Effect of remodeled tumor-induced capillary network on interstitial flow in cancerous tissue

Author(s):  
M. Sefidgar ◽  
K. Raahemifar ◽  
H. Bazmara ◽  
M. Bazargan ◽  
S. M. Mousavi ◽  
...  

Author(s):  
M. Sefidgar ◽  
H. Bazmara ◽  
M. Mousavi ◽  
M. Bazargan ◽  
M. Soltani






Development ◽  
2007 ◽  
Vol 134 (20) ◽  
pp. 3743-3752 ◽  
Author(s):  
A. C. White ◽  
K. J. Lavine ◽  
D. M. Ornitz


2008 ◽  
Vol 295 (1) ◽  
pp. H174-H184 ◽  
Author(s):  
Katherine A. Radek ◽  
Elizabeth J. Kovacs ◽  
Richard L. Gallo ◽  
Luisa A. DiPietro

Physiological angiogenesis is regulated by various factors, including signaling through vascular endothelial growth factor (VEGF) receptors. We previously reported that a single dose of ethanol (1.4 g/kg), yielding a blood alcohol concentration of 100 mg/dl, significantly impairs angiogenesis in murine wounds, despite adequate levels of VEGF, suggesting direct effects of ethanol on endothelial cell signaling (40). To examine the mechanism by which ethanol influences angiogenesis in wounds, we employed two different in vitro angiogenesis assays to determine whether acute ethanol exposure (100 mg/dl) would have long-lasting effects on VEGF-induced capillary network formation. Ethanol exposure resulted in reduced VEGF-induced cord formation on collagen and reduced capillary network structure on Matrigel in vitro. In addition, ethanol exposure decreased expression of endothelial VEGF receptor-2, as well as VEGF receptor-2 phosphorylation in vitro. Inhibition of ethanol metabolism by 4-methylpyrazole partially abrogated the effect of ethanol on endothelial cell cord formation. However, mice treated with t-butanol, an alcohol not metabolized by alcohol dehydrogenase, exhibited no change in wound vascularity. These results suggest that products of ethanol metabolism are important factors in the development of ethanol-induced changes in endothelial cell responsiveness to VEGF. In vivo, ethanol exposure caused both decreased angiogenesis and increased hypoxia in wounds. Moreover, in vitro experiments demonstrated a direct effect of ethanol on the response to hypoxia in endothelial cells, as ethanol diminished nuclear hypoxia-inducible factor-1α protein levels. Together, the data establish that acute ethanol exposure significantly impairs angiogenesis and suggest that this effect is mediated by changes in endothelial cell responsiveness to both VEGF and hypoxia.



As is well known, the glomeruli of the frog’s kidney are supplied with blood only by the renal arteries, whereas the renal tubules have a double supply. On the one hand, they receive blood by way of the renal portal veins; on the other hand, the efferent vessels from the glomeruli open into the capillary network round the tubules. The whole of the tubule receives blood from each of these two sources, so that the capillary network around the tubules can be fully injected either from the renal arteries or from the renal portal veins. Taking advantage of this fact it has been shown by Beddard and one of us (F. A. B.) that after complete occlusion of the glomeruli the tubules, when adequately supplied with oxygen, maintain their normal histological appearance, and may secrete urine. In the present experiments an attempt has been made to determine the function of the glomerulus and to ascertain whether the tubules possess the capacity to absorb water and solids.



1959 ◽  
Vol 5 (1) ◽  
pp. 35-39 ◽  
Author(s):  
Maurice H. Bernstein ◽  
Daniel C. Pease

The fine structure of the tapetum of the cat eye has been investigated by electron microscopy. The tapetum is made up of modified choroidal cells, seen as polygonal plates grouped around penetrating blood vessels which terminate in the anastomosing capillary network of the choriocapillaris. The tapetal cells are rectangular in cross-section, set in regular brick-like rows, and attain a depth of some thirty-five cell layers in the central region. This number is gradually reduced peripherally, and is replaced at the margin of the tapetum by normal choroidal tissue. The individual cells are packed with long slender rods 0.1 µ by 4 to 5 µ. The rods are packed in groups and with their long axes oriented roughly parallel to the plane of the retinal surface. Each cell contains several such groups. Cells at the periphery or in the outer layers of the tapetum are frequently seen to contain both tapetal rods and melanin granules, the latter typical of the choroidal melanocytes. Also melanocyte granules may have intermediate shapes. These observations plus the similar density of the two inclusions lead to the belief that the tapetal rods may be melanin derivatives. A fibrous connective tissue layer lies between the tapetum and the retina. The subretinal capillary network, the choriocapillaris, rests on this layer and is covered by the basement membrane of the retinal epithelium. The cytoplasm of the retinal epithelium exhibits marked absorptive modifications where it comes in contact with the vessels of the choriocapillaris. This fibrous layer and the basement membrane of the retinal epithelium apparently comprise the structural elements of Bruch's membrane.



2000 ◽  
Vol 526 (2) ◽  
pp. 425-434 ◽  
Author(s):  
P. J. Coleman ◽  
D. Scott ◽  
R. M. Mason ◽  
J. R. Levick


2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Maria P McGee ◽  
Michael Morykwas ◽  
James Jordan ◽  
Louis Argenta

Interstitial edema is an early response to myocardial ischemia, leading to fibrosis and remodeling in several heart failure conditions. We aimed to clarify whether osmotic, frictional, or mechanical forces drive fluid accumulation. Equilibrium and dynamic interstitial hydration parameters were determined, compared, and analyzed using osmotic stress approaches in explants from ischemic and nonischemic myocardial regions of pig heart. They were isolated after injury induced by ligating 3-4 branches of the left anterior descending coronary artery, for 85 min followed by 3 hours’ reperfusion. Their volume changed (Δ V max ) linearly with colloidosmotic pressure in both ischemic and nonischemic areas, yielding interstitial compliance values of 1.04 ± 0.09 and 1.08 ± 0.05 µl/g/ mmHg , which do not differ significantly, and hydration potentials from the abscissa intercepts at Δ V max = 0, of -121.4 ± 28 and -14.7 ± 7.6 mmHg, which do (mean ± SE, n = 5 , P-value = 0.001). These hydration potential differences manifest ex-vivo influx rates 8.5 ± 2.7- fold slower in ischemic than nonischemic myocardium. Surprisingly, interstitial flow resistance values derived from net-flow rates at an imposed pressure difference of 216 mmHg were 0.23 ± 0.08 and 0.19 ± 0.01 µl -1 . g. min and did not differ significantly between the areas. The similarity in interstitial compliance and fluid resistance indicates that the more negative hydration potential and faster efflux rates in at-risk regions after reperfusion are due to increased hydrostatic pressure rather than decreased osmotic or frictional forces. Tissue distends due to interstitial fluid accumulation against matrix mechanical forces, including elastic recoil of the collagen elastin mesh and fibroblast action, consistent with impaired drainage and persistent diastolic-like conditions during reperfusion of at-risk areas in vivo . These results indicate changes in pressure gradient magnitude and may have clinical and therapeutic implications; for example, reversal of paracrine interstitial flows during early remodeling



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