Blood flow through new microvessels: factors that affect regrowth of vasa vasorum

A segment of abdominal aorta in dogs was transplanted to its original position (high PO2) or to the femoral vein (low PO2), and a segment of thoracic aorta was transplanted to its original position. Two days after grafting to each location, there was no blood flow (measured with microspheres) through vasa vasorum. After 2 and 4 wk, blood flow through vasa was restored to normal, or above normal, levels in all grafts. Vasa in grafts did not have smooth muscle, and they were not responsive to adenosine. Medial necrosis occurred in grafts of thoracic aorta but not in grafts of abdominal aorta. There was cellular degeneration and medial atrophy in grafts of abdominal aorta to the femoral vein. We conclude that 1) revascularization of the aorta by vasa vasorum is rapid; 2) new vasa do not have smooth muscle, and they are not responsive to vasoactive stimuli; and 3) medial necrosis occurs in grafts in which delivery of oxygen to media is compromised, either by low luminal PO2 or by interruption of medial vasa (in thoracic aorta), but not when the abdominal aorta is excised and reanastomosed. Absence of medial necrosis in grafts of abdominal aorta indicates that diffusion from the lumen of the vessel is adequate to nourish the vessel. This finding provides evidence that adventitial vasa, in contrast to medial vasa, are not essential for nourishment of the vessel wall.

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Fatal Hemothorax Following Management of an Esophageal Foreign Body

Journal of the American Animal Hospital Association ◽

10.5326/0390251 ◽

2003 ◽

Vol 39 (3) ◽

pp. 251-256 ◽

Cited By ~ 14

Author(s):

Leah A. Cohn ◽

Melissa R. Stoll ◽

Keith R. Branson ◽

Alice D. Roudabush ◽

Marie E. Kerl ◽

...

Keyword(s):

Blood Flow ◽

Foreign Body ◽

Nutritional Support ◽

Gastrostomy Tube ◽

Vasa Vasorum ◽

Esophageal Foreign Body ◽

Endoscopic Retrieval ◽

Medial Necrosis ◽

Flow Through

A 10.8-year-old, spayed female toy poodle presented with an esophageal foreign body. The foreign body was removed endoscopically, and a gastrostomy tube was placed to provide nutritional support during esophageal healing. The gastrostomy tube was later removed by endoscopic retrieval of the bulb through the esophagus. Immediately afterward, the dog developed hemothorax and eventually died. It was determined that many small arterial branches were avulsed from the aorta. The involved sections of aorta histopathogically evidenced medial necrosis, which was believed to be related to a prior disruption of blood flow through the vasa vasorum.

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Microvascular dilation in response to occlusion: a coordinating role for conducted vasomotor responses

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.1.h279 ◽

2000 ◽

Vol 279 (1) ◽

pp. H279-H284 ◽

Cited By ~ 11

Author(s):

Kim A. Dora ◽

David N. Damon ◽

Brian R. Duling

Keyword(s):

Endothelial Cells ◽

Blood Flow ◽

Shear Stress ◽

Smooth Muscle ◽

Third Order ◽

Vasomotor Responses ◽

Vasodilatory Response ◽

Flow Through ◽

Stress Dependent ◽

Dependent Mechanism

In rat cremasteric microcirculation, mechanical occlusion of one branch of an arteriolar bifurcation causes an increase in flow and vasodilation of the unoccluded daughter branch. This dilation has been attributed to the operation of a shear stress-dependent mechanism in the microcirculation. Instead of or in addition to this, we hypothesized that the dilation observed during occlusion is the result of a conducted signal originating distal to the occlusion. To test this hypothesis, we blocked the ascending spread of conducted vasomotor responses by damaging the smooth muscle and endothelial cells in a 200-μm segment of second- or third-order arterioles. We found that a conduction blockade eliminated or diminished the occlusion-associated increase in flow through the unoccluded branch and abolished or strongly attenuated the vasodilatory response in both vessels at the branch. We also noted that vasodilations induced by ACh (10−4 M, 0.6 s) spread to, but not beyond, the area of damage. Taken together, these data provide strong evidence that conducted vasomotor responses have an important role in coordinating blood flow in response to an arteriolar occlusion.

