangue

AbstractEnhancing the collateral blood supply during the acute phase of cerebral ischemia may limit both the extension of the core infarct, by rescuing the penumbra area, and the degree of disability. Many imaging techniques have been applied to rodents in preclinical studies, to evaluate the magnitude of collateral blood flow and the time course of responses during the early phase of ischemic stroke. The collateral supply follows several different routes at the base of the brain (the circle of Willis) and its surface (leptomeningeal or pial arteries), corresponding to the proximal and distal collateral pathways, respectively. In this review, we describe and illustrate the cerebral collateral systems and their modifications following pre-Willis or post-Willis occlusion in rodents. We also review the potential pharmaceutical agents for stimulating the collateral blood supply tested to date. The time taken to establish a collateral blood flow supply through the leptomeningeal anastomoses differs between young and adult animals and between different species and genetic backgrounds. Caution is required when transposing preclinical findings to humans, and clinical trials must be performed to check the added value of pharmacological agents for stimulating the collateral blood supply at appropriate time points. However, collateral recruitment appears to be a rapid, beneficial, endogenous mechanism that can be stimulated shortly after artery occlusion. It should be considered a treatment target for use in addition to recanalization strategies.


2008 ◽  
Vol 29 (3) ◽  
pp. 495-503 ◽  
Author(s):  
Yoshitsugu Nuki ◽  
Melissa M Matsumoto ◽  
Eric Tsang ◽  
William L Young ◽  
Nico van Rooijen ◽  
...  

Sustained hemodynamic stresses, especially sustained high blood flow, result in flow-induced outward vascular remodeling. Mechanisms that link hemodynamic stresses to vascular remodeling are not well understood. Inflammatory cells, known for their release of proteinases, including matrix metalloproteinases (MMPs), are emerging as key mediators for various tissue remodeling. Using a flow-augmented common carotid artery model in rats, we tested whether macrophages play critical roles in adaptive outward vascular remodeling in response to an increase in blood flow. Left common carotid artery ligation caused a sustained increase in blood flow with a gradual increase in luminal diameter in the right common carotid artery. Macrophages infiltrated into the vascular wall that peaked 3 days after flow augmentation. The time course of MMP-9 expression coincided with infiltration of macrophages. Macrophage depletion by liposome-encapsulated dichloromethylene diphosphonate significantly reduced flow-induced outward vascular remodeling, as indicated by the smaller luminal diameter of flow-augmented right common carotid artery in the clodronate-treated group compared with the phosphate-buffered saline-treated group ( P<0.05). These data show critical roles of macrophages in flow-induced outward vascular remodeling. Inflammatory cell infiltration and their subsequent release of cytokines may be key processes for flow-induced outward vascular remodeling.


Author(s):  
John L. Beggs ◽  
Peter C. Johnson ◽  
Astrid G. Olafsen ◽  
C. Jane Watkins

The blood supply (vasa nervorum) to peripheral nerves is composed of an interconnected dual circulation. The endoneurium of nerve fascicles is maintained by the intrinsic circulation which is composed of microvessels primarily of capillary caliber. Transperineurial arterioles link the intrinsic circulation with the extrinsic arterial supply located in the epineurium. Blood flow in the vasa nervorum is neurogenically influenced (1,2). Although a recent hypothesis proposes that endoneurial blood flow is controlled by the action of autonomic nerve fibers associated with epineurial arterioles (2), our recent studies (3) show that in addition to epineurial arterioles other segments of the vasa nervorum are also innervated. In this study, we examine blood vessels of the endoneurium for possible innervation.


2008 ◽  
Vol 22 (2) ◽  
pp. 81-90 ◽  
Author(s):  
Natalie Werner ◽  
Neval Kapan ◽  
Gustavo A. Reyes del Paso

The present study explored modulations in cerebral blood flow and systemic hemodynamics during the execution of a mental calculation task in 41 healthy subjects. Time course and lateralization of blood flow velocities in the medial cerebral arteries of both hemispheres were assessed using functional transcranial Doppler sonography. Indices of systemic hemodynamics were obtained using continuous blood pressure recordings. Doppler sonography revealed a biphasic left dominant rise in cerebral blood flow velocities during task execution. Systemic blood pressure increased, whereas heart period, heart period variability, and baroreflex sensitivity declined. Blood pressure and heart period proved predictive of the magnitude of the cerebral blood flow response, particularly of its initial component. Various physiological mechanisms may be assumed to be involved in cardiovascular adjustment to cognitive demands. While specific contributions of the sympathetic and parasympathetic systems may account for the observed pattern of systemic hemodynamics, flow metabolism coupling, fast neurogenic vasodilation, and cerebral autoregulation may be involved in mediating cerebral blood flow modulations. Furthermore, during conditions of high cardiovascular reactivity, systemic hemodynamic changes exert a marked influence on cerebral blood perfusion.


1996 ◽  
Vol 81 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. L. Naylor ◽  
Z. I. Pozeg ◽  
R. L. Hughson

Shoemaker, J. K., H. L. Naylor, Z. I. Pozeg, and R. L. Hughson. Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans. J. Appl. Physiol. 81(4): 1516–1521, 1996.—The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter ( D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (γ˙ = 8 ⋅ MBV/ D), and forearm blood flow (FBF = MBV ⋅ π r 2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (∼10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and γ˙ was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 ± 3 beats/min) compared with placebo (57 ± 3 beats/min) ( P < 0.05) without change to MPP. With placebo, D increased in both arm positions from ∼4.3 mm at rest to ∼4.5 mm at 5 min of exercise ( P < 0.05). This response was not altered with Ibu ( P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow ( P > 0.05) in either arm position. The γ˙ was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise ( P < 0.05). Because PG inhibition altered the time course ofγ˙ at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.


