Microvascular response to blockade of prostaglandin synthesis in rat skeletal muscle

1982 ◽  
Vol 243 (1) ◽  
pp. H51-H60 ◽  
Author(s):  
J. E. Faber ◽  
P. D. Harris ◽  
I. G. Joshua
Keyword(s):  
Skeletal Muscle ◽  
Cremaster Muscle ◽  
Local Blood Flow ◽  
Local Inhibition ◽  
Microvascular Response ◽  
Before And After ◽  
Endogenous Prostaglandins ◽  
The Moment ◽  
Arteriolar Tone ◽  
Arteriolar Diameter

The contribution of endogenous prostaglandins (PGs) to the control of arteriolar diameter in the microcirculation is incompletely defied and has only been studied in drug-anesthetized animals. To test the possibility that endogenous PGs are tonically released to exert a net dilator influence at certain levels in the microcirculation, television microscopy was used to quantitate the arteriolar responses in the rat cremaster muscle to local blockade of PG synthesis with indomethacin. Rats were decerebrated by a midcollicular transection and were allowed to recover from surgical anesthesia. The cremaster muscle with intact circulation and innervation was suspended by sutures in a temperature-controlled Krebs bath. Diameters, vasomotion frequency, and vasomotion amplitude of arterioles at several anatomic levels were measured before and after local inhibition of PG synthesis in the presence and absence of alpha-adrenergic receptor blockade. Inhibition of PG synthesis produced marked constriction (42-66% of control) at all arteriolar levels, with greater responses occurring in the smaller arterioles. PG synthesis blockade increased vasomotion frequency in arterioles that exhibited spontaneous vasomotion during control periods, and blockade induced vasomotion in vessels lacking spontaneous vasomotion. Pretreatment with phentolamine significantly attenuated the constriction and augmentation of vasomotion. These data indicate that dilator PGs participate in the moment-to-moment regulation of arteriolar tone and local blood flow in skeletal muscle. Further, their mechanism of action may involve alterations in neuronal norepinephrine release or alpha-receptor sensitivity.

Regulation of arteriolar tone and responses via L-arginine pathway in skeletal muscle

1992 ◽  
Vol 262 (4) ◽  
pp. H987-H992 ◽  
Author(s):  
G. Kaley ◽  
A. Koller ◽  
J. M. Rodenburg ◽  
E. J. Messina ◽  
M. S. Wolin
Keyword(s):  
Skeletal Muscle ◽  
Vascular Tone ◽  
Topical Administration ◽  
Systemic Blood Pressure ◽  
Vasoactive Agents ◽  
Skeletal Muscle Microcirculation ◽  
Arteriolar Tone ◽  
Dose Dependent ◽  
Arteriolar Diameter

With in vivo television microscopy, changes in arteriolar diameter to topical administration of various vasoactive agents were examined in the absence or in the presence of NG-monomethyl-L-arginine (L-NMMA, topical 100 microM) or NG-nitro-L-arginine (L-NNA, 2.5 microM, 20 microliters/min ia), specific inhibitors of endothelium-derived relaxing factor (EDRF) biosynthesis. In cremaster muscle arterioles (15-22 microns) of rats (n = 6-11), dilations to acetylcholine (1-100 ng) were significantly inhibited (60-70%) by either of the arginine analogues. This inhibition was reversed by subsequent administration of 1 mM L-arginine. Dose-dependent constriction to norepinephrine was enhanced by L-NMMA. Indomethacin treatment reduced arteriolar dilation to bradykinin (BK, 1-100 ng), which was significantly inhibited by additional administration of L-NNA. Application of L-NNA first, followed by additional indomethacin, elicited similar results. Dilations to sodium nitroprusside and adenosine were not reduced in the presence of the inhibitors. L-NMMA or L-NNA caused no change in systemic blood pressure but elicited a significant reduction in arteriolar diameter; this effect was not reversed by 1 mM L-arginine. These data demonstrate the presence of an L-arginine pathway to produce EDRF (nitric oxide) in skeletal muscle microcirculation that mediates and/or modulates arteriolar responses to vasoactive agents and could contribute to the regulation of basal vascular tone.