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Cell Death–associated ADAMTS4 and Versican Degradation in Vascular Tissue

Journal of Histochemistry & Cytochemistry ◽

10.1369/jhc.2009.953901 ◽

2009 ◽

Vol 57 (9) ◽

pp. 889-897 ◽

Cited By ~ 26

Author(s):

Richard D. Kenagy ◽

Seung-Kee Min ◽

Alexander W. Clowes ◽

John D. Sandy

Keyword(s):

Blood Flow ◽

Cell Death ◽

Smooth Muscle ◽

Smooth Muscle Cell ◽

Fas Ligand ◽

Vascular Tissue ◽

Transcript Abundance ◽

High Flow ◽

The Other ◽

Flow Through

High blood flow through baboon polytetrafluorethylene aorto-iliac grafts increases neointimal vascular smooth muscle cell (SMC) death, neointimal atrophy, and cleavage of versican to generate the DPEAAE neoepitope, a marker of ADAMTS-mediated proteolysis. In this study, we have determined the effect of high blood flow on transcript abundance in the neointima for ADAMTS1, −4, −5, −8, −9, −15, and −20. We found that after 24 hr of flow, the mRNA for ADAMTS4 was significantly increased, whereas that for the other family members was unchanged. Because vascular SMC death is markedly increased in the graft after 24 hr of high flow, we next examined the possibility that the ADAMTS4 induction and the cell death are causally related. The addition of Fas ligand to SMC cultures increased both ADAMTS4 mRNA and cell death ∼5-fold, consistent with the idea that ADAMTS4-dependent cleavage of versican may be partly responsible for cell death and tissue atrophy under these conditions.

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3D Simulation Of Blood Flow Through New Designed Stent Graft In Abdominal Aorta

Atherosclerosis ◽

10.1016/j.atherosclerosis.2019.06.482 ◽

2019 ◽

Vol 287 ◽

pp. e160

Author(s):

N. Begic ◽

A. Botonjic Karahusic ◽

T. Kostic

Keyword(s):

Blood Flow ◽

Stent Graft ◽

Abdominal Aorta ◽

3D Simulation ◽

Flow Through

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Blood flow through vasa vasorum in arteries and veins: effects of luminal PO2

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1986.250.3.h434 ◽

1986 ◽

Vol 250 (3) ◽

pp. H434-H442 ◽

Cited By ~ 8

Author(s):

D. D. Heistad ◽

M. L. Armstrong ◽

S. Amundsen

Keyword(s):

Blood Flow ◽

Inferior Vena Cava ◽

Inferior Vena ◽

Superior Vena ◽

Acute Hypoxia ◽

Vena Cava ◽

Vasa Vasorum ◽

Aortic Media ◽

Flow Through ◽

Arteries And Veins

We have examined effects of chronic reduction of intraluminal PO2 on blood flow through vasa vasorum, by comparing large arteries and veins, and effects of acute hypoxia on flow through vasa. Microspheres were used to measure flow in anesthetized dogs. Values obtained with different sizes of microspheres suggest that spheres 9 and 15 micron in diam, but not 50 micron, are appropriate for measurement of blood flow through vasa vasorum. Flow [expressed as ml X min-1 X 100 g-1 (SE)] through medial vasa was similar in the aorta (9.0 +/- 2.1) and pulmonary artery (9.3 +/- 1.1) although, on the basis of wall thickness and number of lamellae, one would predict much higher levels of flow to aortic media. Two veins that we studied have a thick muscular wall. Both veins had high levels of flow through medial vasa: 33 +/- 4.4 to the subdiaphragmatic inferior vena cava and 18 +/- 5.4 to the portal vein. Two other veins are apparently conduit vessels, with dense connective tissue and minimal smooth muscle. Both veins had minimal flow through medial vasa: 2.4 +/- 1.0 to superior vena cava, and 1.9 +/- 0.8 to supradiaphragmatic inferior vena cava. Thus, because flow through vasa differs greatly in different veins, structure of the vessel (as well as intraluminal PO2) is an important determinant of flow through vasa. Acute hypoxia increased conductance of medial vasa vasorum of arteries and veins when neurohumoral constrictor effects were blocked by phenoxybenzamine.(ABSTRACT TRUNCATED AT 250 WORDS)

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Influence of serum cholesterol on atherogenesis and intimal hyperplasia after angioplasty: inhibition by amlodipine

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00617.2004 ◽

2005 ◽

Vol 288 (2) ◽

pp. H591-H600 ◽

Cited By ~ 9

Author(s):

Mark B. Kahn ◽

Kathleen Boesze-Battaglia ◽

David W. Stepp ◽

Artium Petrov ◽

Yong Huang ◽

...

Keyword(s):

