Skeletal Muscle Microcirculation and Changes in Transmural and Perfusion Pressure

2015 ◽  
pp. 93-108 ◽  
Author(s):  
G. J. Tangelder ◽  
D. W. Slaaf ◽  
R. S. Reneman
Keyword(s):  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Skeletal Muscle Microcirculation

Pulsatile Pressure and Flow in the Skeletal Muscle Microcirculation

1990 ◽  
Vol 112 (4) ◽  
pp. 437-443 ◽  
Author(s):  
Shou-Yan Lee ◽  
G. W. Schmid-Scho¨nbein
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Time Dependent ◽  
Physiological Importance ◽  
Pulsatile Pressure ◽  
Theoretical Predictions ◽  
Skeletal Muscle Microcirculation

Although blood flow in the microcirculation of the rat skeletal muscle has negligible inertia forces with very low Reynolds number and Womersley parameter, time-dependent pressure and flow variations can be observed. Such phenomena include, for example, arterial flow overshoot following a step arterial pressure, a gradual arterial pressure reduction for a step flow, or hysteresis between pressure and flow when a pulsatile pressure is applied. Arterial and venous flows do not follow the same time course during such transients. A theoretical analysis is presented for these phenomena using a microvessel with distensible viscoelastic walls and purely viscous flow subject to time variant arterial pressures. The results indicate that the vessel distensibility plays an important role in such time-dependent microvascular flow and the effects are of central physiological importance during normal muscle perfusion. In-vivo whole organ pressure-flow data in the dilated rat gracilis muscle agree in the time course with the theoretical predictions. Hemodynamic impedances of the skeletal muscle microcirculation are investigated for small arterial and venous pressure amplitudes superimposed on an initial steady flow and pressure drop along the vessel.

Coordinated diameter oscillations at arteriolar bifurcations in skeletal muscle

1987 ◽  
Vol 253 (3) ◽  
pp. H568-H573 ◽  
Author(s):  
J. U. Meyer ◽  
L. Lindbom ◽  
M. Intaglietta
Keyword(s):  
Skeletal Muscle ◽  
Fundamental Frequency ◽  
Narrow Band ◽  
Photometric System ◽  
Band Frequency ◽  
Skeletal Muscle Microcirculation

The spontaneous rhythmical luminal changes (vasomotion) at bifurcations in the microvasculature of the rabbit tenuissimus muscle were investigated by means of a microscope video photometric system. Video scenes, containing two terminal arterioles originating from one transverse arteriole, showed that adjacent terminal arterioles constricted synchronously in 26 out of 31 contraction cycles. The onset of 60 constrictions in the parent transverse vessels was synchronized with the activity in terminal arterioles in 75% of the cycles and delayed in 25%. Vasomotion in the parent transverse vessels was notably smaller than in the terminal vessels. All the terminal arterioles in the different animals oscillated at the fundamental frequency of 18.9 +/- 3.5 cycles/min. We conclude that in the skeletal muscle microcirculation 1) coordinated spontaneous diameter oscillations occur in arterioles that are in proximity, 2) diameter changes are most pronounced in the terminal arterioles, and 3) coordinated vasomotion in this tissue exhibits a characteristic narrow band frequency. The presence of a microvascular pacemaker is hypothesized.

scholarly journals Aerobic Exercise Attenuates Pressure Overload-Induced Cardiac Dysfunction through Promoting Skeletal Muscle Microcirculation and Increasing Muscle Mass

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Ling-Yan Yuan ◽  
Pei-Zhao Du ◽  
Min-Min Wei ◽  
Qi Zhang ◽  
Le Lu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Function ◽  
Aerobic Exercise ◽  
Muscle Mass ◽  
Cardiac Dysfunction ◽  
Pressure Overload ◽  
Transverse Aortic Constriction ◽  
Aortic Constriction ◽  
Protein Levels ◽  
Skeletal Muscle Microcirculation