Dilation of isolated skeletal muscle arterioles by insulin is endothelium dependent and nitric oxide mediated

1996 ◽  
Vol 270 (6) ◽  
pp. H2120-H2124 ◽  
Author(s):  
Y. L. Chen ◽  
E. J. Messina
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Cardiac Output ◽  
Flow State ◽  
Insulin Administration ◽  
Cremaster Muscle ◽  
Response Curves ◽  
Solution Ph ◽  
First Order ◽  
Before And After

Studies in humans and animals have shown that insulin administration increases cardiac output and both forearm and hindlimb blood flow. In this study we tested the hypothesis that insulin dilates skeletal muscle arterioles and that the dilation is endothelium dependent. First-order arterioles (77 microns) from rat cremaster muscle were isolated, pressurized (65 mmHg), equilibrated in a Krebs bicarbonate-buffered solution (pH 7.4) gassed with 10% O2 (5% CO2-85% N2), and studied in a no-flow state. Cumulative concentration-response curves to insulin (10 microU/ml-10 mU/ml) were obtained in intact arterioles before and after either endothelium removal or administration of indomethacin (Indo, 10(-5) M) or nitro-L-arginine (L-NNA, 10(-4) M). Insulin evoked concentration-dependent increases in control diameter of 13-61%, which were completely inhibited by endothelium removal or L-NNA. In contrast, Indo had no effect on insulin-evoked arteriolar dilation. These results indicate that dilation to insulin in skeletal muscle arterioles is endothelium dependent and mediated by nitric oxide.

ATP-mediated release of arachidonic acid metabolites from venular endothelium causes arteriolar dilation

2001 ◽  
Vol 280 (6) ◽  
pp. H2616-H2622 ◽  
Author(s):  
Leah W. Hammer ◽  
Alison L. Ligon ◽  
Robert L. Hester
Keyword(s):  
Air Bubbles ◽  
Cremaster Muscle ◽  
In Vivo Microscopy ◽  
Relaxing Factor ◽  
Acid Metabolites ◽  
Male Golden Hamsters ◽  
Arteriolar Tone ◽  
Arteriolar Diameter ◽  
Venular Endothelium

This study was designed to test the hypothesis that venular administration of ATP resulted in endothelium-dependent dilation of adjacent arterioles through a mechanism involving cyclooxygenase products. Forty-three male golden hamsters were anesthetized with pentobarbital sodium (60 mg/kg ip), and the cremaster muscle was prepared for in vivo microscopy. ATP (100 μM) injected into venules dilated adjacent arterioles from a mean diameter of 51 ± 4 to 76 ± 6 μm ( P < 0.05, n = 6). To remove the source of endothelial-derived relaxing factors, the venules were then perfused with air bubbles to disrupt the endothelium. Resting arteriolar diameter was not altered after disruption of the venular endothelium (51 ± 5 μm), and the responses to venular ATP infusions were significantly attenuated (59 ± 4 μm, P < 0.05). To determine whether the relaxing factor was a cyclooxygenase product, ATP infusion studies were repeated in the absence and presence of indomethacin (28 μM). Under control conditions, ATP (100 μM) infusion into the venule caused an increase in mean arteriolar diameter from 55 ± 4 to 78 ± 3 μm ( P < 0.05, n = 6). In the presence of indomethacin, mean resting arteriolar tone was not significantly altered (49 ± 4 μm), and the response to ATP was significantly attenuated (54 ± 4 μm, P < 0.05, n = 6). These studies show that increases in venular ATP concentrations stimulate the release of cyclooxygenase products, possibly from the venular endothelium, to vasodilate the adjacent arteriole.

Endothelial regulation of wall shear stress and blood flow in skeletal muscle microcirculation

1991 ◽  
Vol 260 (3) ◽  
pp. H862-H868 ◽  
Author(s):  
A. Koller ◽  
G. Kaley
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Flow Velocity ◽  
Cremaster Muscle ◽  
Skeletal Muscle Microcirculation ◽  
Wall Shear ◽  
Arteriolar Diameter ◽  
Dependent Mechanism

