Microvascular remodeling and accelerated hyperemia blood flow restoration in arterially occluded skeletal muscle exposed to ultrasonic microbubble destruction

2004 ◽  
Vol 287 (6) ◽  
pp. H2754-H2761 ◽  
Author(s):  
Ji Song ◽  
Patrick S. Cottler ◽  
Alexander L. Klibanov ◽  
Sanjiv Kaul ◽  
Richard J. Price
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Occlusion ◽  
Pulsed Ultrasound ◽  
Medial Region ◽  
Lateral Region ◽  
Microvascular Remodeling ◽  
Flow Restoration ◽  
Normal Rat ◽  
Ultrasound Microbubbles

We showed previously that microbubble destruction with pulsed 1-MHz ultrasound creates a bioeffect that stimulates arteriogenesis and a chronic increase in hyperemia blood flow in normal rat muscle. Here we tested whether ultrasonic microbubble destruction can be used to create a microvascular remodeling response that restores hyperemia blood flow to rat skeletal muscle affected by arterial occlusion. Pulsed ultrasound (1 MHz) was applied to gracilis muscles in which the lateral feed artery was occluded but the medial feed artery was left intact. Control muscles were similarly occluded but did not receive ultrasound, microbubbles, or both. Hyperemia blood flow and number of smooth muscle (SM) α-actin-positive vessels, >30-μm arterioles, and capillaries per fiber were determined 7, 14, and 28 days after treatment. In ultrasound-microbubble-treated muscles, lateral region hyperemia blood flow was increased at all time points and restored to normal at day 28. The number of SM α-actin vessels per fiber was increased over control in this region at days 7 and 14 but decreased by day 28, when larger-diameter arterioles became more prevalent in the medial region. The number of capillaries per fiber was increased over control only at day 7 in the lateral region and only at days 7 and 14 in the medial region, indicating that the angiogenesis response was transient and likely did not contribute significantly to flow restoration at day 28. We conclude that ultrasonic microbubble destruction can be tailored to stimulate an arteriogenesis response that restores hyperemia blood flow to skeletal muscle in a rat model of arterial occlusion.

scholarly journals The role of perfusion in the oxygen extraction capability of skin and skeletal muscle

2016 ◽  
Vol 310 (10) ◽  
pp. H1277-H1284 ◽  
Author(s):  
Clare E. Thorn ◽  
Angela C. Shore
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Occlusion ◽  
Flow Regulation ◽  
Reflectance Spectroscopy ◽  
Oxygen Extraction ◽  
Forearm Skin ◽  
Obese Subjects ◽  
The Difference

Oxygen extraction (OE) by all cells is dependent on an adequate supply of oxygen in proximal blood vessels and the cell's need and ability to uptake that oxygen. Here the role of blood flow in regulating OE in skin and skeletal muscle was investigated in lean and obese men. OE was derived by two optical reflectance spectroscopy techniques: 1) from the rate of fall in mean blood saturation during a 4 min below knee arterial occlusion, and thus no blood flow, in calf skin and skeletal muscle and 2) in perfused, unperturbed skin, using the spontaneous falls in mean blood saturation induced by vasomotion in calf and forearm skin of 24 subjects, 12 lean and 12 obese. OE in perfused skin was significantly higher in lean compared with obese subjects in forearm (Mann-Whitney, P < 0.004) and calf ( P < 0.001) and did not correlate with OE in unperfused skin (ρ = −0.01, P = 0.48). With arterial occlusion and thus no blood flow, skin OE in lean and obese subjects no longer differed ( P = 0.23, not significant). In contrast in skeletal muscle with arterial occlusion and no blood flow, the difference in OE between lean and obese subjects occurred, with obese subjects exhibiting significantly higher OE ( P < 0.012). The classic model of metabolic blood flow regulation to support oxygen extraction is evident in perfused skin; OE is perturbed without blood flow and reduced in obesity. In resting skeletal muscle other mechanism(s), independent of blood flow, are implicated in oxygen extraction.

