Comparison of Stern Wedge and Stern Flap on Fast Monohull Vessel Resistance

Factors affecting fetal vessel resistance have been studied in vitro in bilaterally perfused lobules of human placentae. Potent and efficacious constrictors in this preparation (in order of potency) include endothelin-1 > the thromboxane mimetic U46619 > endothelin-3 > prostaglandin F2 alpha. Inhibitors of eicosanoid synthesis did not affect fetal vessel basal perfusion pressure, nor did they potentiate the effects of the vasoconstrictor U46619. In contrast, the nitric oxide inhibitors N omega-nitro-L-arginine (NOLA), haemoglobin and methylene blue all increased fetal vessel basal perfusion pressure and also increased U46619-induced constriction. Similarly, NOLA markedly potentiated the constrictor effects of endothelin-1, angiotensin II, 5-hydroxytryptamine and bradykinin. These studies therefore provide evidence that NO is important in the maintenance of low basal fetal vessel impedance and also reduces the effects of a number of vasoconstrictor autacoids. Nitric oxide synthase (NOS) activity of human placental homogenates has been measured and shown to be mainly calcium-dependent. Human placental NOS activity was not affected by labour state but was reduced in pre-eclampsia. No evidence was found that in pre-eclampsia raised concentrations of the endogenous NOS inhibitor asymmetric dimethylarginine were responsible for the reduced placental NOS activity. Hence, these studies provide evidence that NO is an important endogenous dilator of the fetal vessels of the human placenta and that reduced NOS activity could contribute to the pathogenesis and/or effects of pre-eclampsia.

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Arterial hypertension and unusual ascending aortic dilatation in a neonate with acute kidney injury: mechanistic computer modelling

10.31219/osf.io/anrkv ◽

2018 ◽

Author(s):

Sanjay R Kharche

Keyword(s):

Acute Kidney Injury ◽

Kidney Injury ◽

Ascending Aorta ◽

Small Vessel ◽

Aortic Dilatation ◽

Small Vessels ◽

Left Ventricle Hypertrophy ◽

Vessel Resistance ◽

Underlying Mechanisms ◽

Ventricle Hypertrophy

Background: Neonatal asphyxia caused acute kidney injury and severe hypertension in a newborn patient. An unusually dilatated ascending aorta developed within a few weeks. Dialysis and hypertensive treatment led to partial recovery of the aortic diameters. It was hypothesized that the aortic dilatation may be associated with cardiovascular changes induced by the acute kidney injury. Mathematical modelling was used to better understand the underlying mechanisms of hypertension and aortic dilatation.Methods: Patient observation included systolic blood pressure recording and echocardiographic exams. To explore underlying mechanisms of aortic dilatation and hypertension, a previous whole-body lumped parameter hemodynamics model was adapted to this study. Computer simulations were designed to permit dissection of individual mechanisms. The hypertension inducing effects of altering systemic vascular resistances, stiffnesses, and heart rate on blood flows and pressures were simulated.Results: In agreement with our clinical diagnosis, the mathematical model showed that an increase of systemic small vessel resistance is the prime cause of hypertension. Further, aortic stiffening may also cause hypertension, it was found to be secondary to the potency of systemic small vessel resistance. The cardiac output, as quantified using pressure-volume loop area, reduced significantly due to hypertension. Simultaneous left ventricle hypertrophy and small vessel blocking increased ascending aorta blood flow as well as pressure indicating an enlarged ascending aorta. In contrast, increased arterial stiffness appeared to lower the aortic blood flow and pressures.Conclusions and discussion: Systemic small vessel resistance is an important factor in arterial hypertension, and may also be a key clinical therapeutic target. Left ventricle hypertrophy may also be simultaneously ameliorated when treating systemic small vessels. Treatment of arterial stiffness appears to provide significant benefit but may be secondary to treatment of the systemic small vessels. The quantitative grading of pathophysiological mechanisms provided by the modelling may contribute to treatment recommendations. Further development and individualization of the model will augment its applicability in clinical practice.

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Effects of arginine vasopressin on cerebral microvascular pressure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.1.h70 ◽

1988 ◽

Vol 255 (1) ◽

pp. H70-H76 ◽

Cited By ~ 7

Author(s):

