scholarly journals Regional Blood Flow in Skeletal Muscle Measured by the Heated Thermocouple Method during Electrical Nerve Stimulation of the Canine Gracilis Muscle.

1991 ◽  
Vol 164 (2) ◽  
pp. 145-156 ◽  
Author(s):  
KIYOYUKI SHICHINO ◽  
TOKIHITO YUKIMURA ◽  
KATSUYUKI MIURA ◽  
KENJIRO YAMAMOTO ◽  
MAMORU OKUBO ◽  
...  
1965 ◽  
Vol 208 (3) ◽  
pp. 417-424 ◽  
Author(s):  
Lawrence D. Dorr ◽  
Michael J. Brody

The hypothesis that sympathetic innervation to skeletal muscle vasculature contains functionally distinct adrenergic and cholinergic fibers was investigated utilizing the dog isolated perfused gracilis muscle. The use of hemicholinium in an attempt to abolish cholinergic dilatation, but not adrenergic constriction, in response to intermittent nerve stimulation was not successful. Continuous nerve stimulation produced vasoconstriction which was maintained for the duration of stimulation. Conversely, when cholinergic vasodilatation was unmasked, continuous stimulation resulted in a dilator response which disappeared rapidly. These experiments suggested that release of the adrenergic transmitter could not be dependent upon an intermediate cholinergic link in the sympathetic nerve. This postulate was supported further by experiments utilizing electrical stimulation of medullary vasoconstrictor areas. Whereas cholinergic vasodilatation was unmasked routinely by peripheral stimulation following reserpine, guanethidine or ß-TM 10, this response was never seen when medullary vasoconstrictor neurons were activated following these agents. It was concluded that sympathetic cholinergic nerves to skeletal muscle vessels possess a purely vasodilator function, and do not play an intermediate role involving release of the adrenergic transmitter.


2017 ◽  
Vol 10 (2) ◽  
pp. 120-124 ◽  
Author(s):  
Fahimeh Kamali ◽  
Hossein Mirkhani ◽  
Ahmadreza Nematollahi ◽  
Saeed Heidari ◽  
Elahesadat Moosavi ◽  
...  

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie

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.


1992 ◽  
Vol 72 (4) ◽  
pp. 1563-1570 ◽  
Author(s):  
G. Piedimonte ◽  
J. I. Hoffman ◽  
W. K. Husseini ◽  
W. L. Hiser ◽  
J. A. Nadel

Stimulation of sensory nerves in the airway mucosa causes local release of the neuropeptides substance P and calcitonin gene-related peptide (CGRP). In this study we used a modification of the reference-sample microsphere technique to measure changes in regional blood flow and cardiac output distribution produced in the rat by substance P, CGRP, and capsaicin (a drug that releases endogenous neuropeptides from sensory nerves). Three sets of microspheres labeled with different radionuclides were injected into the left ventricle of anesthetized F344 rats before, immediately after, and 5 min after left ventricular injections of capsaicin, substance P, or CGRP. The reference blood sample was withdrawn from the abdominal aorta and was simultaneously replaced with 0.9% NaCl at 37 degrees C. We found that stimulation of sensory nerves with a low dose of capsaicin causes a large and selective increase in microvascular blood flow in the extrapulmonary airways. The effect of capsaicin is mimicked by systemic injection of substance P but not by CGRP, suggesting that substance P is the main agent of neurogenic vasodilation in rat airways.


1988 ◽  
Vol 66 (1) ◽  
pp. 101-105 ◽  
Author(s):  
P. Kubes ◽  
C. K. Chapler ◽  
S. M. Cain

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.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (4) ◽  
pp. 571-571
Author(s):  
FORST E. BROWN

In Reply.— Rowlingson and Carron suggest consideration of transcutaneous electrical nerve stimulation (TENS) in the management of frostbite. As they mentioned, sympathetic blocks have been effective in the management of early frostbite; blood flow increase has resulted in the salvage of damaged digits. Interarterial reserpine and prostacycline also have been shown to overcome digital vasoconstriction. In the two patients we described, persistent vasoconstriction as seen in reflex sympathetic dystrophy (RSD) was not the problem. Moreover, the changes seen in the radiographs were not comparable to those seen in RSD.


2020 ◽  
Vol 67 (3) ◽  
pp. 179-185
Author(s):  
Lorena Giner-Bernal ◽  
Jaime Ruiz-Tovar ◽  
Javier Violeta ◽  
María Mercader ◽  
Jaime Miralles ◽  
...  

1989 ◽  
Vol 257 (3) ◽  
pp. H954-H960
Author(s):  
G. C. Haidet ◽  
T. I. Musch ◽  
D. B. Friedman ◽  
G. A. Ordway

To test the hypothesis that stimulation of adrenergic receptors in the heart is maximal during maximal exercise, and to determine whether generalized stimulation of adrenergic receptors during strenuous exercise produces significant alterations in the normal regional distribution of blood flow that occurs during exercise, we evaluated the cardiovascular effects of the infusion of dobutamine (40 micrograms.kg-1.min-1) in mongrel dogs during treadmill running. During maximal exercise, the dobutamine infusion resulted in a significant (P less than 0.05) increase in heart rate. Exercise capacity, total body O2 consumption (VO2), and maximal arteriovenous O2 difference, however, each were reduced during the infusion of this drug. A concomitant reduction in maximal blood flow to locomotive skeletal muscle occurred. The infusion of dobutamine also resulted in an increase in heart rate at a strenuous level of submaximal exercise. However, unlike during maximal exercise, VO2 was unchanged. Blood flow to locomotive skeletal muscle increased, and there was a concomitant reduction in arteriovenous O2 difference. Blood flow reductions that normally occur in splanchnic circulations during strenuous and during maximal exercise were generally somewhat attenuated during the infusion of this drug. Thus, dobutamine, a sympathomimetic agent, produces significant cardiovascular effects when infused in high doses during exercise. Our results demonstrate that beta-adrenergic receptor reserve exists in the heart during maximal exercise in dogs. In addition, the peripheral responses that occur during the infusion of the drug provide additional evidence that different degrees of adrenergic receptor reserve normally appear to be present within different regional circulations during strenuous and during maximal exercise.


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