Angiogenesis in Skletal Muscle

Physiology ◽  
1986 ◽  
Vol 1 (5) ◽  
pp. 160-163
Author(s):  
HW Burton ◽  
JA Faulkner
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Vasoactive Agents ◽  
Adult Skeletal Muscle ◽  
Capillary Growth ◽  
Vascular Bed ◽  
Chronic Electrical Stimulation ◽  
Capillary Bed ◽  
Ischemic Muscle

Capillary growth is rarely observed in normal adult skeletal muscle, but angiogenesis may occur after injury to a capillary bed or after endurance training or chronic electrical stimulation. Revascularization of ischemic muscle may arise as inward growth from surrounding vascularized tissue, as outward growth from endothelial cells in ischemic muscle, or a combination of the two processes. A regenerated vascular bed shows diminished response to vasoactive agents and impaired regulation of blood flow during contractions.

Capillary growth in relation to blood flow and performance in overloaded rat skeletal muscle

1998 ◽  
Vol 85 (6) ◽  
pp. 2025-2032 ◽  
Author(s):  
S. Egginton ◽  
O. Hudlická ◽  
M. D. Brown ◽  
H. Walter ◽  
J. B. Weiss ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Tibialis Anterior Muscle ◽  
Mechanical Stimulus ◽  
Angiogenic Factor ◽  
Protein Distribution ◽  
Blood Flows ◽  
Capillary Growth ◽  
Capillary Bed ◽  
And Performance

Rat extensor digitorum longus muscles were overloaded by stretch after removal of the synergist tibialis anterior muscle to determine the relationship between capillary growth, muscle blood flow, and presence of growth factors. After 2 wk, sarcomere length increased from 2.4 to 2.9 μm. Capillary-to-fiber ratio, estimated from alkaline phosphatase-stained frozen sections, was increased by 33% ( P < 0.0001) and 60% ( P < 0.01), compared with control muscles (1.44 ± 0.06) after 2 and 8 wk, respectively. At 2 wk, the increased capillary-to-fiber ratio was not associated with any changes in mRNA for basic fibroblast growth factor (FGF-2) or its protein distribution. FGF-2 immunoreactivity was present in nerves and large blood vessels but was negative in capillaries, whereas the activity of low-molecular endothelial-cell-stimulating angiogenic factor (ESAF) was 50% higher in stretched muscles. Muscle blood flows measured by radiolabeled microspheres during contractions were not significantly different after 2 or 8 wk (132 ± 37 and 177 ± 22 ml ⋅ min−1 ⋅ 100 g−1, respectively) from weight-matched controls (156 ± 12 and 150 ± 10 ml ⋅ min−1 ⋅ 100 g−1, respectively). Resistance to fatigue during 5-min isometric contractions (final/peak tension × 100) was similar in 2-wk overloaded and contralateral muscles (85 vs. 80%) and enhanced after 8 wk to 92%, compared with 77% in contralateral muscles and 67% in controls. We conclude that increased blood flow cannot be responsible for initiating expansion of the capillary bed, nor does it explain the reduced fatigue within overloaded muscles. However, stretch can present a mechanical stimulus to capillary growth, acting either directly on the capillary abluminal surface or by upregulating ESAF, but not FGF-2, in the extracellular matrix.

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.

Carbohydrate ingestion, with transient endogenous insulinaemia, produces both sympathetic activation and vasodilatation in normal humans

2002 ◽  
Vol 102 (5) ◽  
pp. 523-529 ◽  
Author(s):  
Eleanor M. SCOTT ◽  
John P. GREENWOOD ◽  
Giovanni VACCA ◽  
John B. STOKER ◽  
Stephen G. GILBEY ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Sympathetic Activity ◽  
Healthy Subjects ◽  
Muscle Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Carbohydrate Ingestion ◽  
Vascular Bed ◽  
Carbohydrate Meal

It has been shown that sustained insulin infusion causes an increase in sympathetic vasoconstrictor discharge but, despite this, also causes peripheral vasodilatation. The present study was designed to determine in healthy subjects the effect of ingestion of a carbohydrate meal, with its attendant physiological insulinaemia, on vascular resistance in and sympathetic vasoconstrictor discharge to the same vascular bed, and the relationship between these parameters. Fifteen healthy subjects were studied for 2h following ingestion of a carbohydrate meal. Calf vascular resistance was measured by venous occlusion plethysmography, and muscle sympathetic nerve activity was assessed by peroneal microneurography. Five of the subjects also ingested water on a separate occasion, as a control. Following the carbohydrate meal, the serum insulin concentration increased to 588±72pmol/l. This was associated with a 47% increase in skeletal muscle blood flow (P < 0.001), a 39% fall in vascular resistance (P < 0.001) and a 57% increase in sympathetic activity (P < 0.001). There was a significant correlation between the increase in insulin and the changes in blood flow, vascular resistance and sympathetic activity. In conclusion, we have shown that ingestion of a carbohydrate meal, with its attendant physiological insulinaemia, was associated with overriding skeletal muscle vasodilatation, despite an increase in sympathetic vasoconstrictor discharge to the same vascular bed. These mechanisms may be important in ensuring optimal glucose uptake and maintenance of blood pressure postprandially.