Smooth Muscle ◽

Thoracic Aorta ◽

Abdominal Aorta ◽

Collagen Synthesis ◽

Balloon Dilation ◽

Fold Increase ◽

Lesion Size ◽

Normal Diet ◽

Membrane Bilayer ◽

Cellular Processes

The objectives of the present study were to determine whether serum hypercholesterolemia (HC) promotes the development of spontaneous and angioplasty-induced lesions and whether amlodipine inhibits these lesions and cellular processes underlying their genesis. Rabbits were fed normal, 0.5%, or 2% cholesterol diets for 9 wk, which resulted in the development of increasing HC. After week one, balloon dilation of the abdominal aorta was performed while the thoracic aorta was not disturbed and monitored for the development of spontaneous lesions. Lesion size increased with the degree of HC and was accompanied by increased collagen synthesis and smooth muscle cell (SMC) proliferation at each site. Amlodipine (5 mg/kg po) inhibited lesion size by 50% ( P < 0.01) at both sites in cholesterol-fed animals but not at angioplasty sites in animals on a normal diet. Local collagen synthesis was inhibited at both sites by amlodipine in the diet animals. The increase in HC was accompanied by a 1.7-fold increase in basal Ca2+ uptake in SMCs in the thoracic aorta, which was not altered by amlodipine, nifedipine, Ni2+, or La3+, revealing an uninhibitable calcium leak during atherogenesis. In culture, cholesterol enrichment increased SMC proliferation, collagen synthesis, and the secretion of a soluble SMC mitogen, which were inhibited by amlodipine (10−9 M). Finally, in SMC membranes, amlodipine uniquely restored the cholesterol-expanded membrane bilayer width without any effect on membrane fluidity. This study establishes a causal role between serum HC and the development of spontaneous and angioplasty-induced lesions and the ability of amlodipine to disrupt this action by a novel remodelling action on the SMC membrane.

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Increase of cerebral blood flow produced by low dosages of cyanide

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.204.2.309 ◽

1963 ◽

Vol 204 (2) ◽

pp. 309-313 ◽

Cited By ~ 10

Author(s):

Mauricio Russek ◽

Adolfo Fernandez F. ◽

Cordelia Vega

Keyword(s):

Blood Flow ◽

Hind Limb ◽

Jugular Vein ◽

Great Increase ◽

Femoral Vein ◽

Sagittal Sinus ◽

Flow Through ◽

Significant Change ◽

The Brain ◽

Oxygen Difference

In cats and rabbits lightly anesthetized with pentobarbital or immobilized with Flaxedil and in encéphale isolé cats, the intravenous injection of NaCN in doses of 0.05 to 0.5 mg/kg produced a great increase in blood flow from the head (jugular vein) without any significant change in the blood flow from a hind limb (femoral vein). This would indicate that the increase in blood flow from the head was probably due to the brain and not to the nonnervous structures. This assumption was further supported by the large increase in the blood flow through the sagittal sinus. The greatest increase in jugular flow, threefold, was produced by 0.2–0.3 mg/kg of cyanide. This dose did not produce any significant change in the arterial, jugular, and femoral vein oxygen concentration, and hence in the A-V oxygen difference of head and limb. The results would indicate that the consumption of the brain is augmented by these dosages of cyanide.

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A Novel Model of Tobacco Smoke–Mediated Aortic Injury

Vascular and Endovascular Surgery ◽

10.1177/15385744211063054 ◽

2021 ◽

pp. 153857442110630

Author(s):

Amir F. Azarbal ◽

Tana Repella ◽

Eric Carlson ◽

Elise C. Manalo ◽

Braden Palanuk ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Thoracic Aorta ◽

Abdominal Aorta ◽

Tobacco Smoke ◽

Inflammatory Cells ◽

Smoke Exposure ◽

Tobacco Smoke Exposure ◽

Osmotic Minipumps ◽

Thoracic And Abdominal

Objective Tobacco smoke exposure is a major risk factor for aortic aneurysm development. However, the initial aortic response to tobacco smoke, preceding aneurysm formation, is not well understood. We sought to create a model to determine the effect of solubilized tobacco smoke (STS) on the thoracic and abdominal aorta of mice as well as on cultured human aortic smooth muscle cells (HASMCs). Methods Tobacco smoke was solubilized and delivered to mice via implanted osmotic minipumps. Twenty male C57BL/6 mice received STS or vehicle infusion. The descending thoracic, suprarenal abdominal, and infrarenal abdominal segments of the aorta were assessed for elastic lamellar damage, smooth muscle cell phenotype, and infiltration of inflammatory cells. Cultured HASMCs grown in media containing STS were compared to cells grown in standard media in order to verify our in vivo findings. Results Tobacco smoke solution caused significantly more breaks in the elastic lamellae of the thoracic and abdominal aorta compared to control solution ( P< .0001) without inciting an inflammatory infiltrate. Elastin breaks occurred more frequently in the abdominal aorta than the thoracic aorta ( P < .01). Exposure to STS-induced aortic microdissections and downregulation of α-smooth muscle actin (α-SMA) by vascular smooth muscle cells (VSMCs). Treatment of cultured HASMCs with STS confirmed the decrease in α-SMA expression. Conclusion Delivery of STS via osmotic minipumps appears to be a promising model for investigating the early aortic response to tobacco smoke exposure. The initial effect of tobacco smoke exposure on the aorta is elastic lamellar damage and downregulation of (α-SMA) expression by VSMCs. Elastic lamellar damage occurs more frequently in the abdominal aorta than the thoracic aorta and does not seem to be mediated by the presence of macrophages or other inflammatory cells.

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