Effects of Manual Acupuncture with Sparrow Pecking on Muscle Blood Flow of Normal and Denervated Hindlimb in Rats

2008 ◽  
Vol 26 (3) ◽  
pp. 149-159 ◽  
Author(s):  
Hisashi Shinbara ◽  
Masamichi Okubo ◽  
Eiji Sumiya ◽  
Fumihiko Fukuda ◽  
Tadashi Yano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Dependent Manner ◽  
Manual Acupuncture ◽  
Sprague Dawley ◽  
Axon Reflex ◽  
Hindlimb Muscles ◽  
Arterial Blood ◽  
The Right

Introduction In clinical practice, it has been thought that acupuncture might serve to wash out pain-generating metabolic end-products by improving blood circulation in muscles. We investigated the effects of manual acupuncture (MA) on muscle blood flow (MBF) of normal and denervated hindlimbs in rats. Method Sprague-Dawley rats (n=100) anaesthetised with urethane (1.2g/kg ip) were used. Manual acupuncture with sparrow pecking (SP) at different doses (1, 10 or 30 pecks) was given to the right ventral hindlimb muscles (tibial anterior and extensor digitorum longus muscles) or the right dorsal hindlimb muscles (gastrocnemius, plantaris and soleus muscles). MBF with or without MA was measured using the radiolabelled microsphere technique. The blood pressure was recorded through the right common carotid artery until MBF measurement started. Denervation of hindlimb was conducted by cutting the sciatic and femoral nerves. Results In normal rats, significantly increased MBF after MA were observed only in muscles which were penetrated by an acupuncture needle. The size of the increase depended on the number of times of pecking and seemed to be sustained at least until 60 minutes after MA. However, the increase was observed after both acute and chronic denervation. On the other hand, the mean arterial blood pressure (MAP) did not change significantly before, during or after MA. Conclusion These results suggest that MA could increase muscle blood flow locally in a dose-dependent manner and that this increase may be caused by local vasodilators, as well as the axon reflex. A further study is needed to elucidate the mechanism.

Participation of Calcitonin Gene Related Peptide Released via Axon Reflex in the Local Increase in Muscle Blood Flow following Manual Acupuncture

2013 ◽  
Vol 31 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Hisashi Shinbara ◽  
Masamichi Okubo ◽  
Keisaku Kimura ◽  
Kunio Mizunuma ◽  
Eiji Sumiya
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Calcitonin Gene Related Peptide ◽  
Manual Acupuncture ◽  
Sprague Dawley ◽  
Axon Reflex ◽  
Related Peptide ◽  
Local Increase ◽  
Arterial Blood ◽  
Calcitonin Gene

Objective The purpose of this study was to determine how calcitonin gene related peptide (CGRP) via axon reflex participates in increasing local muscle blood flow (MBF) following manual acupuncture (MA). Methods Male Sprague–Dawley rats (N=56, 270–350 g) were used. We examined (1) the effects of MA on MBF in the tibialis anterior (TA) muscle in normal rats; (2) the effects of MA on MBF in the TA injected with saline or hCGRP8-37 (low: 2×10−4 mol/litre; high: 2×10−3 mol/litre), a competitive CGRP receptor antagonist, in rats; and (3) the effects of MA on MBF in the TA in capsaicin-treated rats. The capsaicin-treated rats were injected with capsaicin dissolved in an ethanol solution within 24 h after birth (50 mg/kg subcutaneously). MA was applied to the right TA for 1 min. 51Cr-labelled microspheres (15 μm in diameter) were used to measure MBF. Results MA significantly increased MBF without changing arterial blood pressure in normal rats (p<0.05). MA also significantly increased MBF in saline-injected, low hCGRP8-37-injected and high hCGRP8-37-injected rats (p<0.001, 005 and 0.05, respectively). The increases in low and high hCGRP8-37-injected rats were lower than those in saline-injected rats, but the difference was not significant. However, MA did not significantly increase MBF in capsaicin-treated rats (p=0.38). Conclusions We obtained conflicting results, suggesting that the participation of CGRP released via axon reflex may be limited to a local increase in MBF following MA.

