scholarly journals Blood flow reprograms lymphatic vessels to blood vessels

2012 ◽  
Vol 122 (7) ◽  
pp. 2702-2702
Author(s):  
Chiu-Yu Chen ◽  
Cara Bertozzi ◽  
Zhiying Zou ◽  
Lijun Yuan ◽  
John S. Lee ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Lymphatic Vessels

scholarly journals Blood flow reprograms lymphatic vessels to blood vessels

2012 ◽  
Vol 122 (6) ◽  
pp. 2006-2017 ◽  
Author(s):  
Chiu-Yu Chen ◽  
Cara Bertozzi ◽  
Zhiying Zou ◽  
Lijun Yuan ◽  
John S. Lee ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Lymphatic Vessels

scholarly journals Causes, consequences, and remedies for growth-induced solid stress in murine and human tumors

2012 ◽  
Vol 109 (38) ◽  
pp. 15101-15108 ◽  
Author(s):  
Triantafyllos Stylianopoulos ◽  
John D. Martin ◽  
Vikash P. Chauhan ◽  
Saloni R. Jain ◽  
Benjamin Diop-Frimpong ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Sonic Hedgehog ◽  
Simple Technique ◽  
Fluid Pressure ◽  
Lymphatic Vessels ◽  
Human Tumors ◽  
Tumor Perfusion ◽  
Solid Stress ◽  
Carcinoma Associated Fibroblasts

The presence of growth-induced solid stresses in tumors has been suspected for some time, but these stresses were largely estimated using mathematical models. Solid stresses can deform the surrounding tissues and compress intratumoral lymphatic and blood vessels. Compression of lymphatic vessels elevates interstitial fluid pressure, whereas compression of blood vessels reduces blood flow. Reduced blood flow, in turn, leads to hypoxia, which promotes tumor progression, immunosuppression, inflammation, invasion, and metastasis and lowers the efficacy of chemo-, radio-, and immunotherapies. Thus, strategies designed to alleviate solid stress have the potential to improve cancer treatment. However, a lack of methods for measuring solid stress has hindered the development of solid stress-alleviating drugs. Here, we present a simple technique to estimate the growth-induced solid stress accumulated within animal and human tumors, and we show that this stress can be reduced by depleting cancer cells, fibroblasts, collagen, and/or hyaluronan, resulting in improved tumor perfusion. Furthermore, we show that therapeutic depletion of carcinoma-associated fibroblasts with an inhibitor of the sonic hedgehog pathway reduces solid stress, decompresses blood and lymphatic vessels, and increases perfusion. In addition to providing insights into the mechanopathology of tumors, our approach can serve as a rapid screen for stress-reducing and perfusion-enhancing drugs.

Innervation of endoneurial microvessels in human sural nerve

1992 ◽  
Vol 50 (1) ◽  
pp. 920-921
Author(s):  
John L. Beggs ◽  
Peter C. Johnson ◽  
Astrid G. Olafsen ◽  
C. Jane Watkins
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Blood Supply ◽  
Peripheral Nerves ◽  
Sural Nerve ◽  
Nerve Fibers ◽  
Arterial Supply ◽  
Autonomic Nerve ◽  
Vasa Nervorum ◽  
Endoneurial Blood Flow

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.

COMPARISON OF ANTIHYPERTENSIVE EFFECT OF MOXONIDINE VERSUS CLONIDINE IN RENAL FAILURE PATIENTS.

2018 ◽  
Vol 6 (9) ◽  
Author(s):  
DR.MATHEW GEORGE ◽  
DR.LINCY JOSEPH ◽  
MRS.DEEPTHI MATHEW ◽  
ALISHA MARIA SHAJI ◽  
BIJI JOSEPH ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Blood Flow ◽  
Blood Vessel ◽  
Blood Vessels ◽  
High Blood Pressure ◽  
Antihypertensive Effect ◽  
The Body ◽  
Ability To Work ◽  
Blood Flows

Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body. Factors that can increase this force include higher blood volume due to extra fluid in the blood and blood vessels that are narrow, stiff, or clogged(1). High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.

