scholarly journals Humoral regulation of blood flow to choroid plexus: role of arginine vasopressin.

1988 ◽  
Vol 63 (2) ◽  
pp. 373-379 ◽  
Author(s):  
F M Faraci ◽  
W G Mayhan ◽  
W J Farrell ◽  
D D Heistad
Keyword(s):  
Blood Flow ◽  
Choroid Plexus ◽  
Arginine Vasopressin ◽  
Humoral Regulation

Effect of vasopressin on production of cerebrospinal fluid: possible role of vasopressin (V1)-receptors

1990 ◽  
Vol 258 (1) ◽  
pp. R94-R98 ◽  
Author(s):  
F. M. Faraci ◽  
W. G. Mayhan ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Arginine Vasopressin ◽  
Indicator Dilution ◽  
Dilution Method ◽  
Ventriculocisternal Perfusion ◽  
Csf Production ◽  
Humoral Regulation

The goal of this study was to examine the role of arginine vasopressin in humoral regulation of choroid plexus function. Production of cerebrospinal fluid (CSF) was measured in anesthetized rabbits with an indicator dilution method, by using ventriculocisternal perfusion of artificial CSF containing blue dextran. Rabbits received either vehicle, vasopressin or vasopressin in the presence of the V1-antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]arginine vasopressin ([d(CH2)5Tyr(Me)]-AVP). Under control conditions, blood flow to the choroid plexus (measured with microspheres) averaged 369 +/- 26 (mean +/- SE) ml.min-1.100 g-1 and CSF production averaged 9.9 +/- 0.9 microliters/min. Intravenous infusion of vasopressin (2 mU.kg-1.min-1 for 90 min) decreased blood flow to the choroid plexus by 50-60% for the entire period of infusion. Vasopressin decreased production of CSF by 35 +/- 8%. Blood flow to the choroid plexus and production of CSF did not change significantly from control values in animals that received vehicle. In the presence of the V1-antagonist (10 micrograms/kg), infusion of vasopressin had no effect on blood flow to the choroid plexus or production of CSF. Thus circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has important effects on formation of CSF, as well as on blood flow to the choroid plexus. These findings are consistent with the hypothesis that effects of vasopressin on both variables are mediated through vasopressin (V1)-receptors.

Effect of atriopeptin on blood flow to cerebrum and choroid plexus

1989 ◽  
Vol 257 (6) ◽  
pp. R1365-R1369
Author(s):  
K. A. Schalk ◽  
J. L. Williams ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Choroid Plexus ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain ◽  
Increased Blood Flow

The goal of this study was to determine whether atriopeptin alters blood flow to cerebrum and choroid plexus. In anesthetized rabbits, blood flow (microspheres) to cerebrum and choroid plexus under control conditions was 36 +/- 3 (mean +/- SE) and 573 +/- 78 ml.min-1.100 g-1, respectively. Infusion of atriopeptin (75, 225, 1,150 ng.kg-1.min-1 iv) increased blood flow to choroid plexus by 22 +/- 11, 53 +/- 26, and 51 +/- 13%, respectively. In contrast, blood flow to cerebrum was not altered by atriopeptin, presumably because the blood-brain barrier prevented access to cerebral vascular smooth muscle. Because a major role of atriopeptin may be to modulate responses to angiotensin II, we examined effects of atriopeptin on vasoconstrictor responses to angiotensin II in the choroid plexus. Angiotensin II was infused in the presence or absence of atriopeptin (300 ng.kg-1.min-1 iv). Angiotensin II (100 ng.kg-1.min-1 iv) decreased blood flow to choroid plexus by 49 +/- 12% and by 47 +/- 14% during simultaneous infusion of atriopeptin. In summary, atriopeptin 1) increases blood flow to choroid plexus, but not cerebrum, and 2) does not appear to attenuate vasoconstrictor effects of angiotensin II in the choroid plexus.

Role of blood flow and impaired autoregulation in the pathogenesis of diabetic retinopathy

Diabetes ◽  
1995 ◽  
Vol 44 (6) ◽  
pp. 603-607 ◽  
Author(s):  
E. M. Kohner ◽  
V. Patel ◽  
S. M. Rassam
Keyword(s):  
Blood Flow ◽  
Diabetic Retinopathy

Exercise with blood flow restriction as a new tool for health improvement in hypertensive elderly women: the role of purinergic enzymes

2020 ◽  
Vol 60 (11) ◽  
Author(s):  
Aline Mânica ◽  
Clodoaldo A. De SÁ ◽  
Angélica Barili ◽  
Vanessa S. Corralo ◽  
Beatriz S. Bonadiman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Elderly Women ◽  
Blood Flow Restriction ◽  
Health Improvement ◽  
Flow Restriction

Role of Nitric Oxide on Papillary Blood Flow and Pressure Natriuresis

Hypertension ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Francisco J. Fenoy ◽  
Paloma Ferrer ◽  
Luis Carbonell ◽  
Miguel García-Salom
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pressure Natriuresis

scholarly journals Computational Analysis of Coronary Blood Flow: The Role of Asynchronous Pacing and Arrhythmias

Mathematics ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 1205
Author(s):  
Timur Gamilov ◽  
Philipp Kopylov ◽  
Maria Serova ◽  
Roman Syunyaev ◽  
Andrey Pikunov ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Long Qt Syndrome ◽  
Premature Ventricular Contraction ◽  
Cardiac Pacing ◽  
Long Qt ◽  
Computational Evaluation ◽  
Qt Syndrome

In this work we present a one-dimensional (1D) mathematical model of the coronary circulation and use it to study the effects of arrhythmias on coronary blood flow (CBF). Hydrodynamical models are rarely used to study arrhythmias’ effects on CBF. Our model accounts for action potential duration, which updates the length of systole depending on the heart rate. It also includes dependency of stroke volume on heart rate, which is based on clinical data. We apply the new methodology to the computational evaluation of CBF during interventricular asynchrony due to cardiac pacing and some types of arrhythmias including tachycardia, bradycardia, long QT syndrome and premature ventricular contraction (bigeminy, trigeminy, quadrigeminy). We find that CBF can be significantly affected by arrhythmias. CBF at rest (60 bpm) is 26% lower in LCA and 22% lower in RCA for long QT syndrome. During bigeminy, trigeminy and quadrigeminy, respectively, CBF decreases by 28%, 19% and 14% with respect to a healthy case.

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