scholarly journals Muscle metaboreflex-induced vasoconstriction in the ischemic active muscle is exaggerated in heart failure

2018 ◽  
Vol 314 (1) ◽  
pp. H11-H18 ◽  
Author(s):  
Jasdeep Kaur ◽  
Danielle Senador ◽  
Abhinav C. Krishnan ◽  
Hanna W. Hanna ◽  
Alberto Alvarez ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Exercise Intolerance ◽  
Adrenergic Blockade ◽  
Active Muscle ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Ischemic Muscle

When oxygen delivery to active muscle is insufficient to meet the metabolic demand during exercise, metabolites accumulate and stimulate skeletal muscle afferents, inducing a reflex increase in blood pressure, termed the muscle metaboreflex. In healthy individuals, muscle metaboreflex activation (MMA) during submaximal exercise increases arterial pressure primarily via an increase in cardiac output (CO), as little peripheral vasoconstriction occurs. This increase in CO partially restores blood flow to ischemic muscle. However, we recently demonstrated that MMA induces sympathetic vasoconstriction in ischemic active muscle, limiting the ability of the metaboreflex to restore blood flow. In heart failure (HF), increases in CO are limited, and metaboreflex-induced pressor responses occur predominantly via peripheral vasoconstriction. In the present study, we tested the hypothesis that vasoconstriction of ischemic active muscle is exaggerated in HF. Changes in hindlimb vascular resistance [femoral arterial pressure ÷ hindlimb blood flow (HLBF)] were observed during MMA (via graded reductions in HLBF) during mild exercise with and without α1-adrenergic blockade (prazosin, 50 µg/kg) before and after induction of HF. In normal animals, initial HLBF reductions caused metabolic vasodilation, while reductions below the metaboreflex threshold elicited reflex vasoconstriction, in ischemic active skeletal muscle, which was abolished after α1-adrenergic blockade. Metaboreflex-induced vasoconstriction of ischemic active muscle was exaggerated after induction of HF. This heightened vasoconstriction impairs the ability of the metaboreflex to restore blood flow to ischemic muscle in HF and may contribute to the exercise intolerance observed in these patients. We conclude that sympathetically mediated vasoconstriction of ischemic active muscle during MMA is exaggerated in HF. NEW & NOTEWORTHY We found that muscle metaboreflex-induced vasoconstriction of the ischemic active skeletal muscle from which the reflex originates is exaggerated in heart failure. This results in heightened metaboreflex activation, which further amplifies the reflex-induced vasoconstriction of the ischemic active skeletal muscle and contributes to exercise intolerance in patients.

Regulation of connexin gene expression during skeletal muscle regeneration in the adult rat

2009 ◽  
Vol 296 (3) ◽  
pp. C593-C606 ◽  
Author(s):  
A. Trovato-Salinaro ◽  
N. Belluardo ◽  
M. Frinchi ◽  
J. von Maltzahn ◽  
K. Willecke ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Blood Vessels ◽  
Temporal Analysis ◽  
Skeletal Muscle Regeneration ◽  
Cell Nuclei ◽  
Adult Skeletal Muscle ◽  
Adult Rat ◽  
Connexin Gene ◽  
Spatial And Temporal Analysis

In the adult skeletal muscle, various kinds of trauma promote proliferation of satellite cells that differentiate into myoblasts forming new myofibers or to repair the damaged one. The aim of present work was to perform a comparative spatial and temporal analysis of connexin (Cx) 37, Cx39, Cx40, Cx43, and Cx45 expression in the adult regenerating skeletal muscle in response to crush injury. Within 24 h from injury, Cx37 expression was upregulated in the endothelial cells of blood vessels, and, 5 days after injury, Cx37-expressing cells were found inside the area of lesion and formed clusters generating new blood vessels with endothelial cells expressing Cx37. Three days after injury, Cx39 mRNA was selectively expressed in myogenin-positive cells, forming rows of closely apposed cell nuclei fusing in myotubes. Cx40 mRNA-labeled cells were observed within 24 h from injury in the endothelium of blood vessels, and, 5 days after lesion, Cx40-labeled cells were found inside the area of lesion-forming rows of myogenin-positive, closely apposed cells coexpressing Cx39. Within 24 h from lesion, both Cx43 and Cx45 mRNAs were upregulated in individual cells, and some of them were positive for M-cadherin. Three days after injury, a large number of both Cx43 and Cx45 mRNA-labeled and myogenin-positive cells were found inside the area of lesion. Taken together, these results show that at least four Cxs, out of five expressed in regenerating skeletal muscle, can be differentially involved in communication of myogenic cells during the process of cell proliferation, aggregation, and fusion to form new myotubes or to repair damaged myofibers.

scholarly journals Muscle-derived Gr1dimCD11b+ cells enhance neovascularization in an ischemic hind limb mouse model