Contributions of Nitric Oxide and Prostaglandins to the Local Increase in Muscle Blood Flow following Manual Acupuncture in Rats

2015 ◽  
Vol 33 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Hisashi Shinbara ◽  
Masamichi Okubo ◽  
Keisaku Kimura ◽  
Kunio Mizunuma ◽  
Eiji Sumiya
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Tibialis Anterior Muscle ◽  
Dependent Manner ◽  
Manual Acupuncture ◽  
Sprague Dawley ◽  
Significant Difference ◽  
Synthase Inhibitor ◽  
The Right

Objective To investigate the contributions of nitric oxide (NO) and prostaglandins (PGs) to the increase in local muscle blood flow (MBF) observed following manual acupuncture (MA). Methods Male Sprague-Dawley rats (n=112; 250–310 g) were injected intraperitoneally with a non-selective NO synthase inhibitor (NG-nitro-L-arginine methyl ester hydrochloride: L-NAME; 10, 50 or 500 mg/kg), a non-selective cyclo-oxygenase inhibitor (indomethacin; 10, 50 or 500 mg/kg), a combination of L-NAME and indomethacin (500 mg/kg each) or saline only under urethane anaesthesia (1.2 g/kg). We used the sparrow pecking technique for 1 min with a stainless steel acupuncture needle (0.20×30 mm) as the acupuncture stimulation method. The stimulus point was on the right tibialis anterior muscle. 51Chromium-labelled microspheres were used for MBF measurement. Results MA increased MBF in the saline-injected group (p<0.001). This increase was partially inhibited by L-NAME in a dose-dependent manner (p>0.05, p<0.05 and p<0.001 for 10, 50 and 500 mg/kg, respectively). On the other hand, indomethacin did not suppress the increase (p>0.05 each for 10, 50 and 500 mg/kg). No significant difference was observed between the inhibitory effects of combined administration of L-NAME and indomethacin and single administration of L-NAME (p>0.05). Conclusions These results suggest that NO is a major factor in the MA-induced increase in MBF, while PGs do not contribute significantly to this increase. As complete inhibition was not achieved by administration of L-NAME±indomethacin, it appears that non-NO and non-PG vasodilators are additionally involved.

Muscular blood flow distribution patterns as a function of running speed in rats

1982 ◽  
Vol 243 (2) ◽  
pp. H296-H306 ◽  
Author(s):  
M. H. Laughlin ◽  
R. B. Armstrong
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Flow Distribution ◽  
Distribution Patterns ◽  
Left Renal Artery ◽  
Sprague Dawley ◽  
Vastus Intermedius ◽  
Slow Twitch ◽  
The Right ◽  
White Gastrocnemius

Muscle blood flow (BF) was measured using the radiolabeled microsphere technique within and among nine major muscles of rats before exercise and during treadmill walking or running at speeds of 15, 30, 45, 60, and 75 m/min. Measurements were made during exercise after 1 min of steady walking or running. Male Sprague-Dawley rats were chronically instrumented with 2 Silastic catheters, one in the ascending aorta via the right carotid artery for microsphere infusion and one in the left renal artery for arterial reference blood sample withdrawal. The preexercise results demonstrated that 1) BF to deep slow-twitch muscles was three to four times that to peripheral fast muscles (e.g., soleus and gastrocnemius BFs were 138 and 33 ml . min-1 . 100 g-1, respectively); 2) BFs to red portions within mixed muscles were three to four times those to white portions (e.g, red and white gastrocnemius BFs were 54 and 18 ml . min-1 . 100 g-1, respectively; and 3) there was a direct relationship (P less than 0.05) between BFs to muscles and their slow-twitch oxidative fiber populations. The results obtained during exercise demonstrated that 1) at the slowest speed studied (15 m/min) BFs to the red portions of muscles increased, whereas BFs to the white portions of the same muscles decreased; 2) BFs to all muscles (except soleus) were increased during running at 75 m/min when there was a range of flows of 30 ml . 100 g-1 . min-1 (white gastrocnemius) to 321 (vastus intermedius), 3) at all running speeds the increases in BF to muscles were directly related to the fast-twitch, high-oxidative fiber populations of the muscles; and 4) BFs to visceral tissues and fat were decreased during exercise.

