scholarly journals THE GRADIENT OF PERMEABILITY OF THE SKIN VESSELS AS INFLUENCED BY HEAT, COLD, AND LIGHT

1932 ◽  
Vol 55 (3) ◽  
pp. 431-439 ◽  
Author(s):  
Stephen Hudack ◽  
Philip D. McMaster
Keyword(s):  
Vascular Permeability ◽  
Vessel Wall ◽  
Functional Changes ◽  
Small Vessels ◽  
Vascular Walls ◽  
Gradient Of Permeability

The mounting gradient of permeability along the small vessels of the corium is essentially unaltered by active hyperemia produced by heat, cold, or light. Only when the vascular walls are so damaged that rapid leakage ensues, as shown by the development of edema, does the permeability of the capillary web as a whole approximate that of the venules. It is plain that the normal gradient of vascular permeability depends upon the integrity of the vessel wall. The method of experiment described can be utilized for a study of the functional changes which result in the lesions due to burning and freezing.

scholarly journals On-site education of VEGF-recruited monocytes improves their performance as angiogenic and arteriogenic accessory cells

2013 ◽  
Vol 210 (12) ◽  
pp. 2611-2625 ◽  
Author(s):  
Inbal Avraham-Davidi ◽  
Simon Yona ◽  
Myriam Grunewald ◽  
Limor Landsman ◽  
Clement Cochain ◽  
...  
Keyword(s):  
Underlying Mechanism ◽  
Target Organ ◽  
Functional Changes ◽  
Small Vessels ◽  
Accessory Cells ◽  
Improved Performance

Adult neovascularization relies on the recruitment of monocytes to the target organ or tumor and functioning therein as a paracrine accessory. The exact origins of the recruited monocytes and the mechanisms underlying their plasticity remain unclear. Using a VEGF-based transgenic system in which genetically tagged monocytes are conditionally summoned to the liver as part of a VEGF-initiated angiogenic program, we show that these recruited cells are derived from the abundant pool of circulating Ly6Chi monocytes. Remarkably, however, upon arrival at the VEGF-induced organ, but not the naive organ, monocytes undergo multiple phenotypic and functional changes, endowing them with enhanced proangiogenic capabilities and, importantly, with a markedly increased capacity to remodel existing small vessels into larger conduits. Notably, monocytes do not differentiate into long-lived macrophages, but rather appear as transient accessory cells. Results from transfers of presorted subpopulations and a novel tandem transfer strategy ruled out selective recruitment of a dedicated preexisting subpopulation or onsite selection, thereby reinforcing active reprogramming as the underlying mechanism for improved performance. Collectively, this study uncovered a novel function of VEGF, namely, on-site education of recruited “standard” monocytes to become angiogenic and arteriogenic professional cells, a finding that may also lend itself for a better design of angiogenic therapies.

Flow Driven Self-Assembly of Von Willebrand Factor Strands and Cables in Synthetic Blood Vessels

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 261-261
Author(s):  
Junmei Chen ◽  
Ying Zheng ◽  
Jose A. Lopez
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels ◽  
Von Willebrand Factor ◽  
Thrombotic Microangiopathy ◽  
Cleavage Site ◽  
Vessel Wall ◽  
Small Vessels ◽  
Microvascular Thrombosis ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Abstract 261 Endothelial activation and microvascular thrombosis are hallmarks of thrombotic microangiopathy—a group of life-threatening disorders that includes thrombotic thrombocytopenic purpura and hemolytic uremic syndrome. Activated endothelial cells release von Willebrand factor (VWF), which can form long strands under flow that remain attached to the endothelium until they are cleaved off by the metalloprotease ADAMTS13. Failure to remove these strands, either because of ADAMTS13 deficiency or oxidation of its cleavage site on VWF, results in microvascular thrombosis. Until now, studies of VWF strands under flow have been performed either in flow chambers with cultured endothelial cells, which does not account for either vessel caliber or geometry, or in live mice, in which it is impossible to study individually the contributions of the various blood components. Recently, we developed a technique to engineer microvessels in vitro that enables us to precisely control several vessel parameters, including lumen diameter and branching architecture, flow patterns, and applied shear stresses, in addition to being able to test individual components of the blood in a system with only human components (PNAS 2012, 109:9342–9347). In the current study, we used this system to examine the effects of a number of variables on the formation of VWF strands from the endothelium of stimulated vessels. We found that VWF fibers can extend across the vessel lumen and attach to opposite sides of the vessel wall in agonist-treated microvessels of up to 200 μm in diameter. Depending on flow conditions, smaller strands can self-associate to form longer and thicker cables. The VWF cables produced solely from VWF contributed by the vessel wall reached lengths up to 5 cm, and became so thick as to be visible, unstained, by light microscopy. When plasma or recombinant VWF was perfused over the VWF cables, the fluid-phase VWF associated with the vessel-bound cables, further thickening them and sometimes inducing web-like structures. The location and structure of the VWF fibers were dependent on vessel geometry and flow pattern; secondary flows that developed at bends or bifurcations in the vessel induced circular clumping of the VWF strands. When whole blood was perfused into the vessels, the transluminal VWF fiber webs caught flowing platelets and leukocytes to form aggregates in the middle of blood stream that sometimes occluded the vessels. The region where the vessel is most likely to occlude also depends on geometry. After this type of trapping, leukocytes were seen to transmigrate across the endothelium. The structure and size of the cables also depended on the agonist employed to stimulate VWF release from the endothelium. Phorbol myristate acetate and shiga-like toxin–2 both produced thicker cables than histamine did, and these were more resistant to ADAMTS13 cleavage. This difference is potentially a result of the former agonists stimulating an endothelial respiratory burst and oxidation of the ADAMTS13 cleavage site on VWF. In summary, our data show that VWF secreted from activated endothelial cells can form transluminal fibers and cables in small vessels. Some of the fibers or cables are resistant to ADAMTS13 cleavage, a likely consequence of their thickness and possibly, oxidation. The webs of VWF fibers or cables in the lumen of small vessels obstruct blood flow by binding to circulating platelets and leukocytes, and are also capable of shredding erythrocytes as they flow past. These findings provide insights into the mechanisms of microangiopathy, and raise the possibility that VWF cables alone, even in the absence of bound platelets, may be capable of occluding small blood vessels and produce many of the characteristic signs of thrombotic microangiopathy. Disclosures: No relevant conflicts of interest to declare.