Background. Aerobic exercise has been proven to have a positive effect on cardiac function after hypertension; however, the mechanism is not entirely clarified. Skeletal muscle mass and microcirculation are closely associated with blood pressure and cardiac function. Objective. This study was designed to investigate the effects of aerobic exercise on the skeletal muscle capillary and muscle mass, to explore the possible mechanisms involved in exercise-induced mitigation of cardiac dysfunction in pressure overload mice. Methods. In this study, 60 BALB/C mice aged 8 weeks were randomly divided into 3 groups: control (CON), TAC, and TAC plus exercise (TAE) group and utilized transverse aortic constriction (TAC) to establish hypertensive model; meanwhile, treadmill training is used for aerobic exercise. After 5 days of recovery, mice in the TAE group were subjected to 10-week aerobic exercise. Carotid pressure and cardiac function were examined before mice were executed by Millar catheter and ultrasound, respectively. Muscle mass of gastrocnemius was weighed; cross-sectional area and the number of capillaries of gastrocnemius were detected by HE and immunohistochemistry, respectively. The mRNA and protein levels of VEGF in skeletal muscle were determined by RT-PCR and western blot, respectively. Results. We found that ① 10-week aerobic exercise counteracted hypertension and attenuated cardiac dysfunction in TAC-induced hypertensive mice; ② TAC decreased muscle mass of gastrocnemius and resulted in muscle atrophy, while 10-week aerobic exercise could reserve transverse aortic constriction-induced the decline of muscle mass and muscle atrophy; and ③ TAC reduced the number of capillaries and the protein level of VEGF in gastrocnemius, whereas 10-week aerobic exercise augmented the number of capillaries, the mRNA and protein levels of VEGF in mice were subjected to TAC surgery. Conclusions. This study indicates that 10-week aerobic exercise might fulfill its blood pressure-lowering effect via improving skeletal muscle microcirculation and increasing muscle mass.

scholarly journals Impaired skeletal muscle microcirculation in systemic sclerosis

2012 ◽  
Vol 14 (5) ◽  
pp. R209 ◽  
Author(s):  
Sasan Partovi ◽  
Anja-Carina Schulte ◽  
Markus Aschwanden ◽  
Daniel Staub ◽  
Daniela Benz ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Systemic Sclerosis ◽  
Skeletal Muscle Microcirculation

Release of nitric oxide and prostaglandin H2 to acetylcholine in skeletal muscle venules

1997 ◽  
Vol 272 (6) ◽  
pp. H2541-H2546 ◽  
Author(s):  
G. Dornyei ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Thromboxane A2 ◽  
No Synthase ◽  
Gracilis Muscle ◽  
Vasoactive Agents ◽  
Before And After ◽  
Higher Doses

The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (approximately 225 microns in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane A2-prostaglandin H2 (PGH2) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/- 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH2 from the venular endothelium.

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.

Myogenic responses of isolated rat skeletal muscle venules: modulation by norepinephrine and endothelium

1996 ◽  
Vol 271 (1) ◽  
pp. H267-H272 ◽  
Author(s):  
G. Dornyei ◽  
E. Monos ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Skeletal Muscle ◽  
Adrenergic Receptor ◽  
Perfusion Pressure ◽  
Receptor Activation ◽  
Intraluminal Pressure ◽  
Negative Slope ◽  
Internal Diameter ◽  
Myogenic Response ◽  
First Order ◽  
Diameter Curve

The pressure-induced myogenic response of large venules of skeletal muscle and its possible interactions with adrenergic receptor activation and endothelial factors have not yet been elucidated. Therefore, first-order venules of rat gracilis muscle were isolated, cannulated, and placed in an organ chamber. Changes in internal diameter of the vessels as a function of perfusion pressure (PP) were obtained. In response to increases in PP (0.5-17.5 mmHg), the diameter of venules increased from 197.1 +/- 23.96 to 369 +/- 14.1 microns. In passive conditions (in Ca(2+)-free solution), the pressure-diameter curve of venules shifted significantly upward. In the presence of norepinephrine (NE; 10(-6) M) in the bath solution, the pressure-diameter curve of active venules shifted significantly downward, and in the pressure-normalized diameter curve, a negative slope developed (-6.1 +/- 4.6). In both the absence and presence of NE, removal of endothelium significantly reduced venular diameters in the pressure ranges of 3-5 and 2-5 mmHg, respectively, but did not change significantly the characteristics of the pressure-diameter curves. These findings indicate that the smooth muscle of venules actively responds to changes in intraluminal pressure. This response is greatly facilitated by NE and modulated by the endothelium. The myogenic response of skeletal muscle venules, especially in the presence of NE, could have a role in the regulation of the resistance and capacitance of venules and, consequently, blood flow and tissue exchange in skeletal muscle.

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