Physiology ◽  
2009 ◽  
Vol 24 (1) ◽  
pp. 58-71 ◽  
Author(s):  
George Osol ◽  
Maurizio Mandala

Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodeling of the entire uterine circulation, as well as the creation of a new fetal vascular organ: the placenta. The process of remodeling involves a number of cellular processes, including hyperplasia and hypertrophy, rearrangement of existing elements, and changes in extracellular matrix. In this review, we provide information on uterine blood flow increases during pregnancy, the influence of placentation type on the distribution of uterine vascular resistance, consideration of the patterns, nature, and extent of maternal uterine vascular remodeling during pregnancy, and what is known about the underlying cellular mechanisms.


2016 ◽  
Vol 214 (7) ◽  
pp. 793-795 ◽  
Author(s):  
Claudio A. Franco ◽  
Holger Gerhardt

Bone morphogenic proteins (BMPs) and blood flow regulate vascular remodeling and homeostasis. In this issue, Baeyens et al. (2016. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201603106) show that blood flow sensitizes endothelial cells to BMP9 signaling by triggering Alk1/ENG complexing to suppress cell proliferation and to recruit mural cells, thereby establishing endothelial quiescence.


1973 ◽  
Vol 95 (2) ◽  
pp. 250-256 ◽  
Author(s):  
T. E. Cooper ◽  
J. P. Groff

This paper discusses the use of heat for producing clinical lesions in tissue and presents the design and analysis of a resistively heated surgical probe. The probe surface temperature is accurately maintained and controlled by using a Wheatstone bridge. The probe was embedded in a clear agar–water test medium, and the temperature field generated by the probe was measured with liquid crystals, a material that provides a visual display of certain isotherms. Experimental results compare within approximately 10 percent of a two-dimensional numerical solution. A one-dimensional theoretical model is also developed which examines the influence of blood flow on the temperature field.


2005 ◽  
Vol 99 (4) ◽  
pp. 1462-1470 ◽  
Author(s):  
Nicole D. Paterson ◽  
John M. Kowalchuk ◽  
Donald H. Paterson

The effects of prior heavy-intensity exercise on O2 uptake (V̇o2) kinetics of a second heavy exercise may be due to vasodilation (associated with metabolic acidosis) and improved muscle blood flow. This study examined the effect of prior heavy-intensity exercise on femoral artery blood flow (Qleg) and its relationship with V̇o2 kinetics. Five young subjects completed five to eight repeats of two 6-min bouts of heavy-intensity one-legged, knee-extension exercise separated by 6 min of loadless exercise. V̇o2 was measured breath by breath. Pulsed-wave Doppler ultrasound was used to measure Qleg. V̇o2 and blood flow velocity data were fit using a monoexponential model to identify phase II and phase III time periods and estimate the response amplitudes and time constants (τ). Phase II V̇o2 kinetics was speeded on the second heavy-intensity exercise [mean τ (SD), 29 ( 10 ) s to 24 ( 10 ) s, P < 0.05] with no change in the phase II (or phase III) amplitude. Qleg was elevated before the second exercise [1.55 (0.34) l/min to 1.90 (0.25) l/min, P < 0.05], but the amplitude and time course [τ, 25 ( 13 ) s to 35 ( 13 ) s] were not changed, such that throughout the transient the Qleg (and ΔQleg/ΔV̇o2) did not differ from the prior heavy exercise. Thus V̇o2 kinetics were accelerated on the second exercise, but the faster kinetics were not associated with changes in Qleg. Thus limb blood flow appears not to limit V̇o2 kinetics during single-leg heavy-intensity exercise nor to be the mechanism of the altered V̇o2 response after heavy-intensity prior exercise.


1986 ◽  
Vol 61 (2) ◽  
pp. 592-598 ◽  
Author(s):  
C. E. Riva ◽  
C. J. Pournaras ◽  
M. Tsacopoulos

A study has been undertaken to determine whether local changes in PO2 could be a factor in the regulation of retinal blood flow during 100% O2 breathing. For this purpose we have measured simultaneously in eyes of anesthetized and artificially ventilated miniature pigs the change in local preretinal PO2 and retinal blood flow using O2-sensitive microelectrodes and laser Doppler velocimetry. Although preretinal intervascular PO2 changed little, periarteriolar PO2 increased markedly during 100% O2 breathing. When measured less than 50 microns from the arteriolar wall, the time course of this increase preceded that of the decrease in retinal blood flow. The results indicate that O2 diffusing through the wall of the large retinal arterioles represents the most important component of periarteriolar PO2. This diffusion coupled with the decrease in retinal blood flow could play a major role in the regulation of inner retinal PO2. The data also suggest that diffusional shunting of O2 between retinal arterioles and veins could explain the unexpected increase in venous O2 saturation during 100% O2 breathing that has been previously reported by others. The finding that retinal periarteriolar PO2 is always higher than the PO2 in the outer retina does not support the previously formulated hypothesis that O2 from the choroid is responsible for the constriction of the arterioles during hyperoxia.


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