Role of chemical factors in regulation of flow through kidney, hindlimb, and heart

1965 ◽  
Vol 208 (5) ◽  
pp. 813-824 ◽  
Author(s):  
J. B. Scott ◽  
R. M. Daugherty ◽  
J. M. Dabney ◽  
F. J. Haddy
Keyword(s):  
Blood Flow ◽  
Metabolic Rate ◽  
Flow Resistance ◽  
Reactive Hyperemia ◽  
Venous Outflow ◽  
Chemical Factors ◽  
Study Support ◽  
Dog Blood ◽  
Flow Through

In the anesthetized dog, blood flow or metabolic rate was varied in kidney, hindlimb, or heart (experimental organ) while simultaneously diverting a portion of the venous outflow through forelimb or kidney (bioassay organ). The resistance to blood flow through the experimental organ gradually rose in the first few minutes following a large increase in flow and gradually fell following a large decrease in flow. Resistance to blood flow through an experimental organ (hindlimb) fell following increase in metabolic rate. In each case, bioassay organ resistance changed in the same direction when the assay organ was the forelimb and in the opposite direction when the assay organ was the kidney. These findings suggest that active hyperemia, reactive hyperemia, and autoregulation of blood flow result, at least in part, from alteration in the chemical environment of the blood vessels. Other findings in this study support the possibility that adenosine triphosphate contributes to the change in environment.

ROLE OF SLIP VELOCITY IN BLOOD FLOW THROUGH STENOSED ARTERIES: A NON-NEWTONIAN MODEL

2007 ◽  
Vol 07 (03) ◽  
pp. 337-353 ◽  
Author(s):  
J. C. MISRA ◽  
G. C. SHIT
Keyword(s):  
Blood Flow ◽  
Skin Friction ◽  
Flow Rate ◽  
Slip Velocity ◽  
Flow Resistance ◽  
Volumetric Flow Rate ◽  
Flow Through ◽  
Analytical Expressions ◽  
Insight Into

A mathematical model is developed in this paper for studying blood flow through a stenosed arterial segment by taking into account the slip velocity at the wall of the artery. Consideration of the non-Newtonian character of blood is made, where a constitutive relation of blood is described by the Herschel–Bulkley equation. The effect of slip at the arterial wall in the presence of mild, moderate, and severe stenosis growth at the lumen of an artery is investigated. Analytical expressions for skin friction, flow resistance, and the flow rate are derived by using the model. The derived expressions are computed numerically by considering an illustrative example. The study provides an insight into the effects of slip velocity on the volumetric flow rate of blood, flow resistance, and skin friction.

Role of adenosine in postprandial and reactive hyperemia in canine jejunum

1992 ◽  
Vol 263 (4) ◽  
pp. G487-G493 ◽  
Author(s):  
D. R. Sawmiller ◽  
C. C. Chou
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Adenosine Deaminase ◽  
Reactive Hyperemia ◽  
Concentration Difference ◽  
Adenosine Concentration ◽  
Anesthetized Dogs ◽  
Series Of Experiments ◽  
Increased Blood Flow

The role of adenosine in postprandial jejunal hyperemia was investigated by determining the effect of placement of predigested food into the jejunal lumen on blood flow and oxygen consumption before and during intra-arterial infusion of dipyridamole (1.5 microM arterial concn) or adenosine deaminase (9 U/ml arterial concn) in anesthetized dogs. Neither drug significantly altered resting jejunal blood flow and oxygen consumption. Before dipyridamole or deaminase, food placement increased blood flow by 30-36%, 26-42%, and 21-46%, and oxygen consumption by 13-22%, 21-22%, and 26-29%, during 0- to 3-, 4- to 7-, and 8- to 11-min placement periods, respectively. Adenosine deaminase abolished the entire 11-min hyperemia, whereas dipyridamole significantly enhanced the initial 7-min hyperemia (45-49%). Both drugs abolished the initial 7-min food-induced increase in oxygen consumption. Dipyridamole attenuated (14%), whereas deaminase did not alter (28%), the increased oxygen consumption that occurred at 8-11 min. Adenosine deaminase also prevented the food-induced increase in venoarterial adenosine concentration difference. In separate series of experiments, luminal placement of food significantly increased jejunal lymphatic adenosine concentration and release. Also, reactive hyperemia was accompanied by an increase in venous adenosine concentration and release. This study provides further evidence to support the thesis that adenosine plays a role in postprandial and reactive hyperemia in the canine jejunum.