Contribution of Adenosine to the Increase in Skeletal Muscle Blood Flow Caused by Manual Acupuncture in Rats

2017 ◽  
Vol 35 (4) ◽  
pp. 284-288 ◽  
Author(s):  
Hisashi Shinbara ◽  
Satomi Nagaoka ◽  
Yasuyuki Izutani ◽  
Masamichi Okubo ◽  
Keisaku Kimura ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Acupuncture Analgesia ◽  
Manual Acupuncture ◽  
Sprague Dawley ◽  
Skeletal Muscle Blood Flow ◽  
Adenosine Receptor Antagonist ◽  
Below The Knee ◽  
Green Fluorescent

Background and aim Adenosine is believed to play an important role in local acupuncture analgesia. The aim of this study was to investigate the contribution of adenosine to the increase in skeletal muscle blood flow (MBF) caused by manual acupuncture (MA). Methods Thirty-two male Sprague-Dawley rats (310–360 g) were anaesthetised and divided into four equal groups (n=8 each): Saline, Saline+MA, Theophylline, and Theophylline+MA. In the two MA groups, the sparrow-pecking MA technique was applied at 30 repetitions per min for 1 min to a depth of 15–18 mm using a stainless steel acupuncture needle (0.20×40 mm). The stimulus point was located on the right tibialis anterior (TA) muscle 7–8 mm below the knee. Animals in the two theophylline groups were intra-arterially injected with 8-(p-sulphophenyl) theophylline, a non-selective adenosine receptor antagonist, at a dose of 30 mg/kg before MA. Animals in the two saline groups received control saline. Fluorescent microspheres (15 µm in diameter, yellow-green fluorescent) were used for MBF measurement in all four groups. Results MA of the TA muscle significantly increased MBF (Saline+MA vs Saline: p=0.001; Saline+MA vs Theophylline: p=0.008). Pre-treatment with theophylline appeared to inhibit this increase (Theophylline vs Theophylline+MA; p=1.000). MBF in the Theophylline+MA group was 43% lower than in the Saline+MA group, although this was not significantly different (p=0.104). Conclusions The results suggest that adenosine leads to an increase in MBF caused by MA. Adenosine may play a role in acupuncture analgesia by washing out algesic substances. Further studies are needed in order to elucidate the precise mechanism.

Cardiovascular and sympathoadrenal responses to heat stress following water deprivation in rats

1996 ◽  
Vol 270 (3) ◽  
pp. R652-R659 ◽  
Author(s):  
M. P. Massett ◽  
D. G. Johnson ◽  
K. C. Kregel
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Body Weight ◽  
Heat Stress ◽  
Water Deprivation ◽  
Plasma Catecholamines ◽  
Sprague Dawley ◽  
Heating Rates ◽  
Systemic Hemodynamic ◽  
Arterial Blood

This study was designed to characterize the regional and systemic hemodynamic and sympathoadrenal responses to heating after 24 and 48 h of water deprivation in chloralose-anesthetized, male Sprague-Dawley rats (n = 7 per group). Water deprivation produced significant decreases in body weight of 8.1 and 13.7% in the 24- and 48-h groups (P < 0.05), respectively. After water deprivation, rats were exposed to an ambient temperature of 43 degrees C. After correction for body weight differences, heating rates were faster in the 48-h group compared with both euhydrated and 24-h groups. Mean arterial blood pressure (MAP), heart rate, and colonic (Tco) and tail (Ttail) temperatures increased above baseline in all groups during heating. Renal and mesenteric artery blood flow velocities decreased, and vascular resistances increased in response to heating. Compared with euhydrated controls, 48-h water-deprived rats exhibited attenuated pressor (delta MAP = 36 +/- 3 vs. 18 +/- 3 mmHg) and visceral vasoconstrictor (% delta in mesenteric resistance = 122.6 +/- 27.3 vs. 54.9 +/- 6.9%) responses during heating. Tail-skin blood flow estimated from Ttail was also lower at baseline and the onset of heating in water-deprived rats. However, peak Ttail and Tco values were similar across groups. Plasma catecholamines measured in separate groups of rats (n = 6 per group) were significantly higher at baseline and the end of heating in the 48-h group compared with euhydrated and 24-h groups. Despite this exaggerated sympathoadrenal response, the 48-h group exhibited attenuated hemodynamic responses to nonexertional heating compared with euhydrated and 24-h water-deprived rats. These data suggest that cardiovascular and thermoregulatory adjustments can compensate for small changes in hydration state (i.e., 24 h), but more severe levels of hypohydration significantly alter blood pressure and body temperature regulation during heat stress.

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.

