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.

scholarly journals Role of adenosine in coronary blood flow regulation after reductions in perfusion pressure.

1985 ◽  
Vol 56 (4) ◽  
pp. 517-524 ◽  
Author(s):  
W P Dole ◽  
N Yamada ◽  
V S Bishop ◽  
R A Olsson
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Perfusion Pressure ◽  
Flow Regulation ◽  
Blood Flow Regulation

scholarly journals Role of nitric oxide in optic nerve head blood flow regulation while experimental increase of ocular perfusion pressure

2011 ◽  
Vol 11 (Suppl 2) ◽  
pp. A47
Author(s):  
Reinhard Told ◽  
Doreen Schmidl ◽  
Michael Lasta ◽  
Agnes Boltz ◽  
Berthold Pemp ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Optic Nerve ◽  
Optic Nerve Head ◽  
Perfusion Pressure ◽  
Flow Regulation ◽  
Ocular Perfusion Pressure ◽  
Ocular Perfusion ◽  
Blood Flow Regulation

Microvascular pressure in venules of skeletal muscle during arterial pressure reduction

1986 ◽  
Vol 250 (5) ◽  
pp. H838-H845 ◽  
Author(s):  
S. D. House ◽  
P. C. Johnson
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Pressure Gradient ◽  
Pressure Difference ◽  
Reactive Hyperemia ◽  
Sartorius Muscle ◽  
Pressure Reduction ◽  
Large Vein ◽  
The Difference

It has been suggested from whole organ studies that the viscosity of blood in skeletal muscle venules varies inversely with flow over physiological flow ranges. If this is the case, the hydrostatic pressure gradient in venules should change less than flow as flow is altered. To test this hypothesis, pressure in venules of cat sartorius muscle was measured during stepwise arterial pressure reduction to 20 mmHg. Large vein pressure remained constant at about 5 mmHg. Average pressures in the large venules (40–185 microns) ranged from 13.6 to 10.0 mmHg. The difference between pressure in these venules and large vein pressure fell in proportion to the reduction in blood pressure and blood flow. Pressures in the smallest venules studied (25 microns) averaged 19.7 +/- 6.2 (SD) mmHg. The pressure difference between the smallest venules and the large vein fell less than the arteriovenous pressure difference or blood flow when arterial pressure was reduced. During reactive hyperemia the pressure gradient between the smallest venules and the large vein rose proportionately less than blood flow. The stability of pressure in the smallest venules is consistent with the hypothesis that blood viscosity varies inversely with flow rate.

scholarly journals Role of Perfusion Pressure in Major Organ Blood Flow during Cardiopulmonary Bypass in Canines

2000 ◽  
Vol 39 (5) ◽  
pp. 748
Author(s):  
Young Lan Kwak ◽  
Young Hwan Park ◽  
Sang Beom Nam ◽  
Young Jun Oh ◽  
Seung Ho Kim ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Perfusion Pressure ◽  
Organ Blood Flow ◽  
Major Organ

Arteriolar network response to pressure reduction during sympathetic nerve stimulation in cat skeletal muscle

1994 ◽  
Vol 266 (3) ◽  
pp. H1251-H1259 ◽  
Author(s):  
P. Ping ◽  
P. C. Johnson
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Similar Degree ◽  
Sartorius Muscle ◽  
Pressure Reduction ◽  
Third Order ◽  
Sympathetic Nerve Stimulation ◽  
Resistance Change

Previous studies in this laboratory have shown that autoregulation of blood flow and dilation of midsized (second-order) arterioles were significantly enhanced during sympathetic nerve stimulation of cat sartorius muscle apparently because of a greater myogenic response of the arterioles. Quite typically, blood flow increased with arterial pressure reduction to 80, 60, and 40 mmHg (superregulation) during sympathetic nerve stimulation. To determine the contribution of the various orders of arterioles to the enhanced autoregulation, we measured diameters in all orders of arterioles and measured red cell velocity in first-, second-, and third-order arterioles. Without sympathetic nerve stimulation, all orders of arterioles except the first order dilated to pressure reduction, but flow autoregulation was weak. With sympathetic nerve stimulation, arteriolar dilation to pressure reduction was significantly enhanced in all six orders of arterioles, and flow rose significantly. The resistance change in the arteriolar network during pressure reduction as calculated from diameter changes was greatest in third- and fourth-order arterioles. Experimentally determined flow changes to pressure reduction and to sympathetic nerve stimulation were quantitatively similar to those predicted from diameter changes in a model of the arteriolar network. Calculated wall shear stress (from viscosity and shear rate) for first-, second-, and third-order arterioles decreased during pressure reduction with and without sympathetic nerve stimulation. We concluded that endothelium-mediated dilation due to shear stress would tend to oppose autoregulation of blood flow to a similar degree under both circumstances.

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.

Role of Endothelin-1 in Choroidal Blood Flow Regulation during Isometric Exercise in Healthy Humans

2003 ◽  
Vol 44 (2) ◽  
pp. 728 ◽  
Author(s):  
Gabriele Fuchsja¨ger-Mayrl ◽  
Alexandra Luksch ◽  
Magdalena Malec ◽  
Elzbieta Polska ◽  
Michael Wolzt ◽  
...  
Keyword(s):  
Blood Flow ◽  
Isometric Exercise ◽  
Flow Regulation ◽  
Choroidal Blood Flow ◽  
Endothelin 1 ◽  
Healthy Humans ◽  
Blood Flow Regulation

K+ATP channels and adenosine are not necessary for coronary autoregulation

1997 ◽  
Vol 273 (3) ◽  
pp. H1299-H1308 ◽  
Author(s):  
D. W. Stepp ◽  
K. Kroll ◽  
E. O. Feigl
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Left Main Coronary Artery ◽  
Perfusion Pressure ◽  
Carbon Dioxide Tension ◽  
Coronary Pressure ◽  
Adenosine Concentration ◽  
The Face

Autoregulation is defined as the intrinsic ability of an organ to maintain constant flow in the face of changing perfusion pressure. The present study evaluated the role of several potential mediators of coronary autoregulation: interstitial adenosine, ATP-sensitive K+ (K+ATP) channels, and myocardial oxygen and carbon dioxide tensions as reflected by coronary venous oxygen and carbon dioxide tensions. The left main coronary artery was cannulated, and blood was perfused at controlled pressures in closed-chest dogs. Interstitial adenosine concentration was estimated from arterial and venous adenosine concentrations with a previously described mathematical model. Autoregulation of coronary blood flow was observed between 100 and 60 mmHg. Glibenclamide, an inhibitor of K+ATP channels, reduced coronary blood flow by 19% at each perfusion pressure, but autoregulation was preserved. After stepwise reductions in coronary pressure to values > or = 70 mmHg, adenosine concentrations did not increase above basal levels. Adenosine concentration was elevated at 60 mmHg, suggesting a role for adenosine at the limit of coronary autoregulation. Adenosine is not required because glibenclamide, an inhibitor of adenosine-mediated vasodilation, did not reduce autoregulation or increase adenosine concentration. Coronary venous oxygen and carbon dioxide tensions were little changed during autoregulation before the inhibition of K+ATP channels and adenosine vasodilation with glibenclamide. However, coronary venous carbon dioxide tension rose progressively with decreasing coronary pressure after glibenclamide. The increase in carbon dioxide indirectly suggests that carbon dioxide-mediated vasodilation compensated for the loss of K+ATP-channel function. In summary, neither K+ATP channels nor adenosine is necessary to maintain coronary flow in the autoregulatory range of coronary arterial pressure from 100 to 60 mmHg.

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