Differences in reactive hyperemia between the intestinal mucosa and muscularis

1984 ◽  
Vol 247 (6) ◽  
pp. G617-G622
Author(s):  
A. P. Shepherd ◽  
G. L. Riedel
Keyword(s):  
Blood Flow ◽  
Metabolic Rate ◽  
Laser Doppler Velocimetry ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Oxygen Demand ◽  
Laser Doppler ◽  
Doppler Velocimetry ◽  
Total Blood ◽  
Total Blood Flow

In a previous study of regional intestinal blood flow by laser-Doppler velocimetry, we noted that the mucosa displayed reactive hyperemia following arterial occlusion but that the muscularis did not. Therefore, to determine whether this observation is generally valid, we compared responses of the mucosa and muscularis externa to arterial occlusion. We measured total blood flow to isolated loops of canine small bowel with an electromagnetic flow probe on the supply artery; blood flow either in the mucosa or in the muscularis was measured by laser-Doppler velocimetry. Mucosal and total blood flow consistently showed reactive hyperemia in response to a 60-s occlusion, but the muscularis did not. To determine whether metabolic rate influenced reactive hyperemia, we increased enteric oxygen uptake by placing 5% bile and transportable solutes in the lumen; these agents increased oxygen consumption by 36%. After a 60-s occlusion, the durations of both total and mucosal reactive hyperemia were significantly prolonged by increased metabolic rate. Similarly, the payback-to-debt ratios in both total and mucosal blood flows were significantly increased at elevated metabolic rate. These data support the conclusions that reactive hyperemia occurs more frequently and has a greater magnitude in the mucosa compared with the muscularis and both total and mucosal reactive hyperemia are strongly influenced by the preocclusive oxygen demand. These findings therefore constitute further evidence that metabolic factors contribute to reactive hyperemia in the intestinal circulation.

scholarly journals Essential Role of Hemoglobin βCys93 in Cardiovascular Physiology

Physiology ◽  
2020 ◽  
Vol 35 (4) ◽  
pp. 234-243 ◽  
Author(s):  
Richard T. Premont ◽  
Jonathan S. Stamler
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Tissue Hypoxia ◽  
Microvascular Blood Flow ◽  
Cardiovascular Physiology ◽  
Transient Ischemia ◽  
Microcirculatory Blood Flow ◽  
Physiological Basis ◽  
Hb S

The supply of oxygen to tissues is controlled by microcirculatory blood flow. One of the more surprising discoveries in cardiovascular physiology is the critical dependence of microcirculatory blood flow on a single conserved cysteine within the β-subunit (βCys93) of hemoglobin (Hb). βCys93 is the primary site of Hb S-nitrosylation [i.e., S-nitrosothiol (SNO) formation to produce S-nitrosohemoglobin (SNO-Hb)]. Notably, S-nitrosylation of βCys93 by NO is favored in the oxygenated conformation of Hb, and deoxygenated Hb releases SNO from βCys93. Since SNOs are vasodilatory, this mechanism provides a physiological basis for how tissue hypoxia increases microcirculatory blood flow (hypoxic autoregulation of blood flow). Mice expressing βCys93A mutant Hb (C93A) have been applied to understand the role of βCys93, and RBCs more generally, in cardiovascular physiology. Notably, C93A mice are unable to effect hypoxic autoregulation of blood flow and exhibit widespread tissue hypoxia. Moreover, reactive hyperemia (augmentation of blood flow following transient ischemia) is markedly impaired. C93A mice display multiple compensations to preserve RBC vasodilation and overcome tissue hypoxia, including shifting SNOs to other thiols on adult and fetal Hbs and elsewhere in RBCs, and growing new blood vessels. However, compensatory vasodilation in C93A mice is uncoupled from hypoxic control, both peripherally (e.g., predisposing to ischemic injury) and centrally (e.g., impairing hypoxic drive to breathe). Altogether, physiological studies utilizing C93A mice are confirming the allosterically controlled role of SNO-Hb in microvascular blood flow, uncovering essential roles for RBC-mediated vasodilation in cardiovascular physiology and revealing new roles for RBCs in cardiovascular disease.

Intracoronary adenosine enhances myocardial reactive hyperemia after brief coronary occlusion

1985 ◽  
Vol 248 (6) ◽  
pp. H812-H817
Author(s):  
D. Saito ◽  
T. Hyodo ◽  
K. Takeda ◽  
Y. Abe ◽  
H. Tani ◽  
...  
Keyword(s):  
Blood Flow ◽  
Left Atrium ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Control Level ◽  
Direct Effects ◽  
Intracoronary Infusion ◽  
Hyperemic Flow ◽  
Hyperemic Response

Adenosine is a prime candidate for the role of mediator between myocardial metabolic state and coronary blood flow. However, there are few reports concerning the direct effects of exogenously added adenosine on coronary autoregulation. The present investigation in the open-chest dog studied the effects of a threshold dose of intracoronary adenosine infusion on reactive hyperemia following brief coronary occlusions. The infused dose did not increase nonocclusive flow by greater than 10%. Adenosine enhanced total hyperemic flow at all occlusions tested (5, 10, 15, 20, and 30 s). Aminophylline pretreatment reduced reactive hyperemia below the control level even in the presence of an intracoronary infusion of adenosine. Adenosine injected into the left atrium and intracoronarily infused papaverine did not affect hyperemic response to 5- and 15-s coronary occlusions. The results suggest that a minimum dose of exogenously added adenosine enhances myocardial reactive hyperemia, possibly by potentiating the effects of endogenous adenosine released during ischemia.

