THE ROLE OF ARTERIOVENOUS ANASTOMOSES IN COLD-INDUCED VASODILATION, REWARMING, AND REACTIVE HYPEREMIA AS DETERMINED BY 24Na CLEARANCE

1967 ◽  
Vol 45 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Merrill A. Edwards
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Arteriovenous Anastomoses ◽  
Total Flow ◽  
Initial Flow

The rate of removal of 24Na from a deposit in the rabbit's foot was used to determine the degree of involvement of arteriovenous anastomoses in the blood flow of cold-induced vasodilation, in the rewarming following intense vasoconstriction, and in reactive hyperemia. The results indicate that in the first two cases the total flow is through the arteriovenous anastomoses. In reactive hyperemia an initial flow which is partly capillary and partly through the anastomoses gives way to a flow which is entirely through the anastomoses.

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.

Role of oxygen in autoregulation of blood flow in isolated vessels

1964 ◽  
Vol 206 (5) ◽  
pp. 951-954 ◽  
Author(s):  
Oliver Carrier ◽  
James R. Walker ◽  
Arthur C. Guyton
Keyword(s):  
Blood Flow ◽  
Normal Level ◽  
Constant Pressure ◽  
Constant Flow ◽  
Average Increase ◽  
Flow Conditions ◽  
Low Oxygen ◽  
Local Blood Flow ◽  
Initial Flow

The role of oxygen in control of local blood flow was investigated in isolated arterial segments 1 cm in length and 0.5–1.0 mm in diameter by perfusion with blood of various Po2 levels. A decrease in vascular resistance always occurred when the Po2 was lowered and an increase occurred when it was raised. In 20 vessels, using constant-pressure perfusion, an average increase in conductance of 2.38 times normal level was obtained when the Po2 was lowered from 100 to 30 mm Hg. When this datum was plotted according to initial flow, the smaller vessels gave the greatest response to low oxygen (2.73 times normal; sem ± 0.15), whereas the largest gave the least (1.76 times normal; sem ± 0.10). Forty-three vessels perfused under constant-flow conditions gave results which were consistent with and confirmed the constant-pressure results. In all of these experiments pH, Pco2, and temperature were monitored and kept at physiological levels. The results indicate that oxygen could well be a factor in the autoregulation of blood flow.

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.

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.

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.

A restrospective perspective

2005 ◽  
Vol 98 (2) ◽  
pp. 762-763 ◽  
Author(s):  
John Gamble
Keyword(s):  
Blood Flow ◽  
Adrenergic Receptors ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Venous Occlusion Plethysmography ◽  
Limb Blood Flow ◽  
Major Area ◽  
Vasoactive Factors ◽  
Health And Disease

Venous occlusion plethysmography is a simple but elegant technique that has contributed to almost every major area of vascular biology in humans. The general principles of plethysmography were appreciated by the late 1800s, and the application of these principles to measure limb blood flow occurred in the early 1900s. Plethysmography has been instrumental in studying the role of the autonomic nervous system in regulating limb blood flow in humans and important in studying the vasodilator responses to exercise, reactive hyperemia, body heating, and mental stress. It has also been the technique of choice to study how human blood vessels respond to a variety of exogenously administered vasodilators and vasoconstrictors, especially those that act on various autonomic and adrenergic receptors. In recent years, plethysmography has been exploited to study the role of the vascular endothelium in health and disease. Venous occlusion plethysmography is likely to continue to play an important role as investigators seek to understand the physiological significance of newly identified vasoactive factors and how genetic polymorphisms affect the cardiovascular system in humans.

Failure to abolish reactive hyperemia by indomethacin in denervated kidneys of rabbits

1977 ◽  
Vol 233 (2) ◽  
pp. F89-F93
Author(s):  
C. Aizawa ◽  
N. Honda
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Reactive Hyperemia ◽  
Fractional Flow ◽  
Outer Cortex ◽  
Cortical Blood Flow ◽  
Before And After ◽  
Inner Cortex ◽  
Postocclusive Reactive Hyperemia

The effect of indomethacin (10 mg/kg) on the distribution of cortical blood flow during postocclusive reactive hyperemia was evaluated in denervated kidneys of anesthetized rabbits by the radioactive microsphere technique. Renal denervation caused a slight but not significant increase in renal blood flow with no remarkable alteration in the distribution of cortical blood flow. After release of 1-min occlusion of the renal artery, hyperemic responses developed with a fractional flow redistribution toward the inner cortex. The absolute perfusion rate increased in the inner cortex but did not significantly change in the outer cortex. Indomethacin produced a decrease in renal blood flow despite elevated blood pressure. Even in the indomethacin-treated animals, postocclusive reactive hyperemia appeared concomitantly with the fractional flow redistribution to the inner cortex. The percentage repayment by reactive hyperemia of ischemia during the artery clamping was not significantly different before and after indomethacin administration. The findings indicate that indomethacin did not significantly affect the postocclusive vascular response in denervated kidneys of rabbits, thereby giving evidence against the role of prostaglandins as mediators of reactive hyperemia.

