Role of endothelium in reactive dilation of skeletal muscle arterioles

1990 ◽  
Vol 259 (5) ◽  
pp. H1313-H1316 ◽  
Author(s):  
A. Koller ◽  
G. Kaley
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cremaster Muscle ◽  
Anesthetized Rats ◽  
Vasoactive Factors ◽  
Peak Increase ◽  
Arteriolar Diameter

In cremaster muscle of pentobarbital-anesthetized rats, the role of endothelium in the reactive dilation of an arteriole (mean control diameter: 18.2 +/- 0.5 microns) during and after short (approximately 20 s) or long (approximately 80 s) occlusion of a parent arteriole was investigated. Distal to the occluder, arteriolar diameter increased during the occlusion (mean peak increase: 6.9 +/- 0.4 and 6.7 +/- 1.1 microns, respectively) and increased even further after the release of the occlusion as blood flow was reestablished (additional mean increase: 6.5 +/- 0.7 and 5.8 +/- 0.8 microns, respectively). The duration of arteriolar dilation after the release of the occlusion was dependent on the duration of occlusion (252.2 +/- 37 vs. 411.3 +/- 57 s; P less than 0.05). After impairment of the arteriolar endothelium by light/dye treatment, a dilation was still present during both the shorter and longer occlusions (mean increase: 4.73 +/- 1.4 and 4.73 +/- 1.3 microns, respectively); however, in both cases the additional dilation after release of the occlusion was greatly diminished. The duration of reactive arteriolar responses following impairment of the endothelium was significantly reduced only on release of the shorter occlusions. The results suggest that reactive dilation (hyperemia) of arterioles is the result of multiple, endothelium-dependent and endothelium-independent vasoactive factors.

Endothelial regulation of wall shear stress and blood flow in skeletal muscle microcirculation

1991 ◽  
Vol 260 (3) ◽  
pp. H862-H868 ◽  
Author(s):  
A. Koller ◽  
G. Kaley
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Flow Velocity ◽  
Cremaster Muscle ◽  
Skeletal Muscle Microcirculation ◽  
Wall Shear ◽  
Arteriolar Diameter ◽  
Dependent Mechanism

In the presence of intact endothelium, in control conditions, calculated wall shear rate (WSR) (means +/- SE: 2,658 +/- 123 s-1; n = 21) was independent of arteriolar diameter (16.2-27.2 microns; correlation coefficient: r = 0.12, P greater than 0.05) in cremaster muscle of pentobarbital-anesthetized rats. An increase in blood flow velocity (due to parallel arteriolar occlusion) elicited a significant increase in WSR (to 4,981 +/- 253 s-1) followed by a delayed (6-15 s) increase in diameter (from: 22.5 +/- 0.6 to 29.5 +/- 0.8 microns), which consequently resulted in a significant decrease in WSR (to 3,879 +/- 203 s-1). As a result of the increased flow velocity and dilation, calculated arteriolar blood flow increased by 230%. After impairment of the endothelium of arterioles by a light-dye technique, basal WSR became significantly higher (3,604 +/- 341 s-1), and despite a greater increase in WSR (10,360 +/- 1,471 s-1) the dilation was absent. Now an inverse linear correlation was found between arteriolar diameter and WSR both before (r = 0.58, P less than 0.05) and during increased flow velocity conditions (r = 0.85, P less than 0.05). Also, arteriolar blood flow that was already less after impairment of endothelium increased by only 66% during the period of increased flow velocity due to the absence of dilation. Results suggest that an increase in wall shear stress is the stimulus for the endothelium-dependent mechanism that elicits "flow dependent" arteriolar dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0150882 ◽  
Author(s):  
Jie Song ◽  
Mamoru Tanida ◽  
Toshishige Shibamoto ◽  
Tao Zhang ◽  
Mofei Wang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Sympathetic Nerves ◽  
Anesthetized Rats

Contribution of adenosine to arteriolar autoregulation in striated muscle

1983 ◽  
Vol 244 (4) ◽  
pp. H567-H576 ◽  
Author(s):  
R. J. Morff ◽  
H. J. Granger
Keyword(s):  
Blood Flow ◽  
Striated Muscle ◽  
Perfusion Pressure ◽  
Cremaster Muscle ◽  
Sprague Dawley ◽  
Red Blood Cell Velocity ◽  
Myogenic Factors ◽  
Bath Medium ◽  
Arteriolar Diameter

