The Effects of Lidocaine and Adrenergic Agonists on Rat Sciatic Nerve and Skeletal Muscle Blood Flow In Vivo

The role of sympathetic innervation in the regulation of hindlimb skeletal muscle blood flow (QL) and metabolism was studied prior to and during acute anemia in anesthetized, paralyzed, and ventilated dogs (n = 8). Neural activity in the sciatic nerve was reversibly cold blocked for a 15-min period at control hematocrit (Hct., 51%) and again at 30 min of anemia (Hct., 14%). At the end of each experiment the sciatic nerve was transected and maximally stimulated (frequency, 10 Hz; duration, 2.0 ms). Arterial blood pressure and [Formula: see text] were measured continuously; skeletal muscle vascular hindrance (ZL) and oxygen uptake [Formula: see text] were calculated. When the sciatic nerve was cold blocked prior to and during anemia, ZL decreased to the same absolute value and [Formula: see text] remained unchanged. Prior to anemia the mean [Formula: see text] increased (p < 0.05) from 99 to a peak value of 165 mL∙kg−1∙min−1 during cold block; [Formula: see text] had returned to control by 10 min of cooling. During anemia, [Formula: see text] increased (p < 0.05) from 160 to 307 mL∙kg−1∙min−1 during sympathetic cold block, while maximal sympathetic stimulation decreased [Formula: see text] to 87 mL∙kg−1∙min−1. [Formula: see text] remained above (p < 0.05) the anemia control value (160 mL∙kg−1∙min−1) at 10 min of cooling. Hindrance increased from 0.30 to 0.38 peripheral resistance units/centipoise following the induction of anemia and this was shown to be sympathetically mediated because hindrance was decreased to the same level during cold block prior to and during anemia.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00389.2010 ◽

2010 ◽

Vol 299 (6) ◽

pp. H1936-H1946 ◽

Cited By ~ 31

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.

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In vivo evidence of altered skeletal muscle blood flow in chronic tension‐type headache

Brain ◽

10.1093/brain/awf029 ◽

2002 ◽

Vol 125 (2) ◽

pp. 320-326 ◽

Cited By ~ 74

Author(s):

M. Ashina ◽

B. Stallknecht ◽

L. Bendtsen ◽

J. F. Pedersen ◽

H. Galbo ◽

...

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Muscle Blood Flow ◽

Tension Type Headache ◽

Skeletal Muscle Blood Flow ◽

Chronic Tension Type Headache ◽

Type Headache

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Regional measurement of canine skeletal muscle blood flow by positron emission tomography with H2 15O

Journal of Applied Physiology ◽

10.1152/japplphysiol.00445.2001 ◽

2002 ◽

Vol 92 (4) ◽

pp. 1709-1716 ◽

Cited By ~ 14

Author(s):

Alan J. Fischman ◽

Hongbing Hsu ◽

Edward A. Carter ◽

Yong M. Yu ◽

Ronald G. Tompkins ◽

...

Keyword(s):

Skeletal Muscle ◽

Positron Emission Tomography ◽

Blood Flow ◽

Muscle Blood Flow ◽

Emission Tomography ◽

Time Activity ◽

Skeletal Muscle Blood Flow ◽

Arterial Blood ◽

Positron Emission

Positron emission tomography (PET) with H2 15O was used as an in vivo, relatively noninvasive, quantitative method for measuring regional blood flow to hindlimb skeletal muscle of anesthetized dogs. A hydrooccluder positioned on the femoral artery was used to reduce flow, and high-flow states were produced by local infusion of adenosine. Three to four measurements were made in each animal. Approximately 40 mCi of H2 15O were injected intravenously, and serial images and arterial blood samples were acquired over 2.5 min. Data analysis was performed by fitting tissue and arterial blood time-activity curves to a modified, single-compartment Kety model. The model equation was also solved on a pixel-by-pixel basis to yield maps of regional skeletal muscle blood flow. After each PET determination, flow was measured with radioactive microspheres. Results of the PET measurements demonstrated that basal flow to hindlimb skeletal muscle was 3.83 ± 0.36 ml · min−1 · 100 g−1(mean ± SE). This value was in excellent agreement with the microsphere data, 3.73 ± 0.32 ml · min−1 · 100 g−1( P = 0.69, not significant). Adenosine infusion resulted in flows as high as 30 ml · min−1 · 100 g−1, and the PET and microsphere data were highly correlated over the entire range of flows ( r 2 = 0.98, P < 0.0001). We conclude that muscle blood flow can be accurately measured in vivo by PET with H2 15O and that this approach offers promise for application in human studies of muscle metabolism under varying pathophysiological states.

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Effects of Hemodilution on Skeletal Muscle Blood Flow and Blood Viscosity in vivo after Splanchnic Stasis

European Surgical Research ◽

10.1159/000128492 ◽

1985 ◽

Vol 17 (6) ◽

pp. 366-371 ◽

Cited By ~ 4

Author(s):

L. Gustafsson ◽

L. Appelgren ◽

H.E. Myrvolb

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Blood Viscosity ◽

Muscle Blood Flow ◽

Skeletal Muscle Blood Flow

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.00106.2004 ◽

2004 ◽

Vol 97 (3) ◽

pp. 1130-1137 ◽

Cited By ~ 49

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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