Regulation of canine skeletal muscle and hindlimb blood flow in acute anemia

1988 ◽  
Vol 66 (1) ◽  
pp. 101-105 ◽  
Author(s):  
P. Kubes ◽  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Sympathetic Stimulation ◽  
Arterial Blood ◽  
Measured Resistance ◽  
Muscle Groups

Redistribution of blood flow away from resting skeletal muscle does not occur during anemic hypoxia even when whole body oxygen uptake is not maintained. In the present study, the effects of sympathetic nerve stimulation on both skeletal muscle and hindlimb blood flow were studied prior to and during anemia in anesthetized, paralyzed, and ventilated dogs. In one series (skeletal muscle group, n = 8) paw blood flow was excluded by placing a tourniquet around the ankle; in a second series (hindlimb group, n = 8) no tourniquet was placed at the ankle. The distal end of the transected left sciatic nerve was stimulated to produce a maximal vasoconstrictor response for 4-min intervals at normal hematocrit (Hct.) and at 30 min of anemia (Hct. = 14%). Arterial blood pressure and hindlimb or muscle blood flow were measured; resistance and vascular hindrance were calculated. Nerve stimulation decreased blood flow (p < 0.05) in the hindlimb and muscle groups at normal Hct. Blood flow rose (p < 0.05) during anemia and was decreased (p < 0.05) in both groups during nerve stimulation. However, the blood flow values in both groups during nerve stimulation in anemic animals were greater (p < 0.05) than those at normal Hct. Hindlimb and muscle vascular resistance fell significantly during anemia and nerve stimulation produced a greater increase in vascular resistance at normal Hct. Vascular hindrance in muscle, but not hindlimb, was less during nerve stimulation in anemia than at normal Hct. The data indicate that (i) maximal sympathetic stimulation produced a significant decrease in both skeletal muscle and hindlimb blood flow during anemia, (ii) the reduction in blood flow in these areas was less with sympathetic stimulation during anemia than at normal Hct., and (iii) the anemic stimulus (Hct. = 14%) does not activate maximal sympathetic vasoconstrictor tone in the skeletal muscle.

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 PL - 031 Skeletal muscle blood flow determination using gold standard invasive arterial input function and non-invasive image-based input function by positron emission tomography (PET)

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Ilkka Heinonen ◽  
Kari Kalliokoski ◽  
Vesa Oikonen ◽  
Christopher Mawhinney ◽  
Warren Gregson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Data Analysis ◽  
Arterial Input Function ◽  
Muscle Blood Flow ◽  
Input Function ◽  
Invasive Approach ◽  
Skeletal Muscle Blood Flow ◽  
Non Invasive ◽  
Arterial Blood

Objective Skeletal muscle is unique among organs in that its blood flow, thus oxygen supply that is critical for muscular function, can change over a remarkably large range. Compared to the rest, muscle blood flow can increase over 20-fold during intense exercise. Positron emission tomography (PET) and [15O]-H2O tracer provide a unique tool for the direct measurement of muscle blood flow in specific muscle regions. Quantification of PET blood flow requires knowledge of the arterial input function, which is usually provided by arterial blood sampling. However, arterial sampling is an invasive approach requiring arterial cannulation. In the current study, we aimed to explore the analysis and error estimation based on non-invasive, PET image-based input function for skeletal muscle blood flow in PET [15O]-labeled radiowater study. Methods Thirty healthy untrained men volunteered to participate in this study. [15O]-labeled radio water PET perfusion scans were performed at rest and right after cycling exercise. GE Discovery PET-CT scanner was used for image acquisition. The 15O isotope was produced with a Cyclone 3 cyclotron (IBA Molecular, Belgium). After 455 MBq of 15O-H2O was injected intravenously and after 20 seconds, dynamic scanning images were performed in following frames: 6x5 seconds, 12x10 seconds, 7x30 seconds and 12x10 seconds. Arterial blood was sampled continuously from radial artery during imaging for radioactivity with a detector during PET scanning. All the data analysis was performed using all in-house developed programs. Arterial input function was preprocessed with delay correction. Image-based input function was defined based on sum image of dynamic images. Blood flow was calculated using the 1-tissue compartment model, k1 is considered as blood flow without any further correction. All data analysis was performed by Carimas software (http://www.turkupetcentre.fi/carimas). Data analysis was performed in five parts: 1) Modelling data using input function from artery. 2) By defining femoral artery Volume Of Interest (VOI) on PET images. 3) Modelling data using image-based input function. 4) Calculating the correlation for blood flow between artery (blood) input function and image-based input function. 5) Predicted true blood flow was calculated based on correlation based on the initial linear relationship between blood and image-based input functions. Results Skeletal muscle blood flow had a good linear relationship calculated by femoral artery VOI and by arterial (blood) input function (y = 2,9587x - 0,096, R² = 0,8852, p<0.0001). Further, by using the prediction equation obtained by the linear relationship between VOI-determined (femoral) artery blood flow and direct gold standard (radial) artery input function determined blood flow, image-based input function determined blood flow was well predicted using this non-invasive approach (y = 1,1812x + 0,1219, R² = 0,9259, p<0.0001). Conclusions It is concluded that there is a strong linear correlation between gold standard invasive approach and non-invasive image-based approach to measure skeletal muscle blood flow by PET, but if no further corrections are made, image-based approach overestimates correct blood flow. However, this can be corrected by linear prediction equation, suggesting that invasive arterial input function may not always be needed in the future when measuring skeletal muscle blood flow by PET. This will be of benefit particularly for exercise studies.