scholarly journals THE GRADIENT OF VASCULAR PERMEABILITY

1931 ◽  
Vol 53 (2) ◽  
pp. 195-217 ◽  
Author(s):  
Frederick Smith ◽  
Peyton Rous
Keyword(s):  
Vascular Permeability ◽  
Skeletal Muscles ◽  
Capillary Permeability ◽  
Flight Muscle ◽  
Frog Muscle ◽  
The Other ◽  
Other Hand ◽  
Chicken Muscle ◽  
Gradient Of Permeability ◽  
Collecting System

A mounting gradient of permeability exists along the capillaries of frog muscle. In chicken muscle on the other hand none has been demonstrated; but the close-knit vascularization is arranged in duplicate in such manner that the blood runs in opposite directions through the capillaries of nearly adjacent fibres. In a flight muscle of the pigeon there exists in addition to this artifice what appears to be a special collecting system of venous capillaries. In the mammalian diaphragm indications of such a system are also to be found, and a gradient of capillary permeability like that in the other skeletal muscles is probably present. These vascular conditions are briefly considered in terms of function.

scholarly journals Vascular Inflammation in Lungs of Patients with Fatal Coronavirus Disease 2019 (COVID-19): Possible Role for the NLRP3 Inflammasome

2021 ◽  
Author(s):  
Oindrila Paul ◽  
Jian Qin Tao ◽  
Eric West ◽  
Leslie Litzky ◽  
Michael Feldman ◽  
...  
Keyword(s):  
Respiratory Disease ◽  
Nlrp3 Inflammasome ◽  
Lung Inflammation ◽  
Arterial Thrombosis ◽  
Vessel Wall ◽  
Structural Damage ◽  
Respiratory Diseases ◽  
Vascular Inflammation ◽  
Vascular Changes ◽  
Small Vessels

Abstract Background: Hyperinflammation is a key event that occurs with SARS-CoV-2 infection. In the lung, hyperinflammation leads to structural damage to tissue. To date, numerous lung histological studies have shown extensive alveolar damage, but there is scarce documentation of vascular inflammation in postmortem lung tissue. Methods: Lung sections from 8 COVID-19 affected and 11 non-COVID-19 subjects [of which 8 were acute respiratory disease syndrome (ARDS) affected and 3 were from subjects with non-respiratory diseases] were stained for H & E to ascertain histopathological features including presence of thrombi/microthrombi. Inflammation along the vessel wall was also monitored by quantification of the expression of moieties of the NLRP3 inflammasome pathway (NLRP3 and caspase-1). Results: In lungs from “fatal COVID-19”, vascular changes in the form of microthrombi in small vessels, arterial thrombosis, and organization were extensive as compared to lungs from “non-COVID-19 non respiratory disease” affected subjects. The NLRP3 pathway components were significantly higher in lungs from COVID-19 subjects as compared to non-COVID-19 fatal cases without respiratory disease. No significant differences were observed between COVID-19 lungs and non-COVID-19 ARDS lungs. Conclusion: We posit that inflammasome formation along the vessel wall is a characteristic of lung inflammation that accompanies COVID-19. Thus, the NLRP3 inflammasome pathway seems to be probable candidate that drives amplification of inflammation post SARS-CoV-2 infection.