Abstract 413: Renal Cyclooxygenase-2 Expression And Hemodynamic Role During Angiotensin II-dependent Hypertension

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Alexis A Gonzalez ◽  
Torrance Green ◽  
Camille R Bourgeois ◽  
Christina Luffman ◽  
Minolfa C Prieto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Late Phase ◽  
Renal Hemodynamics ◽  
Cyclooxygenase 2 ◽  
Kidney Cortex ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Cox 2

Intrarenal cyclooxygenase-2 (COX-2) activity is increased during activation of the renin-angiotensin-system (RAS) increasing synthesis of prostaglandin E2 (PGE2) and buffering the vasoconstrictor and antinatriuretic effects of angiotensin II (AngII). While AngII upregulates intrarenal COX-2 expression, it remains unclear if this occurs in a time-dependent manner, thereby impacting renal hemodynamics differently during the early and late phases of the development of high blood pressure in AngII-induced hypertension. Male Sprague-Dawley rats were infused with AngII (0.4 μg/min/kg). Systolic blood pressure (SBP), COX-2 expression and PGE2 tissue content and urinary excretion were evaluated at day 3, 7 and 14 of the AngII infusions. In acute studies we evaluated the effects of COX-2 inhibition at day 5-7 and day 14 on renal hemodynamic parameters. Chronic AngII infusions increased SBP from day 7 through 14: 162 ± 5 mmHg; and 198 ± 15 mmHg versus controls: 114 ± 10 mmHg; P<0.05. COX-2 mRNA and protein levels were high in kidney cortex only at day 3 (mRNA: 241 ± 56%, protein: 160 ± 21%, P<0.05 versus controls). Medullary COX-2 mRNA and protein were increased on days 3 (mRNA: 176 ± 20%, protein: 185 ± 32%, P<0.05 versus controls), 7 (mRNA: 189 ± 23%, protein: 158 ± 15%, P<0.05 versus controls) and 14 (mRNA: 148 ± 15%, protein: 135 ± 13%, P<0.05 versus controls). Urinary and medullary PGE2 increased by day 3 and remained elevated during days 7 and 14. COX-2 inhibition decreased GFR and renal blood flow in AngII infused rats during both the early and late phases. Interestingly, COX-2 inhibition decreased mean arterial blood pressure at day 14 of AngII-infusion (COX-2 inhibition: 124 ± 9 versus 140 ± 7 mmHg, P<0.05) but not during the early normotensive phase (COX-2 inhibition: 110 ± 4 versus 115± 4 mmHg, P=NS). These results indicate that enhanced medullary COX-2 expression and PGE2 production during both the early and late phases attenuates the effects of AngII on renal hemodynamics. However COX-2 inhibition at day 14 reduced blood pressure, suggesting that a vasoconstrictor COX-2 metabolite contributes to the hypertension during the late phase.

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.

Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1802-1808 ◽  
Author(s):  
S. N. Hussain ◽  
C. Roussos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Endotoxic Shock ◽  
Organ Blood Flow ◽  
Similar Reduction ◽  
Arterial Blood

Respiratory muscle blood flow and organ blood flow during endotoxic shock were studied in spontaneously breathing dogs (SB, n = 6) and mechanically ventilated dogs (MV, n = 5) with radiolabeled microspheres. Shock was produced by a 5-min intravenous injection of Escherichia coli endotoxin (0.55:B5, Difco, 10 mg/kg) suspended in saline. Mean arterial blood pressure and cardiac output in the SB group dropped to 59 and 45% of control values, respectively. There was a similar reduction in arterial blood pressure and cardiac output in the MV group. Total respiratory muscle blood flow in the SB group increased significantly from the control value of 51 +/- 4 ml/min (mean +/- SE) to 101 +/- 22 ml/min at 60 min of shock. In the MV group, respiratory muscle perfusion fell from control values of 43 +/- 12 ml/min to 25 +/- 3 ml/min at 60 min of shock. In the SB group, 8.8% of the cardiac output was received by the respiratory muscle during shock in comparison with 1.9% in the MV group. In both groups of dogs, blood flow to most organs was compromised during shock; however, blood flow to the brain, gut, and skeletal muscles was higher in the MV group than in the SB group. Thus by mechanical ventilation a fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during endotoxic shock.

Sign in / Sign up

Export Citation Format

Share Document