Effects of insulin-like growth factor-I and LR3IGF-I on regional blood flow in normal rats

1997 ◽  
Vol 155 (2) ◽  
pp. 351-358 ◽  
Author(s):  
CM Gillespie ◽  
AL Merkel ◽  
AA Martin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Arterial Blood ◽  
Cardiovascular Side Effects ◽  
Igf I ◽  
The Central Nervous System ◽  
The Brain ◽  
Infusion Period

Two studies were conducted to investigate the haemodynamic effects of IGF-I and its analogue LR3IGF-I in normal anaesthetised rats. Infusion of IGF-I intravenously, at a dose of 125 micrograms/kg/h, for 20 min in the first study resulted in renal blood flow being significantly elevated by 35% above baseline. Mean arterial blood pressure (MABP) at this IGF-I dose fell by 18% of baseline, with LR3IGF-I also causing a significant decline in MABP (by 15%) at the dose of 125 micrograms/kg/h. In the second study the intravenous administration of IGF-I or LR3IGF-I, at a dose of 125 micrograms/kg/h, over a period of 60 min, resulted in MABP being significantly lowered by 25% of baseline values. Regional blood flow rates were determined using radioactive microspheres, 15 microns in diameter, injected systemically at the end of the peptide infusion period. The gastrocnemius, a representative skeletal muscle, was the only vascular region to show a significant increase in blood flow after IGF-I (by 58%) or LR3IGF-1 (by 308%) infusion. Vascular resistance in the brain was significantly reduced after infusion of IGF-I (by 60%) or LR3IGF-I (by 48%) as compared with vehicle. Skeletal muscle vascular resistance was also reduced by IGF-I (by 41%) and more particularly by LR3IGF-I (by 77%) in comparison to vehicle. These alterations to vascular tone produced by IGF infusion may be related to the central nervous system and systemic cardiovascular side-effects that have been reported during IGF-I administration in humans.

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.

Oxygen uptake and blood flow in canine skeletal muscle during moderate and severe anemia

1983 ◽  
Vol 61 (2) ◽  
pp. 178-182 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Oxygen Transport ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Arterial Oxygen ◽  
Acute Anemia ◽  
Moderate Anemia ◽  
The Mean