scholarly journals THE GRADIENT OF VASCULAR PERMEABILITY

1931 ◽  
Vol 54 (4) ◽  
pp. 499-514 ◽  
Author(s):  
Frederick Smith ◽  
Peyton Rous
Keyword(s):  
Vascular Permeability ◽  
Human Skin ◽  
Gradient Of Permeability

The permeability of the venules of the skin of the mouse greatly exceeds that of the capillaries. A mounting gradient of permeability exists along the further portion of the latter. The significance of these facts is discussed with relation to conditions in human skin. The cutaneous venules are differentiated for several functions besides those ordinarily attributed to them, and must be considered as specialized organs.

Vorkommen von Laminosioptes cysticola in den Bauchorganen einer Pute

1970 ◽  
Vol 7 (4) ◽  
pp. 321-328 ◽  
Author(s):  
G. Kaliner
Keyword(s):  
Small Intestine ◽  
Histologic Examination ◽  
Small Vessels ◽  
Vascular Walls ◽  
Histologische Untersuchung ◽  
Liver And Kidney ◽  
Renal Vascular ◽  
Considerable Damage

Bei einer sechs Monate alten Pute wurde in der Leber, Niere, den Gefässuänden dieser Organe und in der Subserosa des Dünndarmes Laminosioptes cystitola gefunden, Die histologische Untersuchung ergab eine Perihepatitis, Perinephritis, eine Lokalisierte Entzündung von Leber und Niere und eine Hämosiderose in Leber. Niere und Milz. Eine Anzahl von kleineren Gefässen zeigten Hyalinablagerungen. Auf Grund der Befunde wird angenommen, dass L. cysticola den Wirtsorganismus erheblich stören kann. Mites ( Laminosioptes cyticola) were found in the liver, kidney, hepatic and renal vascular walls, and in the subserosa of the small intestine of a 6-month-old rurkey-hen. The histologic examination of the affected organs revealed a perihepatitis, perinephritis, focal inflammation of liver and kidney, and hemosiderosis of liver, kidney, and spleen. Several small vessels contained hyalin deposits. Based on these findings it is assumed that L. cysticola is capable of causing considerable damage to the tissues of the host.

scholarly journals THE GRADIENT OF VASCULAR PERMEABILITY

1930 ◽  
Vol 51 (5) ◽  
pp. 807-830 ◽  
Author(s):  
Peyton Rous ◽  
H. P. Gilding ◽  
Frederick Smith
Keyword(s):  
Blood Flow ◽  
Urinary Bladder ◽  
Vascular Permeability ◽  
Muscle Fibre ◽  
Skeletal Muscles ◽  
Individual Cell ◽  
Liver Lobule ◽  
Gradient Of Permeability ◽  
Functional States ◽  
The Individual

The permeability of the capillaries in the skeletal muscles of mammals increases progressively along their course and is greatest where they pass into the least venules. The gradient of permeability is so largely independent of functional states as to give grounds for the view that it is determined by inherent local differences. Through the gradient opportunity is equalized along the capillary. In the liver lobule this object is accomplished by an artifice of arrangement whereby the blood flow past the cells is increased with their distance from the source of supply. In the urinary bladder the interlacing of capillaries, their progressive widening, and a consequent gradual slowing of the blood flow act to achieve the same end. Here a gradient of permeability has not been demonstrable. Where cells of different sorts are served by a slender capillary, their differing requirements may render unnecessary any provision to equalize their opportunities; but where shortcomings in local maintenance will reduce the efficiency of an entire fabric, as the muscle fibre, and where cells of like character live competitively along the same channel, as in the liver, some arrangement must exist to ensure an even distribution of the services rendered by the blood. In situations of the kind last mentioned the immediate environment of the individual cell, the "milieu interne" of Bernard, is not only kept as constant as possible but it must be the same, by and large, for all of the cells. The task of serving voluntary muscle is not strictly limited to the capillaries. The intrafascicular arterioles and venules act so effectively to sustain the tissue about them that where they run no capillaries are supplied.

scholarly journals Dynamic Changes in Vascular Permeability, Cerebral Blood Volume, Vascular Density, and Size after Transient Focal Cerebral Ischemia in Rats: Evaluation with Contrast-Enhanced Magnetic Resonance Imaging

2008 ◽  
Vol 28 (8) ◽  
pp. 1491-1501 ◽  
Author(s):  
Chien-Yuan Lin ◽  
Chen Chang ◽  
Wai-Mui Cheung ◽  
Ming-Huang Lin ◽  
Jean-Ju Chen ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Focal Cerebral Ischemia ◽  
Late Phase ◽  
Vascular Density ◽  
Outer Cortex ◽  
Vessel Size ◽  
Small Vessels ◽  
Collateral Vessels