The contribution of adenosine to blood flow autoregulation in striated muscle was evaluated by direct in vivo visualization of arterioles in the rat cremaster muscle. Male Sprague-Dawley rats were anesthetized with pentobarbital sodium, and the cremaster muscle was surgically exposed and maintained in a controlled tissue bath environment with pH 7.40, CO2 tension (PCO2) congruent to 40 mmHg, and O2 tension (PO2) at either a high (congruent to 70 mmHg) or a low (congruent to 10 mmHg) value. Local adenosine activity was blocked in some animals by the addition of theophylline (3 X 10(-5) M) to the bath medium. Individual second (2A)- and third (3A)-order arterioles were observed via closed-circuit television microscopy, and blood flow in each arteriole was calculated from simultaneous measurements of arteriolar diameter and red blood cell velocity. Perfusion pressure to the animal's hindquarters was altered by varying the degree of occlusion of the sacral aorta; arteriolar diameter, velocity, and blood flow responses were plotted as a function of the varying pressure. Both 2A and 3A arterioles exhibited vasodilation and substantial superregulation of blood flow (increased blood flow with decreased perfusion pressure) when bath PO2 was low and adenosine activity was not blocked. Addition of theophylline to the cremaster bath medium significantly reduced the dilation and abolished superregulation, although substantial autoregulation remained. When bath PO2 was high, the degree of arteriolar dilation and autoregulation was reduced compared with the low bath PO2 responses, and blocking adenosine activity had no effect on the responses. These results support the concept that changes in local adenosine levels are involved in the autoregulatory responses observed in the rat cremaster muscle and that the magnitude of adenosine's contribution is directly related to the degree of tissue hypoxia. However, blocking adenosine activity did not totally abolish autoregulation, suggesting that other metabolic and/or myogenic factors may also be contributing to blood flow regulation in this tissue.

Microvascular response to blockade of prostaglandin synthesis in rat skeletal muscle

1982 ◽  
Vol 243 (1) ◽  
pp. H51-H60 ◽  
Author(s):  
J. E. Faber ◽  
P. D. Harris ◽  
I. G. Joshua
Keyword(s):  
Skeletal Muscle ◽  
Cremaster Muscle ◽  
Local Blood Flow ◽  
Local Inhibition ◽  
Microvascular Response ◽  
Before And After ◽  
Endogenous Prostaglandins ◽  
The Moment ◽  
Arteriolar Tone ◽  
Arteriolar Diameter

The contribution of endogenous prostaglandins (PGs) to the control of arteriolar diameter in the microcirculation is incompletely defied and has only been studied in drug-anesthetized animals. To test the possibility that endogenous PGs are tonically released to exert a net dilator influence at certain levels in the microcirculation, television microscopy was used to quantitate the arteriolar responses in the rat cremaster muscle to local blockade of PG synthesis with indomethacin. Rats were decerebrated by a midcollicular transection and were allowed to recover from surgical anesthesia. The cremaster muscle with intact circulation and innervation was suspended by sutures in a temperature-controlled Krebs bath. Diameters, vasomotion frequency, and vasomotion amplitude of arterioles at several anatomic levels were measured before and after local inhibition of PG synthesis in the presence and absence of alpha-adrenergic receptor blockade. Inhibition of PG synthesis produced marked constriction (42-66% of control) at all arteriolar levels, with greater responses occurring in the smaller arterioles. PG synthesis blockade increased vasomotion frequency in arterioles that exhibited spontaneous vasomotion during control periods, and blockade induced vasomotion in vessels lacking spontaneous vasomotion. Pretreatment with phentolamine significantly attenuated the constriction and augmentation of vasomotion. These data indicate that dilator PGs participate in the moment-to-moment regulation of arteriolar tone and local blood flow in skeletal muscle. Further, their mechanism of action may involve alterations in neuronal norepinephrine release or alpha-receptor sensitivity.

Prostaglandins mediate skeletal muscle arteriole dilation in hyperdynamic bacteremia

1990 ◽  
Vol 259 (3) ◽  
pp. H728-H734
Author(s):  
H. G. Cryer ◽  
R. N. Garrison ◽  
P. D. Harris ◽  
B. H. Greenwald ◽  
N. L. Alsip
Keyword(s):  
Skeletal Muscle ◽  
Topical Application ◽  
Serotonin Receptors ◽  
Cremaster Muscle ◽  
Synthesis Inhibitor ◽  
E Coli ◽  
Decerebrate Rat ◽  
Prostaglandin Synthesis Inhibitor ◽  
Baseline Values

Live Escherichia coli bacteremia during the high cardiac output (hyperdynamic) phase of sepsis causes constriction of large arterioles but dilation of small arterioles in skeletal muscle. This study examines the role of dilator prostaglandins, serotonin, and histamine in these differential microvascular responses in the decerebrate rat that avoids the effects of drug anesthesia. Topical application of meclofenamate, a prostaglandin synthesis inhibitor, to the cremaster muscle 60 min after induction of E. coli bacteremia enhanced the constriction of large arterioles from 20 +/- 8 to 46 +/- 9% less than baseline and blunted the dilation of small arterioles from 39 +/- 9 to 17 +/- 7% above baseline values in the cremaster microcirculation. Induction of E. coli bacteremia after pretreatment of the cremaster with meclofenamate constricted large arterioles to 40 +/- 4% less than baseline and small arterioles to 31 +/- 4% less than baseline. This indicates that prostaglandins initiate small arteriole dilation in response to E. coli, but some other dilator factor is activated by prostaglandins to maintain small arteriole dilation during E. coli bacteremia. Topical application of cyproheptadine, an antagonist of both histamine and serotonin receptors, to the cremaster muscle did not alter the E. coli-induced constriction of large arterioles or the dilation of small arterioles in the cremaster microcirculation.