The metabolic and cardiovascular adjustments of the whole body and skeletal muscle were studied during moderate and severe acute anemia. In 15 anesthetized dogs, venous outflow from the gastrocnemius–plantaris muscle group was isolated. Cardiac output [Formula: see text], muscle blood flow [Formula: see text], total body and muscle oxygen uptake [Formula: see text] were determined during a control period, and at 30 and 60 min of either (i) moderate anemia (n = 8) in which the mean hematocrit (Hct) was 25% or (ii) progressive anemia (n = 7) in which the mean Hct values were 25% at 30 min and 16% at 60 min of anemia. Muscle [Formula: see text], [Formula: see text], and [Formula: see text] were increased in both groups at 30 min of anemia. By 60 min, [Formula: see text] and [Formula: see text] declined to preanemic control values in the moderate anemia group; whole body [Formula: see text] was maintained at the control level. Arterial oxygen transport was the same in the two groups at both 30 and 60 min of anemia despite the difference in Hct at 60 min. Muscle [Formula: see text] showed a further and similar rise in both groups between 30 and 60 min of anemia. These data show that the rise in muscle [Formula: see text] during acute anemia was not directly proportional to the degree of the hematocrit reduction. Further, the findings suggest that the muscle [Formula: see text] response was related to the decrease in arterial oxygen transport.

Attenuation of hindlimb vasodilation in heat-stressed baboons during dehydration

1986 ◽  
Vol 250 (1) ◽  
pp. R30-R35 ◽  
Author(s):  
R. M. Thornton ◽  
D. W. Proppe
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Regression Coefficients ◽  
Skeletal Muscle Blood Flow ◽  
Ambient Temperatures ◽  
Arterial Blood

The influence of dehydration on hindlimb vasodilation during environmental heating (EH) was examined in eight unanesthetized chronically instrumented baboons. Mean iliac blood flow (MIBF), arterial blood pressure, and core temperature (Tc) were measured during EH of baboons in euhydrated and dehydrated states. EH consisted of acute exposure to high ambient temperatures (39-44 degrees C) until Tc reached 39.5 degrees C. Dehydration was produced by 68-72 h of fluid deprivation, which caused increases in plasma osmolality [291 +/- 1 (SE) to 338 +/- 6 mosmol/kg H2O] and sodium concentration (143 +/- 2 to 163 +/- 3 meq/l) and a 16% fall in plasma volume. The primary influence of dehydration was attenuation of the progressive rise in MIBF and iliac conductance (IC) during EH. Absolute MIBF and IC levels at Tc = 39.5 degrees C during EH were 44 and 52%, respectively, lower in the dehydrated state. Also, the MIBF-Tc and IC-Tc linear regression coefficients during EH were lower by 33 and 43%, respectively, in the dehydrated state. Since limb skeletal muscle blood flow does not increase during EH, we conclude that dehydration attenuates the heat stress-induced rise in skin blood flow in baboons, an influence that is similar to what occurs in humans.

Neural control of muscle blood flow during exercise

2004 ◽  
Vol 97 (2) ◽  
pp. 731-738 ◽  
Author(s):  
Gail D. Thomas ◽  
Steven S. Segal
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Neural Control ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity ◽  
Arterial Blood

Activation of skeletal muscle fibers by somatic nerves results in vasodilation and functional hyperemia. Sympathetic nerve activity is integral to vasoconstriction and the maintenance of arterial blood pressure. Thus the interaction between somatic and sympathetic neuroeffector pathways underlies blood flow control to skeletal muscle during exercise. Muscle blood flow increases in proportion to the intensity of activity despite concomitant increases in sympathetic neural discharge to the active muscles, indicating a reduced responsiveness to sympathetic activation. However, increased sympathetic nerve activity can restrict blood flow to active muscles to maintain arterial blood pressure. In this brief review, we highlight recent advances in our understanding of the neural control of the circulation in exercising muscle by focusing on two main topics: 1) the role of motor unit recruitment and muscle fiber activation in generating vasodilator signals and 2) the nature of interaction between sympathetic vasoconstriction and functional vasodilation that occurs throughout the resistance network. Understanding how these control systems interact to govern muscle blood flow during exercise leads to a clear set of specific aims for future research.