Postischemic cerebral blood flow and blood volume changes have been associated with angiogenesis; nevertheless, the spatiotemporal changes in vascular permeability, vascular density, and vessel size have not been investigated. Here we report a prolonged increase in vascular permeability from day 3 to day 21 after ischemia, in particular in the reperfused outer cortical layers and leptomeninges. Increased cerebral blood volume (CBV) was observed from day 3 to day 14, whereas increased blood volume in small vessels, primarily capillaries, was noticed from day 7 to day 14 in the reperfused cortex. An initial decrease in vascular density and a reciprocal increase in vessel size were observed within the reperfused cortex at days 1 and 3 after ischemia. Immunohistological analysis confirmed a similar decrease in microvessel density and an increase in vessel size in vessels with a diameter greater than 30 μm. These large-sized vessels exhibited intense basic fibroblast growth factor and endothelial nitric oxide synthase immunoreactivity, suggesting the growth of collateral vessels. By contrast, a late increase in vascular density was noticed in the reperfused outer cortex at days 14 and 21 after ischemia. Together, these findings suggest that the early phase of CBV increase is likely because of the improvement in collateral circulation, whereas the late phase of CBV increase is attributed to the surge of angiogenesis.

scholarly journals Ultrastructural Characterization of Corpus Cavernosum of Ageing, Orchidectomy and Diabetes Rat Experimental Models

2008 ◽  
Vol 14 (S3) ◽  
pp. 97-98 ◽  
Author(s):  
A.L. Cordeiro ◽  
A. Figueiredo ◽  
F. Godinho ◽  
I. Martins ◽  
P. Vendeira ◽  
...  
Keyword(s):  
Risk Factors ◽  
Smooth Muscle ◽  
Corpus Cavernosum ◽  
Experimental Models ◽  
Ultrastructural Organization ◽  
Structural Elements ◽  
Functional Changes ◽  
Small Vessels ◽  
Ultrastructural Characterization

Small vessels of the penis are very sensitive to structural and functional changes, and small disturbances can conduce to any degree of erectile dysfunction (ED). For this motive, ED is now considered as an early manifestation of atherosclerosis and consequently a precursor of systemic vascular disease. Ageing, diabetes and hipogonadic states are recognized risk factors for ED, contributing together to vascular damage of penile tissue. Penile trabeculae of corpus cavernosum in the rat, constituted by connective tissue with abundant collagen fibrils, scarce fibroblasts and fibroelastic components, support smooth muscle fibers in subendothelium location. Corpus cavernosum structural elements act in concert, allowing increase of intra-cavernous arterial flow and smooth muscle relaxing, processes which are fundamental to penis erection. The purpose of this study is to clarify ultrastructural organization of corpus cavernosum of experimental rat models of known ED-risk factors.

scholarly journals Comparative ultrastructural study of human corpus cavernosum during ageing

2008 ◽  
Vol 14 (S3) ◽  
pp. 152-155 ◽  
Author(s):  
N. Tomada ◽  
R. Oliveira ◽  
I. Tomada ◽  
P. Vendeira ◽  
D. Neves
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Corpus Cavernosum ◽  
Arterial System ◽  
Smooth Muscle Relaxation ◽  
Relaxation Processes ◽  
Functional Changes ◽  
Small Vessels ◽  
Aging Study ◽  
Cavernous Tissue

Erectile Dysfunction (ED), the inability to achieve or maintain an erection of sufficient rigidity for completion of sexual act, is a common condition affecting more than 150 million of men worldwide. This disorder is highly associated with aging, however concomitant pathologies such as hyperlipidemia, hypertension, and diabetes also contribute to ED progression. In the Massachusetts Male Aging Study, age was considered an independent variable strongly associated with ED, showing that the prevalence of this disease increased with age from 38% in the youngest group of men (mean age 40 y.) to almost 70% in the oldest group of men examined (mean age 70 y.). It is well demonstrated that aging leads to changes in the cardiovascular system, which results in a decrease in elasticity due to fibrosis and an increase in stiffness of the arterial system, independently of the effects of concurrent pathologies. Vasculogenic ED is the most prevalent condition, affecting nearly 80% of patients with organic etiology. Small vessels of the penis are very sensitive to structural and functional changes, and small disturbances can conduce to ED. ED is now considered by some authors as synonymous to endothelial dysfunction and an early manifestation of atherosclerosis, being a precursor of systemic vascular disease. Human cavernous tissue is mainly constituted by smooth muscle fibers that surround sinusoid vessels. Corpus cavernosum structural elements act in concert, allowing increase of intra-cavernous arterial flow and smooth muscle relaxation processes which are fundamental to penile erection. The aim of this study was to compare the ultrastructural anatomy of the young and aged human corpus cavernosum, in the absence of additional risk factors.

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