Microfluidics of blood in blood vessels stenosis

2016 ◽  
Vol 11 (2) ◽  
pp. 210-217 ◽  
Author(s):  
A.T. Akhmetov ◽  
A.A. Valiev ◽  
A.A. Rakhimov ◽  
S.P. Sametov ◽  
R.R. Habibullina
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Hydraulic Resistance ◽  
Microfluidic Device ◽  
Human Body ◽  
Vascular System ◽  
Hydrodynamic Conditions ◽  
Microstructure Change ◽  
Healthy Part

It is mentioned in the paper that hydrodynamic conditions of a flow in blood vessels with the stenosis are abnormal in relation to the total hemodynamic conditions of blood flow in a vascular system of a human body. A microfluidic device developed with a stepped narrowing for studying of the blood flow at abnormal conditions allowed to reveal blood structure in microchannels simulating the stenosis. Microstructure change is observed during the flow of both native and diluted blood through the narrowing. The study of hemorheological properties allowed us to determine an increasing contribution of the hydraulic resistance of the healthy part of the vessel during the stenosis formation.

scholarly journals Age-Dependent Dysregulation of Muscle Vasculature and Blood Flow Recovery after Hindlimb Ischemia in the mdx Model of Duchenne Muscular Dystrophy

Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 481
Author(s):  
Paulina Podkalicka ◽  
Olga Mucha ◽  
Katarzyna Kaziród ◽  
Iwona Bronisz-Budzyńska ◽  
Sophie Ostrowska-Paton ◽  
...  
Keyword(s):  
Blood Flow ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Blood Vessels ◽  
Mdx Mice ◽  
Hindlimb Ischemia ◽  
Double Positive ◽  
Functional Studies ◽  
Age Dependent ◽  
Dystrophic Mice

Duchenne muscular dystrophy (DMD), caused by a lack of functional dystrophin, is characterized by progressive muscle degeneration. Interestingly, dystrophin is also expressed in endothelial cells (ECs), and insufficient angiogenesis has already been hypothesized to contribute to DMD pathology, however, its status in mdx mice, a model of DMD, is still not fully clear. Our study aimed to reveal angiogenesis-related alterations in skeletal muscles of mdx mice compared to wild-type (WT) counterparts. By investigating 6- and 12-week-old mice, we sought to verify if those changes are age-dependent. We utilized a broad spectrum of methods ranging from gene expression analysis, flow cytometry, and immunofluorescence imaging to determine the level of angiogenic markers and to assess muscle blood vessel abundance. Finally, we implemented the hindlimb ischemia (HLI) model, more biologically relevant in the context of functional studies evaluating angiogenesis/arteriogenesis processes. We demonstrated that both 6- and 12-week-old dystrophic mice exhibited dysregulation of several angiogenic factors, including decreased vascular endothelial growth factor A (VEGF) in different muscle types. Nonetheless, in younger, 6-week-old mdx animals, neither the abundance of CD31+α-SMA+ double-positive blood vessels nor basal blood flow and its restoration after HLI was affected. In 12-week-old mdx mice, although a higher number of CD31+α-SMA+ double-positive blood vessels and an increased percentage of skeletal muscle ECs were found, the abundance of pericytes was diminished, and blood flow was reduced. Moreover, impeded perfusion recovery after HLI associated with a blunted inflammatory and regenerative response was evident in 12-week-old dystrophic mice. Hence, our results reinforce the hypothesis of age-dependent angiogenic dysfunction in dystrophic mice. In conclusion, we suggest that older mdx mice constitute an appropriate model for preclinical studies evaluating the effectiveness of vascular-based therapies aimed at the restoration of functional angiogenesis to mitigate DMD severity.

scholarly journals Innervation of the pancreas by substance P, enkephalin, vasoactive intestinal polypeptide and gastrin/CCK immunoractive nerves.

1979 ◽  
Vol 27 (9) ◽  
pp. 1283-1284 ◽  
Author(s):  
L I Larsson
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Substance P ◽  
Blood Vessels ◽  
Vasoactive Intestinal Polypeptide ◽  
Pancreatic Blood Flow ◽  
Major Site ◽  
Site Of Action ◽  
Immunocytochemical Studies ◽  
Intestinal Polypeptide

Immunocytochemical studies habe shown that many peptides which profoundly affect the endocrine and exocrine functions of the pancreas are localized to neurons. In the cat, such peptidergic nerves appear to innervate ganglia, islets and blood vessels of the pancreas, whereas their contributions to exocrine cells are minor. Our studies suggest that pancreatic ganglia represent one major site of action of the peptides and that, in addition, nerves containing the vasoactive intestinal polypeptide and gastrin/CCK-related peptides profoundly affect pancreatic blood flow and insulin secretion, respectively.