Dissociation between volume blood flow and laser-Doppler signal from rat muscle during changes in vascular tone

1998 ◽  
Vol 274 (4) ◽  
pp. H1248-H1254 ◽  
Author(s):  
Larisa V. Kuznetsova ◽  
Nicole Tomasek ◽  
Gisli H. Sigurdsson ◽  
Andrej Banic ◽  
Dominique Erni ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Vascular Tone ◽  
Muscle Blood Flow ◽  
Laser Doppler ◽  
Ang Ii ◽  
Ganglionic Blockade ◽  
Vasoactive Substances ◽  
Total Muscle

Although the laser-Doppler flowmetry (LDF) signal from skeletal muscle has been shown to provide a good measure of blood flow under some conditions, its behavior during administration of vasoactive substances has never been addressed. The aims of this study were to compare 1) changes in LDF signal with those in total muscle blood flow measured with radioactive microspheres after ganglionic blockade (chlorisondamine) and during administration of angiotensin II (ANG II), phenylephrine (PE), and isoproterenol (Iso) and 2) changes in vascular resistance estimated by the two techniques. The LDF signal from the biceps femoris muscle was investigated in anesthetized male Wistar rats. Ganglionic blockade led to a significant ( P < 0.05) fall in mean arterial pressure (MAP) [medians (lower, upper quartiles): 78 (72, 83) vs. 127 (114, 138) mmHg under basal conditions], muscle blood flow (MBF, microsphere technique; 61%), and the LDF signal (29%). Muscle vascular resistance (MVR = MAP/MBF) was increased (64%, P < 0.05), but vascular resistance estimated as MAP/LDF signal (MVRLDF) was unchanged. During ANG II and PE infusions, MAP rose ( P< 0.05) to 178 (155, 194) and 127 (124, 142) mmHg, respectively; MBF did not change compared with the preinfusion (postganglionic blockade) level and remained significantly ( P< 0.05) lower than baseline, whereas the LDF signal increased up to a level not different from baseline. MVR rose and was significantly ( P < 0.05) higher than baseline, whereas MVRLDF did not differ significantly from baseline. During Iso infusion, MAP fell [58 (56, 60) vs. 94 (92, 102) mmHg, P < 0.05], the LDF signal was reduced (49%, P < 0.05) despite a large increase in MBF (139%, P < 0.05), and MVR fell (74%, P < 0.05), whereas MVRLDF did not change vs. preinfusion level. Our results suggest that 1) changes in the LDF signal from muscle may not correlate with changes in total muscle blood flow measured by the microsphere technique during infusion of vasoactive substances and 2) the use of LDF data for estimation of MVR during changes in vascular tone in rat skeletal muscle is probably not appropriate.

scholarly journals Sympathetic restraint of muscle blood flow during hypoxic exercise

2009 ◽  
Vol 296 (5) ◽  
pp. R1538-R1546 ◽  
Author(s):  
Michael K. Stickland ◽  
Curtis A. Smith ◽  
Benjamin J. Soriano ◽  
Jerome A. Dempsey
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Adrenergic Blockade ◽  
Moderate Exercise ◽  
Intact Control ◽  
Arterial Blood ◽  
Breathing Room ◽  
Response To Exercise

Control of exercising muscle blood flow is a balance between local vasodilatory factors and the increase in global sympathetic vasoconstrictor outflow. Hypoxia has been shown to potentiate the muscle sympathetic nerve response to exercise, potentially limiting the increase in muscle blood flow. Accordingly, we investigated sympathetic restraint to exercising muscle during whole body exercise in hypoxia. Six dogs chronically instrumented with ascending aortic and hindlimb flow probes and a terminal aortic catheter were studied at rest and mild [2.5 miles/h (mph), 5% grade] and moderate (4.0 mph, 10% grade) exercise while breathing room air or hypoxia (PaO2 ∼45 mmHg) in the intact control condition and following systemic α-adrenergic blockade (phentolamine). Hypoxia caused an increase in cardiac output (CO), hindlimb flow (FlowL), and blood pressure (BP), while total (CondT) and hindlimb conductance (CondL) were unchanged at rest and mild exercise but increased with moderate exercise. During both mild and moderate exercise, α-blockade in normoxia resulted in significant vasodilation as evidenced by increases in CO (10%), FlowL (17%), CondT (33%), CondL (43%), and a decrease in BP (−18%), with the increase in CondL greater than the increase in CondT during mild exercise. Compared with the normoxic response, α-blockade in hypoxia during exercise resulted in a significantly greater increase in CondT (59%) and CondL (74%) and a correspondingly greater decrease in BP (−34%) from baseline. These findings indicate that there is considerable hypoxia-induced sympathetic restraint of muscle blood flow during both mild and moderate exercise, which helps to maintain arterial blood pressure in hypoxia.

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