Hindlimb vascular responses to sympathetic augmentation during acute anemia

1985 ◽  
Vol 63 (7) ◽  
pp. 782-786 ◽  
Author(s):  
Stephen M. Cain ◽  
C. K. Chapler
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Sympathetic Activity ◽  
Carotid Arteries ◽  
Muscle Blood Flow ◽  
Recovery Period ◽  
Control Period ◽  
Whole Body ◽  
Block Group ◽  
Limb Blood Flow

The effect of increased sympathetic activity on skeletal muscle blood flow during acute anemic hypoxia was studied in 16 anesthetized dogs. Sympathetic activity was altered by clamping the carotid arteries bilaterally below the carotid sinus. One group (n = 8) was beta blocked by administration of propranolol (1 mg/kg); a second group (n = 8) was untreated. Venous outflow from the left hindlimb was isolated for measurement of blood flow and O2 uptake [Formula: see text]. After a 20-min control period, both carotid arteries were clamped (CC) for 20 min followed by a 20-min recovery period. The sequence was repeated after hematocrit was lowered to about 15% by dextran exchange for blood. Prior to anemia, CC did not alter cardiac output or limb blood flow in either group. After induction of anemia, hindlimb resistance was higher with CC in the beta block than in the no block group. Both limb blood flow and [Formula: see text] fell in the β-block group with CC during anemia. Beta block also prevented the additive increases in whole body [Formula: see text] seen with CC and induction of anemia. The data showed that the increased vasoconstrictor tone that was obtained with beta block during anemia was successful in redistributing the lower viscosity blood away from resting skeletal muscle, even to the point that muscle [Formula: see text] was decreased.

Effects of norepinephrine and alpha-block on O2 uptake and blood flow in dog hindlimb

1981 ◽  
Vol 51 (5) ◽  
pp. 1245-1250 ◽  
Author(s):  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Control Period ◽  
The Other ◽  
Whole Body ◽  
Block Group ◽  
Limb Blood Flow ◽  
O2 Uptake ◽  
O2 Transport ◽  
Constant Rate

Norepinephrine (NE) may increase skeletal muscle O2 demand at the same time that it restricts O2 transport by vasoconstriction. We prevented vasoconstriction with 3.0 mg/kg phenoxybenzamine (alpha-Bl) in 10 anesthetized, paralyzed dogs ventilated at constant rate. Hindlimb and whole-body O2 uptake (VO2) and blood flow were measured for a 20-min control period, 20 min of NE infusion at 1 micrograms . kg-1 . min-1 either intravenously (iv) or intra-arterially (ia), and 20 min of recovery. The sequence was repeated for the other route of infusion. A second group of 10 without alpha-Bl was treated the same. Cardiac output increased with both ia and iv infusions in the no-block group and was unchanged in the alpha-Bl group. Limb blood flow increased 25% during the first 5 min of iv but decreased 40% with ia infusion in the no-block group. Whole-body VO2 was significantly increased 9% in both groups by both routes of NE. Limb VO2 was significantly decreased in the no-block group at 5 min of NE infusion iv when limb blood flow was increased. Limb VO2 did not change significantly in the alpha-Bl group with NE by either route. Hindlimb skeletal muscle did not participate in or contribute to the calorigenic effect of NE on the whole body, and that lack of effect was not due to any effect of NE on rate or distribution of blood flow in the limb.

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.

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.

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.

The role of α-adrenergic receptors in carbon monoxide hypoxia

1986 ◽  
Vol 64 (11) ◽  
pp. 1442-1446 ◽  
Author(s):  
S. M. Villeneuve ◽  
C. K. Chapler ◽  
C. E. King ◽  
S. M. Cain
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Adrenergic Receptors ◽  
Muscle Blood Flow ◽  
Control Period ◽  
Arterial Oxygen ◽  
Adrenergic Blockade ◽  
Limb Blood Flow ◽  
Arterial Oxygen Content

The importance of α-adrenergic receptors in the cardiac output and peripheral circulatory responses to carbon monoxide (CO) hypoxia was studied in anesthetized dogs. Phenoxybenzamine (3 mg/kg i.v.) was injected to block α-receptor activity and the data obtained were then compared with those from a previous study of CO hypoxia in unblocked animals. Values for cardiac output, hindlimb blood flow, vascular resistance, and oxygen uptake were obtained prior to and at 30 and 60 min of CO hypoxia which reduced arterial oxygen content by approximately 50%. α-Adrenergic blockade resulted in a lower (p < 0.05) control value for cardiac output than observed in unblocked animals, but no differences were present between the two groups at 30 or 60 min of CO hypoxia. Similarly, limb blood flow was lower (p < 0.05) during the control period in the α-blocked group but rose to the same level as that in the unblocked animals at 60 min of COH. No change in limb blood flow occurred during CO hypoxia in the unblocked group. These findings demonstrated that during CO hypoxia (i) α-receptor mediated venoconstriction does not contribute to the cardiac output response and (ii) α-receptor mediated vasoconstriction probably does prevent a rise in hindlimb skeletal muscle blood flow.

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.