Vasoconstrictor-induced changes in renal blood flow: role of prostaglandins and histamine

1988 ◽  
Vol 254 (4) ◽  
pp. F470-F476 ◽  
Author(s):  
R. O. Banks
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Histidine Decarboxylase ◽  
Reactive Hyperemia ◽  
Constant Infusion ◽  
Base Line ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Control Value

The role of histamine (H) and prostaglandins (PGs) in the renal vasoconstriction prompted by a 10-min intrarenal infusion of norepinephrine (NE, 0.2 micrograms), antidiuretic hormone (ADH, 10 mU), or angiotensin II (ANG II, 0.05 micrograms) was evaluated in anesthetized dogs (amounts are per min per kg). Renal blood flow (RBF, flow probe) decreased four- to fivefold during the 1st min of infusion with each agonist but then gradually returned toward base line. This “escape” was greatest with ADH, less with NE, and small with ANG II. There was a postinfusion reactive hyperemia (RH) only after NE; NE-RH was 4.26 +/- 0.75 (SE) ml/g. Meclofenamate (MFA) reduced NE-RH to 60 +/- 11% of control and decreased NE escape. The H1-receptor antagonist, chlorpheniramine (CP), decreased NE-RH to 24 +/- 5% of control and reduced NE escape. MFA slowed, but did not block, ADH escape and had little effect on ANG II escape. CP did not affect ADH or ANG II escape. The histidine decarboxylase inhibitor, p-toluenesulfonohydrazine, did not affect NE escape but decreased NE-RH to 22 +/- 6% of control. Bolus injections of ADH during a constant infusion of the hormone were not vasoactive, indicating a tachyphylaxis-like phenomenon; this was not found with ANG II or NE. Finally, the excretion of histamine-like material increased from a control value of 0.69 +/- 0.08 to 1.28 +/- 0.28 micrograms/min during NE-RH. These results indicate that NE releases histamine and PGs from the kidney and that PGs account, primarily, for NE escape, whereas histamine accounts, primarily, for NE-RH.

Voltage-dependent K+ channels regulate the duration of reactive hyperemia in the canine coronary circulation

2008 ◽  
Vol 294 (5) ◽  
pp. H2371-H2381 ◽  
Author(s):  
Gregory M. Dick ◽  
Ian N. Bratz ◽  
Léna Borbouse ◽  
Gregory A. Payne ◽  
Ü. Deniz Dincer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Channel Blocker ◽  
Myocardial Metabolism ◽  
Reactive Hyperemia ◽  
No Donor ◽  
Voltage Dependent ◽  
Hyperemic Flow

We previously demonstrated a role for voltage-dependent K+ (KV) channels in coronary vasodilation elicited by myocardial metabolism and exogenous H2O2, as responses were attenuated by the KV channel blocker 4-aminopyridine (4-AP). Here we tested the hypothesis that KV channels participate in coronary reactive hyperemia and examined the role of KV channels in responses to nitric oxide (NO) and adenosine, two putative mediators. Reactive hyperemia (30-s occlusion) was measured in open-chest dogs before and during 4-AP treatment [intracoronary (ic), plasma concentration 0.3 mM]. 4-AP reduced baseline flow 34 ± 5% and inhibited hyperemic volume 32 ± 5%. Administration of 8-phenyltheophylline (8-PT; 0.3 mM ic or 5 mg/kg iv) or NG-nitro-l-arginine methyl ester (l-NAME; 1 mg/min ic) inhibited early and late portions of hyperemic flow, supporting roles for adenosine and NO. 4-AP further inhibited hyperemia in the presence of 8-PT or l-NAME. Adenosine-induced blood flow responses were attenuated by 4-AP (52 ± 6% block at 9 μg/min). Dilation of arterioles to adenosine was attenuated by 0.3 mM 4-AP and 1 μM correolide, a selective KV1 antagonist (76 ± 7% and 47 ± 2% block, respectively, at 1 μM). Dilation in response to sodium nitroprusside, an NO donor, was attenuated by 4-AP in vivo (41 ± 6% block at 10 μg/min) and by correolide in vitro (29 ± 4% block at 1 μM). KV current in smooth muscle cells was inhibited by 4-AP (IC50 1.1 ± 0.1 mM) and virtually eliminated by correolide. Expression of mRNA for KV1 family members was detected in coronary arteries. Our data indicate that KV channels play an important role in regulating resting coronary blood flow, determining duration of reactive hyperemia, and mediating adenosine- and NO-induced vasodilation.

Sign in / Sign up

Export Citation Format

Share Document