Endothelium regulates skeletal muscle microcirculation by a blood flow velocity-sensing mechanism

1990 ◽  
Vol 258 (3) ◽  
pp. H916-H920 ◽  
Author(s):  
A. Koller ◽  
G. Kaley
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Flow Velocity ◽  
Cremaster Muscle ◽  
Positive Linear Correlation ◽  
Skeletal Muscle Microcirculation ◽  
Per Se ◽  
Dependent Flow

In rat cremaster muscle, utilizing parallel arteriolar occlusion, we found that an increase in red blood cell (RBC) velocity (3.5-26.5 mm/s) per se induced an increase in diameter (1.5-9.4 microns) of arterioles (mean control diam 21.5 +/- 0.6 microns; n = 25). The dilation of arterioles appeared only when RBC velocity increased and started always with a delay (mean 8.4 +/- 0.5 s) after the increase in flow velocity. A positive linear correlation was found between peak changes in RBC velocity and diameter (r = 0.87, P less than 0.05). The velocity sensor as well as the mechanism(s) that mediates this response is likely to be located in endothelial cells, because the dilation to increased RBC velocity was completely eliminated after impairment of arteriolar endothelium with light-dye (L-D) treatment. The in vivo demonstration of this phenomenon in arterioles suggests the existence of a new endothelium-dependent, flow velocity-sensitive mechanism for the regulation of blood flow in the microcirculation.

Effect of oxygen on blood flow autoregulation in cat sartorius muscle

1981 ◽  
Vol 241 (6) ◽  
pp. H807-H815 ◽  
Author(s):  
S. M. Sullivan ◽  
P. C. Johnson
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Important Determinant ◽  
Flow Regulation ◽  
Sartorius Muscle ◽  
Gas Mixture ◽  
Pressure Reduction ◽  
Effect Of Oxygen ◽  
Arteriolar Diameter

To assess the role of O2 in blood flow autoregulation, arteriolar diameter and erythrocyte velocity were measured in individual microvessels of the cat sartorius muscle while ambient O2 tension (PO2) and perfusion pressure were altered. The muscle surface was covered with a layer of silicone fluid equilibrated with a gas mixture containing 0—20% O2. Under control conditions (0% O2) all except the largest arterioles dilated with pressure reduction, and all showed significant blood flow autoregulation. Elevated PO2 diminished flow regulation and dilation in large and small arterioles when arterial pressure was reduced. This effect was generally more pronounced in the small arterioles where elevated PO2 caused complete cessation of blood flow. Complete blood flow stoppage was not routinely seen in larger vessels and may reflect the fact that these vessels also supply deeper tissue regions less affected by the change in ambient PO2. Our results indicate that the PO2 level of the tissue may be an important determinant in blood flow autoregulation.

Age-related changes in regional blood flow in the rat

1985 ◽  
Vol 249 (3) ◽  
pp. H485-H491 ◽  
Author(s):  
R. F. Tuma ◽  
G. L. Irion ◽  
U. S. Vasthare ◽  
L. A. Heinel
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Index ◽  
Regional Blood Flow ◽  
Adult Rats ◽  
Blood Flows ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Regional Blood Flows ◽  
Central Hemodynamic

The purpose of this investigation was to characterize the changes in regional blood flow and central hemodynamic measures that occur in the rat as a result of the aging process. The isotope-labeled microsphere technique was used to measure cardiac output and regional blood flows in conscious and anesthetized adult (12 mo) and senescent (24 mo) Fischer 344 virgin female rats. No significant changes were observed in central hemodynamic measurements or regional blood flows in conscious rats with the exception of a 25% reduction in splenic blood flow. Pentobarbital anesthesia significantly reduced cardiac index and heart rate but elevated total peripheral resistance and mean arterial blood pressure. There was a decrease in blood flow to skeletal muscle, spleen, duodenum, stomach, and brain tissue samples and increased hepatic arterial blood flow in both age groups. The use of anesthesia caused a greater reduction in the cardiac index and brain blood flow in the senescent anesthetized rats than in the adult rats. Heart and kidney blood flows were decreased by anesthesia in the senescent rats but not in the adult rats. Skeletal muscle blood flow, however, was significantly greater in the senescent anesthetized rats than in the younger anesthetized animals. Although body weight and organ weights of the liver, spleen, kidneys, stomach, heart, and brain were significantly greater for the senescent rats, no differences could be demonstrated in tibial length or lean body mass.

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