Blood ◽  
2010 ◽  
Vol 116 (9) ◽  
pp. 1623-1626 ◽  
Author(s):  
Jeong A. Kim ◽  
Keith March ◽  
Hee-Don Chae ◽  
Brian Johnstone ◽  
Su-Jung Park ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Mouse Model ◽  
Hind Limb ◽  
Suppressor Cells ◽  
Myeloid Derived Suppressor Cells ◽  
Matrigel Culture ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Ischemic Muscle

Gr1+CD11b+ cells are characterized as myeloid-derived suppressor cells potentially involved in angiogenesis. We demonstrate that Gr1+CD11b+ cells isolated from ischemic muscle in a hind-limb ischemic C57BL/6 mouse model play a role in vessel formation after ischemic injury. Gr1dimCD11b+ cells, a subpopulation of Gr1+CD11b+ cells, within skeletal muscle were increased in context of ischemia. Strikingly, astrocyte-plexus formed from muscle-derived Gr1dimCD11b+ cells in Matrigel culture, followed by formation of isolectin and von Willebrand Factor–expressing cells, similar to that reported for angiogenesis in retina. When isolated muscle-derived Gr1dimCD11b+ cells were injected into ischemic muscles, recovery of blood flow was significantly enhanced and these cells were incorporated into vessel walls. This suggests that Gr1dimCD11b+ cells are recruited into ischemic regions after ischemia and may be involved in angiogenesis by their capacity to generate vascular cells.

Autonomic Control of Blood Flow in Hind Paw of the Dog

1956 ◽  
Vol 187 (3) ◽  
pp. 469-472 ◽  
Author(s):  
Harold D. Green ◽  
William B. Howard ◽  
Leroy F. Kenan
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Femoral Artery ◽  
Electromagnetic Flowmeter ◽  
Minimal Flow ◽  
Sacral Vertebra ◽  
Dorsalis Pedis Artery ◽  
Vascular Bed ◽  
Potent Vasoconstrictor ◽  
Stimulation Of

Blood flow was measured in the hind paw of the dog by directing blood from the femoral artery through an electromagnetic flowmeter and into the dorsalis pedis artery. The system was such that minimal flow was measured in skeletal muscle in the foot. Under the conditions of these experiments, epinephrine and arterenol, injected intra-arterially, exerted potent vasoconstrictor effects, the former being slightly but not significantly more potent than the latter when equimolecular doses were used. Isoproterenol and methacholine caused weak dilator responses. Ischemia did not induce any reactive vasodilation. Stimulation of the sympathetic chain at approximately the level of the first sacral vertebra induced potent vasoconstriction. All constrictor effects were blocked by 10 mg of phenoxybenzamine (Dibenzyline) given intra-arterially without affecting appreciably the dilator responses to either the methacholine or the isoproterenol. It is concluded that this vascular bed contains potent innervated alpha constrictor receptors but but that adrenergic and cholinergic dilator receptors are minimally present. No evidence was obtained for the presence of cholinergic autonomic dilator fibers.

scholarly journals Muscle metaboreflex improves O2delivery to ischemic active skeletal muscle

1999 ◽  
Vol 276 (4) ◽  
pp. H1399-H1403 ◽  
Author(s):  
Donal S. O’Leary ◽  
Robert A. Augustyniak ◽  
Eric J. Ansorge ◽  
Heidi L. Collins
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Pressor Response ◽  
Systemic Arterial Pressure ◽  
Integrative Approach ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Per Se ◽  
Hb Concentration ◽  
Ischemic Muscle

Ischemia of active skeletal muscle elicits a powerful pressor response, termed the muscle metaboreflex. We recently reported that the muscle metaboreflex pressor response acts to partially restore blood flow to the ischemic active skeletal muscle. However, because this reflex is activated by reductions in O2 delivery rather than blood flow per se, gain of the muscle metaboreflex as analyzed on the basis of blood flow alone may underestimate its true strength if this reflex also acts to increase arterial O2content. In conscious dogs chronically instrumented to measure systemic arterial pressure, cardiac output, and hindlimb blood flow, we activated the muscle metaboreflex via graded, partial reductions in hindlimb blood flow during mild (3.2 km/h) and moderate (6.4 km/h, 10% grade) workloads. At rest, during free-flow exercise, and with metaboreflex activation, we analyzed arterial blood samples for Hb concentration and O2 content and compared muscle metaboreflex gain calculations based on the ability to partially restore flow with those based on the ability to partially restore O2 delivery (blood flow × arterial O2 content). During both mild and moderate exercise, metaboreflex activation caused significant increases in arterial Hb concentration and O2 content. Metaboreflex gain quantified on the ability to partially restore O2 delivery was significantly greater than that based on restoration of blood flow during both mild and moderate workloads (0.52 ± 0.10 vs. 0.39 ± 0.08, P < 0.05, and 0.61 ± 0.05 vs. 0.46 ± 0.04, P < 0.05, respectively). We conclude that the muscle metaboreflex acts to increase both arterial O2 content and blood flow to ischemic muscle such that when combined, O2 delivery is substantially increased and metaboreflex gain is greater when analyzed with a more integrative approach.

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