BLOOD FLOW THROUGH A CIRCULAR PIPE WITH AN IMPULSIVE PRESSURE GRADIENT

2000 ◽  
Vol 10 (02) ◽  
pp. 187-202 ◽  
Author(s):  
GIUSEPPE PONTRELLI
Keyword(s):  
Blood Flow ◽  
Finite Difference ◽  
Finite Difference Method ◽  
Unsteady Flow ◽  
Pressure Gradient ◽  
Collocation Method ◽  
Difference Method ◽  
Flow Through ◽  
Impulsive Pressure

The unsteady flow of a viscoelastic fluid in a straight, long, rigid pipe, driven by a suddenly imposed pressure gradient is studied. The used model is the Oldroyd-B fluid modified with the use of a nonconstant viscosity, which includes the effect of the shear-thinning of many fluids. The main application considered is in blood flow. Two coupled nonlinear equations are solved by a spectral collocation method in space and the implicit trapezoidal finite difference method in time. The presented results show the role of the non-Newtonian terms in unsteady phenomena.

scholarly journals Adenosine Deaminase Inhibitors Enhance Cerebral Anoxic Hyperemia in the Rat

1985 ◽  
Vol 5 (2) ◽  
pp. 295-299 ◽  
Author(s):  
J. W. Phillis ◽  
R. E. DeLong ◽  
J. K. Towner
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Adenosine Deaminase ◽  
Reactive Hyperemia ◽  
Low Doses ◽  
Venous Outflow ◽  
Vascular Regulation ◽  
Vascular Insufficiency ◽  
Basal Flow ◽  
Cerebral Vascular

Cerebral blood flow in the rat was monitored by a venous outflow technique with an extracorporeal circulation, which allows for the continuous recording of flow over periods of several hours. The adenosine deaminase inhibitors erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) (1.0–100 μg/kg) and deoxycoformycin (0.1–1 μg/kg) potentiated the reactive hyperemia elicited by a brief (24-s) anoxic challenge. Basal flow rate was unaltered by EHNA administration and slightly enhanced by deoxycoformycin. The results are consistent with the hypothesis that adenosine plays a significant role in cerebral vascular regulation and suggest that low doses of these deaminase inhibitors may be useful in the treatment of cerebral vascular insufficiency.

scholarly journals Deformation and dynamics of red blood cells in flow through cylindrical microchannels

Soft Matter ◽  
2014 ◽  
Vol 10 (24) ◽  
pp. 4258-4267 ◽  
Author(s):  
Dmitry A. Fedosov ◽  
Matti Peltomäki ◽  
Gerhard Gompper
Keyword(s):  
Blood Flow ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Flow Resistance ◽  
Flow Conditions ◽  
Hydrodynamic Simulations ◽  
Wide Range ◽  
Flow Through ◽  
Cell Partitioning

The behavior of red blood cells (RBCs) in microvessels plays an important role in blood flow resistance and in the cell partitioning within a microcirculatory network. We employ mesoscopic hydrodynamic simulations to study the behavior and deformation of single RBCs in microchannels yielding the construction of diagrams of RBC shapes for a wide range of flow conditions.

scholarly journals Evolutionary Role of Epigenetics in Ischemic Stroke: A Review

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 1616-1620
Author(s):  
Rohini Agrawal ◽  
Prashant Amale ◽  
Shilpa Deshpande ◽  
Manish Deshmukh ◽  
Priti Bhoyar ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Hemorrhagic Stroke ◽  
Neural Stem Progenitor Cells ◽  
Genetic Level ◽  
Flow Through ◽  
After Cancer ◽  
The Brain ◽  
Global Population

Stroke is a Central Nervous System (CNS) disorder which occurs due to the obstruction in the brain blood flow. Stroke is mainly of two types, such as ischemic and hemorrhagic stroke. Ischemic stroke (80%) caused due to obstruction of blood flow through Middle Cerebral Artery (MCA) and characterized by a decreased supply of oxygen and glucose to CNS. In comparison, Hemorrhagic stroke (20%) mainly occurs due to the rupturing of blood vessels. Epidemiologically, it is the common reason of death after cancer and affecting millions of global population. There are many risk factors such as hypertension; hypercholesterolemia etc. which can exaggerate the condition of stroke. Various conventional therapies like Antiplatelets, Thrombolytic are available, but, there is a need to obtain a therapeutic approach that can provide prevention as well as a cure for the stroke. So the present review is primarily focused on epigenetic approach for ischemic stroke by Endogenous Transplantation of Neural Stem/Progenitor Cells (NSPCs). This, in turn, will decrease the level of REST protein at the genetic level and enhance the activity of Na+-Ca+ exchanger activity and lowers the excitotoxicity.

Inhibition of vascular ATP-sensitive K+channels does not affect reactive hyperemia in human forearm

2003 ◽  
Vol 284 (2) ◽  
pp. H711-H718 ◽  
Author(s):  
H. M. Omar Farouque ◽  
Ian T. Meredith
Keyword(s):  
Blood Flow ◽  
Adaptive Response ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Channel Inhibition ◽  
Human Forearm ◽  
Hyperemic Response

The extent to which ATP-sensitive K+ channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K+channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced ( n = 9). The contribution of vascular ATP-sensitive K+ channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K+ channel inhibitor ( n = 12). To document ATP-sensitive K+ channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K+ channel opener, was undertaken ( n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K+ channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.

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