scholarly journals Enhanced Nitrite-Mediated Relaxation of Placental Blood Vessels Exposed to Hypoxia Is Preserved in Pregnancies Complicated by Fetal Growth Restriction

2021 ◽  
Vol 22 (9) ◽  
pp. 4500
Author(s):  
Teresa Tropea ◽  
Carina Nihlen ◽  
Eddie Weitzberg ◽  
Jon O. Lundberg ◽  
Mark Wareing ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Plasma Concentrations ◽  
Growth Restriction ◽  
Alternative Source ◽  
Fetal Plasma ◽  
Placental Blood ◽  
Nitrate And Nitrite

Nitric oxide (NO) is essential in the control of fetoplacental vascular tone, maintaining a high flow−low resistance circulation that favors oxygen and nutrient delivery to the fetus. Reduced fetoplacental blood flow is associated with pregnancy complications and is one of the major causes of fetal growth restriction (FGR). The reduction of dietary nitrate to nitrite and subsequently NO may provide an alternative source of NO in vivo. We have previously shown that nitrite induces vasorelaxation in placental blood vessels from normal pregnancies, and that this effect is enhanced under conditions of hypoxia. Herein, we aimed to determine whether nitrite could also act as a vasodilator in FGR. Using wire myography, vasorelaxant effects of nitrite were assessed on pre-constricted chorionic plate arteries (CPAs) and veins (CPVs) from normal and FGR pregnancies under normoxic and hypoxic conditions. Responses to the NO donor, sodium nitroprusside (SNP), were assessed in parallel. Nitrate and nitrite concentrations were measured in fetal plasma. Hypoxia significantly enhanced vasorelaxation to nitrite in FGR CPAs (p < 0.001), and in both normal (p < 0.001) and FGR (p < 0.01) CPVs. Vasorelaxation to SNP was also potentiated by hypoxia in both normal (p < 0.0001) and FGR (p < 0.01) CPVs. However, compared to vessels from normal pregnancies, CPVs from FGR pregnancies showed significantly lower reactivity to SNP (p < 0.01). Fetal plasma concentrations of nitrate and nitrite were not different between normal and FGR pregnancies. Together, these data show that nitrite-mediated vasorelaxation is preserved in FGR, suggesting that interventions targeting this pathway have the potential to improve fetoplacental blood flow in FGR pregnancies.

Growth regulation of the vascular system: evidence for a metabolic hypothesis

1990 ◽  
Vol 259 (3) ◽  
pp. R393-R404 ◽  
Author(s):  
T. H. Adair ◽  
W. J. Gay ◽  
J. P. Montani
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Growth Regulation ◽  
Vascular System ◽  
Major Influence ◽  
Control Element ◽  
Hypoxic Conditions ◽  
Control Growth ◽  
Vessel Growth ◽  
Tissue Cells

Prolonged imbalances between the perfusion capabilities of the blood vessels and the metabolic requirements of the tissue cells often lead to modification of the vasculature to satisfy the tissue needs. This homeostatic response appears to be bidirectional, since the vascularity of a tissue can increase or decrease in parallel with primary changes in metabolic rate. The factors that mediate the responses are not well understood, but oxygen has been implicated as a major control element, since vessel growth increases during hypoxic conditions and decreases during hyperoxic conditions. The following feedback control hypothesis may apply to many different physiological situations. Decreased oxygenation causes the tissues to become hypoxic, and this initiates a variety of signals that lead to the growth of blood vessels. The increase in vascularity promotes oxygen delivery to the tissue cells by decreasing diffusion distances, increasing capillary surface area, and increasing the maximum rate of blood flow. When the tissues receive adequate amounts of oxygen even during periods of peak activity, the intermediate effectors return to normal levels, and this negative signal, in turn, stops the further development of the vasculature. Although the effector mechanisms of the hypoxic stimulus are still being investigated, adenosine, which is produced in hypoxic tissues, appears to mediate hypoxia-induced increases in vascularity in some instances. Roles for fibroblast growth factor as well as mechanical factors associated with vasodilation and increased blood flow are postulated. Although blood vessel growth is a multifactorial process, a major influence in its regulation appears to be metabolic need. If this view is correct, it may be found that many of the quantitatively significant factors that control growth in a given vasculature are themselves modulated or controlled by metabolic signals reflecting the nutritional status of the tissues which that vasculature supplies.

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