F. M. Faraci ◽

W. G. Mayhan ◽

P. G. Schmid ◽

D. D. Heistad

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Vascular Resistance ◽

Arginine Vasopressin ◽

Cerebral Arteries ◽

Aortic Pressure ◽

Artery Pressure ◽

Large Arteries ◽

Pial Artery ◽

Vessel Resistance

The goal of this study was to examine effects of arginine vasopressin and angiotensin on cerebral microvascular pressure and segmental vascular resistance. We measured pressure (servo-null) in pial arteries that were approximately 200 micron in diameter and cerebral blood flow (microspheres) in anesthetized cats, and we calculated resistance of large and small cerebral vessels. Resistance of large arteries (greater than 200 micron diam) was approximately 45% of total cerebral vascular resistance under control conditions. Vasopressin (40 mU/kg iv) decreased resistance of large arteries by 22 +/- 7%, increased pial artery pressure by 10 +/- 2 mmHg when aortic pressure was maintained at control levels, and increased small vessel resistance by 27 +/- 11%. This increase in small vessel resistance apparently was an autoregulatory response to the increase in pial pressure. Cerebral blood flow was not changed (38 +/- 4 vs. 37 +/- 3 ml.min-1.100 g-1). Intravenous infusion of angiotensin (2 micrograms.kg-1.min-1) increased large artery resistance by 32 +/- 6%, decreased pial artery pressure 6 +/- 3 mmHg with aortic pressure maintained constant, and decreased cerebral blood flow by 12 +/- 1%. Thus circulating vasopressin, at concentrations similar to those observed during hemorrhage, selectively dilates large cerebral arteries and increases microvascular pressure without changes in cerebral blood flow. In contrast to vasopressin, angiotensin selectively increases resistance of large cerebral arteries and decreases cerebral microvascular pressure. Thus vasopressin and angiotensin, at doses that have minimal effects on cerebral blood flow, may play an important role in regulation of cerebral microvascular pressure.

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Effects of Angiotensin and Atrial Natriuretic Peptide on the Cerebral Circulation

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1992.44 ◽

1992 ◽

Vol 12 (2) ◽

pp. 318-325 ◽

Cited By ~ 27

Author(s):

Kinya Tamaki ◽

Yoshisuke Saku ◽

Jun Ogata

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Cerebral Circulation ◽

Systemic Arterial Pressure ◽

Large Artery ◽

Ang Ii ◽

Small Vessels ◽

High Doses ◽

Vessel Resistance ◽

Atrial Natriuretic

The purpose of the present study was to determine effects of angiotensin (ANG) II on the cerebral circulation. We measured the pial artery pressure (PAP) and CBF in anesthetized rabbits. ANG II (5 μg/min) was infused into each carotid artery, and systemic arterial pressure was maintained constant. During infusion of ANG II, there was a significant increase in CBF and fall of PAP, with no change in the large artery resistance (LAR) and a significant decrease in the small vessel resistance (SVR). To investigate whether prostaglandin modulated the ANG II-induced increase in CBF, indomethacin was administered (10 mg/kg i.v.) in another group of animals. Indomethacin itself reduced PAP and increased LAR significantly without changing CBF or SVR. Indomethacin did not attenuate the effects of ANG II on the cerebral circulation. The CMRO2 was assessed during ANG II intracarotid infusion in another group of rabbits. CMRO2 did not change during infusion of ANG II. We also investigated effects of α-atrial natriuretic peptide (ANP) on the cerebral circulation. Infusion of ANP (1 μg/min) decreased LAR by 28% (p < 0.05) without altering SVR. Administration of ANG II after ANP tended to reduce LAR (p > 0.05), with a significant decrease in SVR. The results of the present study suggest that high doses of ANG II can produce cerebral vasodilatation, particularly of small vessels. Blood-borne ANP dilated the large arteries of the cerebral circulation selectively and neither interfered with nor reversed the ANG II-induced increase in CBF.

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Coupling of a cardiovascular model with a thermoregulation model to predict human blood pressure under unsteady environmental conditions

E3S Web of Conferences ◽

10.1051/e3sconf/201911102062 ◽

2019 ◽

Vol 111 ◽

pp. 02062

Author(s):

Yoshito Takahashi ◽

Masayuki Oata ◽

Jun-ichi Asaka ◽

Akihisa Nomoto ◽

Shin-ichi Tanabe

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Human Blood ◽

Environmental Conditions ◽

Lumped Parameter Model ◽

Cardiovascular Model ◽

Lumped Parameter ◽

Gravity Effects ◽

Vessel Resistance ◽

Peak Blood

We coupled a cardiovascular model with a thermoregulation model to predict human blood pressure in unsteady environmental conditions. Our cardiovascular model is a lumped parameter model and consists of 42 segments, which include the entire artery and vein system, divided into 18 segments; the heart, divided into 4 segments; and the pulmonary artery and vein. The vessel parameters were adjusted on the basis of local body blood volume and flow of the thermoregulation model in a thermoneutral environment. Blood pressure under unsteady environmental conditions is predicted by changing the heart rate and vessel resistance of the cardiovascular model which is controlled by blood flow that the thermoregulation model predicts. It is possible to predict the increase in blood pressure under cold environmental conditions and the increase in cardiac output under hot environmental conditions and when bathing. The model was validated by simulating bathing experiments. As the result, the model predicted the peak blood pressure later than the experimental data in a cold environment. To improve the accuracy of the model, it is necessary to consider a method for controlling the heart rate, vessel resistance, and gravity effects after a change in posture.