Rapid force recovery in contracting skeletal muscle after brief ischemia is dependent on O2 availability

1999 ◽  
Vol 87 (6) ◽  
pp. 2225-2229 ◽  
Author(s):  
Michael C. Hogan ◽  
Suzanne Kohin ◽  
Creed M. Stary ◽  
Russell T. Hepple
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Rapid Recovery ◽  
Contracting Muscle ◽  
Force Development ◽  
Short Period ◽  
Flow Restoration ◽  
Ischemic Period ◽  
Normal Blood Flow

We tested the hypothesis that contracting skeletal muscle can rapidly restore force development during reperfusion after brief total ischemia and that this rapid recovery depends on O2 availability and not an alternate factor related to blood flow. Isolated canine gastrocnemius muscle ( n = 5) was stimulated to contract tetanically (isometric contraction elicited by 8 V, 0.2-ms duration, 200-ms trains, at 50-Hz stimulation) every 2 s until steady-state conditions of muscle blood flow (controlled by pump perfusion) and developed force were attained (3 min). While maintaining the same stimulation pattern, muscle blood flow was then reduced to zero (complete ischemia) for 2 min. Normal blood flow was then restored to the contracting muscle; however, two distinct conditions of oxygenation (at the same blood flow) were sequentially imposed: deoxygenated blood (30 s), blood with normal arterial O2content (30 s), a return to deoxygenated blood (30 s), and finally a return to normal arterial O2 content (90 s). During the ischemic period, force development fell to 39 ± 6 (SE)% of normal (from 460 ± 40 to 170 ± 20 N/100 g). When muscle blood flow was restored to normal by perfusion with deoxygenated blood, developed force continued to decline to 140 ± 20 N/100 g. Muscle force rapidly recovered to 310 ± 30 N/100 g ( P < 0.05) during the 30 s in which the contracting muscle was perfused with oxygenated blood and then fell again to 180 ± 30 N/100 g when perfused with blood with low[Formula: see text]. These findings demonstrate that contracting skeletal muscle has the capacity for rapid recovery of force development during reperfusion after a short period of complete ischemia and that this recovery depends on O2availability and not an alternate factor related to blood flow restoration.

Patterns of glycogen loss in muscle fibers: response to arterial occlusion during exercise

1981 ◽  
Vol 51 (3) ◽  
pp. 552-556 ◽  
Author(s):  
R. B. Armstrong ◽  
D. F. Peterson
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Common Iliac Artery ◽  
Fiber Type ◽  
Muscle Fibers ◽  
Arterial Occlusion ◽  
Exercise Bout ◽  
Motor Units ◽  
Rat Skeletal Muscle ◽  
The Right

This experiment was designed to determine if glycogen loss in active rat skeletal muscle fibers could be accentuated by periodic occlusion of blood to the muscles without significantly altering the numbers of types of fibers that lose glycogen. We attempted to augment glycogen loss by periodically occluding blood flow to the muscles while the animals ran on a treadmill. An occluder cuff was placed on the right common iliac artery of 10 rats. While the rats ran for 5 min at 26 m . min-1, blood flow to the right hindlimb was completely occluded for 16 +/- 5 (SD) s during every 30 s of the run. Glycogen loss in soleus (S), plantaris (P), and gastrocnemius (G) muscles was determined biochemically and histochemically. Muscles from both the occluded limb (S, P, and the deep red portion of G) and the nonoccluded limb (S and red G) of the runners showed significant glycogen loss compared with the controls. Furthermore, glycogen concentration was significantly lower in S, P, and red G of the occluded limb than in the same muscles of the nonoccluded limb. Significantly greater numbers of fibers within fiber type populations of P and G showed glycogen loss in the occluded limb, indicating that more motor units were recruited during the exercise bout in these muscles. The data suggest a sensitive link between motor unit recruitment and the metabolic condition of the contracting fibers, as the increased number of fibers showing glycogen loss presumably, resulted from fatigue of active units. We conclude that occlusion of blood flow to active muscles is not a feasible means of accentuating glycogen loss in active fibers while maintaining normal patterns of recruitment.