In the presence of intact endothelium, in control conditions, calculated wall shear rate (WSR) (means +/- SE: 2,658 +/- 123 s-1; n = 21) was independent of arteriolar diameter (16.2-27.2 microns; correlation coefficient: r = 0.12, P greater than 0.05) in cremaster muscle of pentobarbital-anesthetized rats. An increase in blood flow velocity (due to parallel arteriolar occlusion) elicited a significant increase in WSR (to 4,981 +/- 253 s-1) followed by a delayed (6-15 s) increase in diameter (from: 22.5 +/- 0.6 to 29.5 +/- 0.8 microns), which consequently resulted in a significant decrease in WSR (to 3,879 +/- 203 s-1). As a result of the increased flow velocity and dilation, calculated arteriolar blood flow increased by 230%. After impairment of the endothelium of arterioles by a light-dye technique, basal WSR became significantly higher (3,604 +/- 341 s-1), and despite a greater increase in WSR (10,360 +/- 1,471 s-1) the dilation was absent. Now an inverse linear correlation was found between arteriolar diameter and WSR both before (r = 0.58, P less than 0.05) and during increased flow velocity conditions (r = 0.85, P less than 0.05). Also, arteriolar blood flow that was already less after impairment of endothelium increased by only 66% during the period of increased flow velocity due to the absence of dilation. Results suggest that an increase in wall shear stress is the stimulus for the endothelium-dependent mechanism that elicits "flow dependent" arteriolar dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of endothelium in reactive dilation of skeletal muscle arterioles

1990 ◽  
Vol 259 (5) ◽  
pp. H1313-H1316 ◽  
Author(s):  
A. Koller ◽  
G. Kaley
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cremaster Muscle ◽  
Anesthetized Rats ◽  
Vasoactive Factors ◽  
Peak Increase ◽  
Arteriolar Diameter

In cremaster muscle of pentobarbital-anesthetized rats, the role of endothelium in the reactive dilation of an arteriole (mean control diameter: 18.2 +/- 0.5 microns) during and after short (approximately 20 s) or long (approximately 80 s) occlusion of a parent arteriole was investigated. Distal to the occluder, arteriolar diameter increased during the occlusion (mean peak increase: 6.9 +/- 0.4 and 6.7 +/- 1.1 microns, respectively) and increased even further after the release of the occlusion as blood flow was reestablished (additional mean increase: 6.5 +/- 0.7 and 5.8 +/- 0.8 microns, respectively). The duration of arteriolar dilation after the release of the occlusion was dependent on the duration of occlusion (252.2 +/- 37 vs. 411.3 +/- 57 s; P less than 0.05). After impairment of the arteriolar endothelium by light/dye treatment, a dilation was still present during both the shorter and longer occlusions (mean increase: 4.73 +/- 1.4 and 4.73 +/- 1.3 microns, respectively); however, in both cases the additional dilation after release of the occlusion was greatly diminished. The duration of reactive arteriolar responses following impairment of the endothelium was significantly reduced only on release of the shorter occlusions. The results suggest that reactive dilation (hyperemia) of arterioles is the result of multiple, endothelium-dependent and endothelium-independent vasoactive factors.

Effect of NG-monomethyl-L-arginine on arcade arterioles of rat spinotrapezius muscles

1991 ◽  
Vol 261 (1) ◽  
pp. H46-H52 ◽  
Author(s):  
T. Nakamura ◽  
R. L. Prewitt
Keyword(s):  
Specific Inhibitor ◽  
Onset Of Action ◽  
Adrenoceptor Antagonist ◽  
No Formation ◽  
Vasoactive Substances ◽  
Adrenoceptor Agonist ◽  
Before And After ◽  
Arteriolar Tone ◽  
Arteriolar Diameter

The effect of the specific inhibitor of nitric oxide (NO) formation NG-monomethyl-L-arginine (L-NMMA) on resting arteriolar diameter and on actions of both endothelium-dependent and -independent vasoactive substances was investigated using intravital microscopy in rats. The spinotrapezius muscle of anaesthetized normotensive rats was suspended in a Krebs-Henseleit bath containing tetrodotoxin (3 x 10(-7) M), indomethacin (2.8 x 10(-5) M), and propranolol (10(-6) M) to block sympathetic nerve conduction, prostacyclin formation, and beta-adrenergic receptors, respectively. Acetylcholine (ACh), nitroprusside (NP), norepinephrine (NE), phenylephrine (PE), and guanabenz (GB) were topically applied before and after superfusion of L-NMMA (10(-5) to 10(-4) M). Superfusion of L-NMMA reduced arteriolar diameter and caused dose-dependent increases in arteriolar tone. The onset of action of L-NMMA was nearly immediate. L-NMMA inhibited vasodilator responses to the endothelium-dependent vasodilator ACh but not to the endothelium-independent NP. NE induced dose-related vasoconstriction that was significantly potentiated by L-NMMA. These effects were partially reversed by addition of L-arginine (10(-3) M). Potentiation of vasoconstriction elicited by NE was still observed after inhibition of alpha 1-adrenoceptors with prazosin, but potentiation was abolished by the alpha 2-adrenoceptor antagonist yohimbine. L-NMMA potentiated arteriolar vasoconstriction elicited by the alpha 2-adrenergic receptor agonist GB but not by the alpha 1-adrenoceptor agonist PE. These findings with L-NMMA suggest that resting diameter of arterioles is modulated by endogenous NO biosynthesis and that endothelium-dependent vasodilators act through the formation of endogenous NO to exert their action in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Vitamin B6 Deficiency can Reduce Fuel Storage and Utilization in Physically Trained Rats