O2 extraction by canine hindlimb during alpha-adrenergic blockade and hypoxic hypoxia

1980 ◽  
Vol 48 (4) ◽  
pp. 630-635 ◽  
Author(s):  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Blood Flow ◽  
Femoral Vein ◽  
Recovery Period ◽  
Whole Body ◽  
Adrenergic Blockade ◽  
Limb Blood Flow ◽  
O2 Uptake ◽  
Total Blood ◽  
O2 Extraction ◽  
Total Blood Flow

Hindlimb and total blood flow and O2 uptake were measured in anesthetized paralyzed dogs in which venous outflow from the left hindlimb (less paw) was directed through the femoral vein. After ventilation on room air, 10 dogs were given 3 mg/kg phenoxybenzamine + 10 ml/kg dextran and 10 other dogs were isovolemically exchanged with 10 ml/kg dextran without alpha-block while continuing to be ventilated on room air. All animals were then ventilated with 9.1% O2 in N2, followed by a recovery period on room air. Total and limb peripheral resistances were lowered by alpha-block, but total and limb blood flow changed little from control levels. Both total and limb O2 uptake were decreased below control values during hypoxia. Cardiac output and limb blood flow increased during hypoxia in both groups. Although alpha-block caused O2 extraction by the whole body to be less during hypoxia than in unblocked dogs, the hindlimb in both groups extracted O2 equally well. We concluded that skeletal muscle was not overperfused relative to O2 demand when alpha-blocked during hypoxia.

Assessment of muscle blood flow by laser-Doppler flowmetry during hemorrhage in SHR

1990 ◽  
Vol 259 (3) ◽  
pp. H860-H865
Author(s):  
J. H. Lombard ◽  
R. J. Roman
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Laser Doppler Flowmetry ◽  
Muscle Blood Flow ◽  
Control Period ◽  
Tissue Perfusion ◽  
Gracilis Muscle ◽  
Laser Doppler ◽  
Doppler Flowmetry ◽  
Skeletal Muscle Blood Flow

Skeletal muscle blood flow was assessed via laser-Doppler flowmetry (LDF) in the gracilis muscle of anesthetized 12- to 15-wk-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) control rats subjected to graded hemorrhage. Tissue perfusion was assessed at 20 specific sites in the muscle before and 20 min after each of five successive 1-ml withdrawals of blood. Mean LDF signals recorded from the gracilis muscle of SHR and WKY were similar during the prehemorrhage control period. After hemorrhage, mean arterial pressure and calculated vascular resistance of the gracilis muscle were higher in SHR than in WKY, and SHR exhibited a greater reduction of LDF signal in response to hemorrhage than WKY. Although SHR and WKY had a similar number of low flow sites (LDF signal less than 0.17 V) during the control period, successive blood volume withdrawals led to a significantly greater increase in the number of poorly perfused areas in the muscles of the hypertensive animals. The results of this study suggest that LDF is a useful tool to assess tissue perfusion during circulatory stress and that hemorrhage causes a greater decrease in skeletal muscle blood flow in SHR than in WKY. More severe reductions in tissue perfusion may contribute to the reduced ability of hypertensive animals to survive after hypotensive hemorrhage.

scholarly journals Local, but not indirect whole body heating, increases human skeletal muscle blood flow

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Illka Heinonen ◽  
R. Matthew Brothers ◽  
Jukka Kemppainen ◽  
Juhani Knuuti ◽  
Kari K. Kalliokoski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Skeletal Muscle Blood Flow

Muscle Blood Flow and Mitochondrial Function: Influence of Aging

2002 ◽  
Vol 12 (3) ◽  
pp. 368-378 ◽  
Author(s):  
Ronald L. Terjung ◽  
Ryszard Zarzeczny ◽  
H.T. Yang
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Muscle Blood Flow ◽  
The Elderly ◽  
Exchange Capacity ◽  
Oxygen Exchange ◽  
Whole Body ◽  
Tissue Blood Flow ◽  
Fiber Types

Skeletal muscle mitochondrial capacity (mito), tissue blood flow (BF) capacity, and oxygen exchange capacity (e.g., DO2) appear to be well matched. The different skeletal muscle fiber types and muscle remodeled, due to inactivity >(e.g., related to aging or disease) or exercise training, exhibit widely differing aerobics capacities (V̇O2max). Yet, there are remarkably coordinated alterations in these 3 parameters in each of these conditions. With such a balance, there is likely shared control among these parameters in limiting (V̇O2max) of muscle, although this is a matter of considerable debate. The reduction in aerobic capacity in elderly can be improved by submaximal aerobic exercise training; this is related to increases in muscle mitochondria concentration and capillarity, but probably not BF capacity, as this is limited by central cardiovascular function. Thus, exercise-induced biochemical adaptations and angiogenesis occur in the elderly. The increase in muscle capillarity likely contributes to the increased oxygen exchange capacity, typical of endurance type training. The increase in [mito] appears essential to realize the increased in muscle V̇O2max with training and amplifies the rate-limiting influence of the muscle’s oxygen exchange capacity. Further, vascular remodeling induced by exercise in the elderly could be effective at improving flow capacity, if limited by peripheral obstruction. Thus, the limits to aerobic function specific to aged muscle appear most influenced by inactivity, whereas central cardiovascular changes impact whole body performance. Some may consider the aged myocyte as a small, inactive, normal myocyte in need of activity!

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