scholarly journals Erythrocyte and the Regulation of Human Skeletal Muscle Blood Flow and Oxygen Delivery

2002 ◽  
Vol 91 (11) ◽  
pp. 1046-1055 ◽  
Author(s):  
José González-Alonso ◽  
David B. Olsen ◽  
Bengt Saltin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Delivery ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow

scholarly journals Erythrocytes and the regulation of human skeletal muscle blood flow and oxygen delivery: role of erythrocyte count and oxygenation state of haemoglobin

2006 ◽  
Vol 572 (1) ◽  
pp. 295-305 ◽  
Author(s):  
José González-Alonso ◽  
Stefan P. Mortensen ◽  
Ellen A. Dawson ◽  
Niels H. Secher ◽  
Rasmus Damsgaard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Delivery ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Erythrocyte Count ◽  
Skeletal Muscle Blood Flow

scholarly journals Local, but not indirect whole body heating, increases human skeletal muscle blood flow

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Illka Heinonen ◽  
R. Matthew Brothers ◽  
Jukka Kemppainen ◽  
Juhani Knuuti ◽  
Kari K. Kalliokoski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Skeletal Muscle Blood Flow

scholarly journals Combined inhibition of nitric oxide and prostaglandins reduces human skeletal muscle blood flow during exercise

2002 ◽  
Vol 543 (2) ◽  
pp. 691-698 ◽  
Author(s):  
Robert Boushel ◽  
Henning Langberg ◽  
Carsten Gemmer ◽  
Jens Olesen ◽  
Regina Crameri ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow

scholarly journals Erythrocyte-dependent regulation of human skeletal muscle blood flow: role of varied oxyhemoglobin and exercise on nitrite, S-nitrosohemoglobin, and ATP

2010 ◽  
Vol 299 (6) ◽  
pp. H1936-H1946 ◽  
Author(s):  
Stéphane P. Dufour ◽  
Rakesh P. Patel ◽  
Angela Brandon ◽  
Xinjun Teng ◽  
James Pearson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Tissue Perfusion ◽  
Hypoxic Stress ◽  
Skeletal Muscle Blood Flow ◽  
Plasma Nitrite

The erythrocyte is proposed to play a key role in the control of local tissue perfusion via three O2-dependent signaling mechanisms: 1) reduction of circulating nitrite to vasoactive NO, 2) S-nitrosohemoglobin (SNO-Hb)-dependent vasodilatation, and 3) release of the vasodilator and sympatholytic ATP; however, their relative roles in vivo remain unclear. Here we evaluated each mechanism to gain insight into their roles in the regulation of human skeletal muscle blood flow during hypoxia and hyperoxia at rest and during exercise. Arterial and femoral venous hemoglobin O2 saturation (O2Hb), plasma and erythrocyte NO and ATP metabolites, and leg and systemic hemodynamics were measured in 10 healthy males exposed to graded hypoxia, normoxia, and graded hyperoxia both at rest and during submaximal one-legged knee-extensor exercise. At rest, leg blood flow and NO and ATP metabolites in plasma and erythrocytes remained unchanged despite large alterations in O2Hb. During exercise, however, leg and systemic perfusion and vascular conductance increased in direct proportion to decreases in arterial and venous O2Hb ( r2 = 0.86–0.98; P = 0.01), decreases in venous plasma nitrite ( r2 = 0.93; P < 0.01), increases in venous erythrocyte nitroso species ( r2 = 0.74; P < 0.05), and to a lesser extent increases in erythrocyte SNO ( r2 = 0.59; P = 0.07). No relationship was observed with plasma ATP ( r2 = 0.01; P = 0.99) or its degradation compounds. These in vivo data indicate that, during low-intensity exercise and hypoxic stress, but not hypoxic stress alone, plasma nitrite consumption and formation of erythrocyte nitroso species are associated with limb vasodilatation and increased blood flow in the human skeletal muscle vasculature.

scholarly journals Sodium nitroprusside increases human skeletal muscle blood flow, but does not change flow distribution or glucose uptake

1999 ◽  
Vol 521 (3) ◽  
pp. 729-737 ◽  
Author(s):  
Olli-Pekka Pitkänen ◽  
Hanna Laine ◽  
Jukka Kemppainen ◽  
Esa Eronen ◽  
Anu Alanen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Glucose Uptake ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Flow Distribution ◽  
Skeletal Muscle Blood Flow

Biphasic effect of hydrogen peroxide on skeletal muscle arteriolar tone via activation of endothelial and smooth muscle signaling pathways

2004 ◽  
Vol 97 (3) ◽  
pp. 1130-1137 ◽  
Author(s):  
Csongor Csekő ◽  
Zsolt Bagi ◽  
Akos Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Hydrogen Peroxide ◽  
Blood Flow ◽  
Smooth Muscle ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Local Regulation ◽  
Prostaglandin H ◽  
Arteriolar Tone

We hypothesized that hydrogen peroxide (H2O2) has a role in the local regulation of skeletal muscle blood flow, thus significantly affecting the myogenic tone of arterioles. In our study, we investigated the effects of exogenous H2O2 on the diameter of isolated, pressurized (at 80 mmHg) rat gracilis skeletal muscle arterioles (diameter of ∼150 μm). Lower concentrations of H2O2 (10−6–3 × 10−5 M) elicited constrictions, whereas higher concentrations of H2O2 (6 × 10−5–3 × 10−4 M), after initial constrictions, caused dilations of arterioles (at 10−4 M H2O2, −19 ± 1% constriction and 66 ± 4% dilation). Endothelium removal reduced both constrictions (to −10 ± 1%) and dilations (to 33 ± 3%) due to H2O2. Constrictions due to H2O2 were completely abolished by indomethacin and the prostaglandin H2/thromboxane A2 (PGH2/TxA2) receptor antagonist SQ-29548. Dilations due to H2O2 were significantly reduced by inhibition of nitric oxide synthase (to 38 ± 7%) but were unaffected by clotrimazole or sulfaphenazole (inhibitors of cytochrome P-450 enzymes), indomethacin, or SQ-29548. In endothelium-denuded arterioles, clotrimazole had no effect, whereas H2O2-induced dilations were significantly reduced by charybdotoxin plus apamin, inhibitors of Ca2+-activated K+ channels (to 24 ± 3%), the selective blocker of ATP-sensitive K+ channels glybenclamide (to 14 ± 2%), and the nonselective K+-channel inhibitor tetrabutylammonium (to −1 ± 1%). Thus exogenous administration of H2O2 elicits 1) release of PGH2/TxA2 from both endothelium and smooth muscle, 2) release of nitric oxide from the endothelium, and 3) activation of K+ channels, such as Ca2+-activated and ATP-sensitive K+ channels in the smooth muscle resulting in biphasic changes of arteriolar diameter. Because H2O2 at low micromolar concentrations activates several intrinsic mechanisms, we suggest that H2O2 contributes to the local regulation of skeletal muscle blood flow in various physiological and pathophysiological conditions.

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