2008 ◽  
Vol 78 (2) ◽  
pp. 64-69 ◽  
Author(s):  
Choi ◽  
Cho
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Muscle Protein ◽  
Plasma Free Fatty Acid ◽  
Vitamin B ◽  
Liver Protein ◽  
Protein Levels ◽  
Before And After ◽  
Fuel Storage ◽  
Exercise Muscle

This study investigated the effect of vitamin B6 deficiency on the utilization and recuperation of stored fuel in physically trained rats. 48 rats were given either vitamin B6-deficient (B6–) diet or control (B6+) diet for 4 weeks and were trained on treadmill for 30 minutes daily. All animals were then subdivided into 3 groups: before-exercise (BE); during-exercise (DE); after-exercise (AE). The DE group was exercised on treadmill for 1 hour just before being sacrificed. Animals in the AE group were allowed to take a rest for 2 hours after being exercised like the DE group. Glucose and free fatty acids were compared in plasma. Glycogen and triglyceride were compared in liver and skeletal muscle. Protein levels were compared in plasma, liver, and skeletal muscle. Compared with the B6+ group, plasma glucose levels of the B6– group were significantly lower before and after exercise. Muscle glycogen levels of the B6– group were significantly lower than those of the B6+ group regardless of exercise. The liver glycogen level of the B6– group was also significantly lower than that of B6+ group during and after exercise. Before exercise, plasma free fatty acid levels were not significantly different between the B6+ and B6– groups, and plasma free fatty acid levels of the B6– group were significantly lower during and after exercise. The muscle triglyceride level of the B6– group was significantly lower than that of the B6+ group before exercise, and there were no differences between B6+ and B6– groups during and after exercise. Liver triglyceride levels were not significantly different between B6+ and B6– groups. Plasma protein levels of the B6– group were lower than those of B6+ before and after exercise. Muscle protein levels of the B6– group were not significantly different from those of the B6+ group. Liver protein levels of the B6– group were significantly lower than that of the B6+ group after exercise. Liver protein levels of both B6+ and B6– groups were not significantly changed, regardless of exercise. Thus, it is suggested that vitamin B6 deficiency may reduce fuel storage and utilization with exercise in physically trained rats.

EVALUATION OF THE EFECTS OF ELECTRONIC ACUPUNCTURE COMBINED WITH “TAM TY THANG” REMEDY IN THE TREATMENT OF RHEUMATOID ARTHRITIS BY WIND-COLD-DAMP

2017 ◽  
pp. 122-127
Author(s):  
Thi Luu Nguyen ◽  
Thi Tan Nguyen
Keyword(s):  
Rheumatoid Arthritis ◽  
Side Effects ◽  
Prospective Study ◽  
Key Words Rheumatoid Arthritis ◽  
Good Effect ◽  
Good Level ◽  
Relieve Pain ◽  
Level Of Activity ◽  
Before And After ◽  
The Moment

Objectives: To assess the effect of electronic acupuncture combined with “Tam ty thang” remedy in the treatment of rheumatoid arthritis by wind-cold-damp. Materials and methods: prospective study, comparing before and after treatment, including 43 patients who were diagnosed with rheumatoid arthritis by wind-cold-damp according to traditional medicine. Results: good level occupied 69,8%, and fair good level occupied 30,2%.The improved motor function accounted for 95.3%, to relieve pain up to 95,3%, reducing inflammation of VSS in 1 hour at the moment No 31,65, N28 17,88. The improvement in the level of activity of the hand reached 48,8% for good level. Conclusions: The method of electronic acupuncture combined with “Tam ty thang” remedy have a good effect in the treatment of rheumatoid arthritis by wind-cold-damp and it didn’t cause significantly side effects in clinic. Key words: rheumatoid arthritis, electronic acupuncture, “Tam ty thang” remedy

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