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Lung inflation and longitudinal distribution of pulmonary vascular resistance during hypoxia

Journal of Applied Physiology ◽

10.1152/jappl.1979.47.3.532 ◽

1979 ◽

Vol 47 (3) ◽

pp. 532-536 ◽

Cited By ~ 26

Author(s):

C. A. Dawson ◽

D. J. Grimm ◽

J. H. Linehan

Keyword(s):

Vascular Resistance ◽

Pressor Response ◽

Transpulmonary Pressure ◽

Longitudinal Distribution ◽

Local Resistance ◽

Lung Inflation ◽

Hypoxic Conditions ◽

Low Viscosity ◽

Major Increase ◽

Vessel Resistance

Using the low-viscosity bolus method, we examined the influence of lung inflation on the longitudinal distribution of vascular resistance during hypoxia in isolated cat lungs. During hypoxia, increasing transpulmonary pressure decreased vascular resistance but did not change the volume into the lung at which the maximum local resistance was located. This was in contrast to the normoxic situation in which inflation caused an increase in resistance over much of the transpulmonary pressure range studied and moved the maximum local resistance downstream. These results indicate that during hypoxia the major increase in resistance was in extra-alveolar vessels and that distension of these vessels by lung inflation decreased the magnitude of the pressor response. The increase in resistance in alveolar vessels, which occurred on inflation, was similar during control and hypoxic conditions but was a smaller part of the total resistance during hypoxia because of the much larger extra-alveolar vessel resistance.

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Effect of Change in Air Temperature Upon Systemic Small and Large Vessel Resistance

Circulation Research ◽

10.1161/01.res.5.1.58 ◽

1957 ◽

Vol 5 (1) ◽

pp. 58-63 ◽

Cited By ~ 9

Author(s):

F. J. HADDY ◽

MALCOLM FLEISHMAN ◽

JERRY B. SCOTT

Keyword(s):

Air Temperature ◽

Large Vessel ◽

Vessel Resistance

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Effects of transient changes in intra myocardial vessel resistance and compliance on the systolic coronary blood flow by optimized model

Proceedings of the 1996 IEEE IECON. 22nd International Conference on Industrial Electronics, Control, and Instrumentation ◽

10.1109/iecon.1996.571011 ◽

2002 ◽

Cited By ~ 1

Author(s):

H. Hirayama ◽

T. Okizaki ◽

J. Mukai ◽

Y. Fukuyama

Keyword(s):

Blood Flow ◽

Coronary Blood Flow ◽

Optimized Model ◽

Vessel Resistance

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Slackness between vessel and myocardium is necessary for coronary flow reserve

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01184.2011 ◽

2012 ◽

Vol 302 (11) ◽

pp. H2230-H2242 ◽

Cited By ~ 7

Author(s):

Jonathan M. Young ◽

Jenny S. Choy ◽

Ghassan S. Kassab ◽

Yoram Lanir

Keyword(s):

Coronary Flow Reserve ◽

Coronary Flow ◽

Mechanical Energy ◽

Potential Effect ◽

Experimental Measurements ◽

Flow Reserve ◽

Model Predictions ◽

Effectiveness And Efficiency ◽

Vessel Resistance ◽

Experimental Findings

Tone regulation in coronary microvessels has largely been studied in isolated vessels in the absence of myocardial tethering. Here, the potential effect of radial tethering and interstitial space connective tissue (ISCT) between coronary microvessels and the surrounding myocardium was studied. We hypothesized that rigid tethering between microvessels and the myocardium would constrain the active contraction of arterioles and is not compatible with the observed tone regulation. The ISCT between coronary microvessels and myocardium in five swine was found to increase exponentially from 0.22 ± 0.02 μm in capillaries (modified Strahler order 0) of the endocardium to 34.9 ± 7.1 μm in epicardial vessels ( order 10). Microvessels with both soft tethering and ISCT gap were capable of significant changes in vessel resistance (up to an ∼1,600% increase), consistent with experimental measurements of high coronary flow reserve. Additionally, the mechanical energy required for myogenic contraction was estimated. The results indicate that rigid tethering requires up to four times more mechanical energy than soft tethering in the absence of a gap. Hence, the experimental measurements and model predictions suggest that effectiveness and efficiency in tone regulation can be achieved only if the vessel is both softly tethered to and separated from the myocardium in accordance with the experimental findings of ISCT gap. These results have fundamental implications on future simulations of coronary circulation.

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