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

scholarly journals Direct Measurements of the Permeability Surface Area for Insulin and Glucose in Human Skeletal Muscle

2003 ◽  
Vol 88 (10) ◽  
pp. 4559-4564 ◽  
Author(s):  
Soffia Gudbjörnsdóttir ◽  
Mikaela Sjöstrand ◽  
Lena Strindberg ◽  
John Wahren ◽  
Peter Lönnroth
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Tolerance ◽  
Plasma Insulin ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Permeability Surface ◽  
One Step

Abstract To elucidate mechanisms regulating capillary transport of insulin and glucose, we directly calculated the permeability surface (PS) area product for glucose and insulin in muscle. Intramuscular microdialysis in combination with the forearm model and blood flow measurements was performed in healthy males, studied during an oral glucose tolerance test or during a one-step or two-step euglycemic hyperinsulinemic clamp. PS for glucose increased significantly from 0.29 ± 0.1 to 0.64 ± 0.2 ml/min·100 g after oral glucose tolerance test, and glucose uptake increased from 1.2 ± 0.4 to 2.6 ± 0.6 μmol/min·100 g (P &lt; 0.05). During one-step hyperinsulinemic clamp (plasma insulin, 1.962 pmol/liter), PS for glucose increased from 0.2 ± 0.1 to 2.3 ± 0.9 ml/min·100 g (P &lt; 0.05), and glucose uptake increased from 0.6 ± 0.2 to 5.0 ± 1.4 μmol/min·100 g (P &lt; 0.05). During the two-step clamp (plasma insulin, 1380 ± 408 and 3846 ± 348 pmol/liter), the arterial-interstitial difference and PS for insulin were constant. The PS for glucose tended to increase (P = not significant), whereas skeletal muscle blood flow increased from 4.4 ± 0.7 to 6.2 ± 0.8 ml/min·100 ml (P &lt; 0.05). The present data show that PS for glucose is markedly increased by oral glucose, whereas a further vasodilation exerted by high insulin concentrations may not be physiologically relevant for capillary delivery of either glucose or insulin in resting muscle.

Osteonecrosis of the Femoral Head of Laboratory Animals: The Lessons Learned from a Comparative Study of Osteonecrosis in Man and Experimental Animals

2003 ◽  
Vol 40 (4) ◽  
pp. 345-354 ◽  
Author(s):  
J. H. Boss ◽  
I. Misselevich
Keyword(s):  
Blood Flow ◽  
Femoral Head ◽  
Weight Bearing ◽  
Arterial Occlusion ◽  
Lessons Learned ◽  
Laboratory Animals ◽  
Treatment Modalities ◽  
Venous Stasis ◽  
Spontaneously Hypertensive ◽  
Bearing Loads

Animal models of osteonecrosis of the femoral head are indispensable to the understanding of successful treatment modalities for avascular necrosis of the femoral head in adults and in children with Legg-Calvé-Perthes disease. Many of these models adequately reflect the current “vascular deprivation” theory regarding the etiology of the disease. In addition to spontaneous occurrence, surgical- and corticosteroid-induced models are suitable, common experimental ones. Osteonecrosis of spontaneously hypertensive rats appears to be due to defective bone formation and compression of the arteries entering the femoral head at its lateral facets by daily weight-bearing loads. Successful modeling of surgical-induced femoral capital necrosis can be a challenge in animals with a dual epiphyseal blood supply. High doses of corticosteroids are a pivotal risk factor in the development of osteonecrosis. The pathogenesis of corticosteroid-induced osteonecrosis likely resides in reduced blood flow. Steroids may reduce blood flow by numerous mechanisms, including marrow adipocytic hypertrophy leading to sinusoidal compression, venous stasis and, eventually, obstruction of the arteries, and arterial occlusion by fat emboli and lipid-loaded fibrin-platelet thrombi. Other, less common varieties of osteonecrosis include those secondary to endotoxin-induced disseminated intravascular coagulation, immune reactions, immoderately low or high temperatures, and high-impact-related injuries. Common to these diverse forms of osteonecrosis are fibrin thrombi clogging arterioles and small arteries.

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