scholarly journals Lymph flow pattern in pleural diaphragmatic lymphatics during intrinsic and extrinsic isotonic contraction

2016 ◽  
Vol 310 (1) ◽  
pp. H60-H70 ◽  
Author(s):  
Andrea Moriondo ◽  
Eleonora Solari ◽  
Cristiana Marcozzi ◽  
Daniela Negrini
Keyword(s):  
Skeletal Muscle ◽  
Shear Stress ◽  
Muscle Contraction ◽  
Ex Vivo ◽  
Muscle Fibers ◽  
Lymphatic Vessels ◽  
Smooth Muscle Contraction ◽  
Skeletal Muscle Fibers ◽  
Skeletal Muscle Contraction

Peripheral rat diaphragmatic lymphatic vessels, endowed with intrinsic spontaneous contractility, were in vivo filled with fluorescent dextrans and microspheres and subsequently studied ex vivo in excised diaphragmatic samples. Changes in diameter and lymph velocity were detected, in a vessel segment, during spontaneous lymphatic smooth muscle contraction and upon activation, through electrical whole-field stimulation, of diaphragmatic skeletal muscle fibers. During intrinsic contraction lymph flowed both forward and backward, with a net forward propulsion of 14.1 ± 2.9 μm at an average net forward speed of 18.0 ± 3.6 μm/s. Each skeletal muscle contraction sustained a net forward-lymph displacement of 441.9 ± 159.2 μm at an average velocity of 339.9 ± 122.7 μm/s, values significantly higher than those documented during spontaneous contraction. The flow velocity profile was parabolic during both spontaneous and skeletal muscle contraction, and the shear stress calculated at the vessel wall at the highest instantaneous velocity never exceeded 0.25 dyne/cm2. Therefore, we propose that the synchronous contraction of diaphragmatic skeletal muscle fibers recruited at every inspiratory act dramatically enhances diaphragmatic lymph propulsion, whereas the spontaneous lymphatic contractility might, at least in the diaphragm, be essential in organizing the pattern of flow redistribution within the diaphragmatic lymphatic circuit. Moreover, the very low shear stress values observed in diaphragmatic lymphatics suggest that, in contrast with other contractile lymphatic networks, a likely interplay between intrinsic and extrinsic mechanisms be based on a mechanical and/or electrical connection rather than on nitric oxide release.

scholarly journals Defective Acetylcholine Receptor Subunit Switch Precedes Atrophy of Slow-Twitch Skeletal Muscle Fibers Lacking ERK1/2 Kinases in Soleus Muscle

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shuo Wang ◽  
Bonnie Seaberg ◽  
Ximena Paez-Colasante ◽  
Mendell Rimer
Keyword(s):  
Skeletal Muscle ◽  
Acetylcholine Receptor ◽  
Soleus Muscle ◽  
Muscle Fibers ◽  
Neuromuscular Synapse ◽  
Fiber Morphology ◽  
Skeletal Muscle Fibers ◽  
Slow Twitch

Abstract To test the role of extracellular-signal regulated kinases 1 and 2 (ERK1/2) in slow-twitch, type 1 skeletal muscle fibers, we studied the soleus muscle in mice genetically deficient for myofiber ERK1/2. Young adult mutant soleus was drastically wasted, with highly atrophied type 1 fibers, denervation at most synaptic sites, induction of “fetal” acetylcholine receptor gamma subunit (AChRγ), reduction of “adult” AChRε, and impaired mitochondrial biogenesis and function. In weanlings, fiber morphology and mitochondrial markers were mostly normal, yet AChRγ upregulation and AChRε downregulation were observed. Synaptic sites with fetal AChRs in weanling muscle were ~3% in control and ~40% in mutants, with most of the latter on type 1 fibers. These results suggest that: (1) ERK1/2 are critical for slow-twitch fiber growth; (2) a defective γ/ε-AChR subunit switch, preferentially at synapses on slow fibers, precedes wasting of mutant soleus; (3) denervation is likely to drive this wasting, and (4) the neuromuscular synapse is a primary subcellular target for muscle ERK1/2 function in vivo.

Ischemia/reperfusion-induced changes in intracellular free Ca2+ levels in rat skeletal muscle fibers – an in vivo study

2000 ◽  
Vol 440 (2) ◽  
pp. 302-308 ◽  
Author(s):  
Tamás Ivanics ◽  
Zsuzsa Miklós ◽  
Zoltán Ruttner ◽  
Sándor Bátkai ◽  
Dick W. Slaaf ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
In Vivo Study ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Induced Changes

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

2009 ◽  
Vol 297 (1) ◽  
pp. H433-H442 ◽  
Author(s):  
Ashok K. Dua ◽  
Nickesh Dua ◽  
Coral L. Murrant
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Muscle Fibers ◽  
Nitric Oxide Donor ◽  
Contraction Frequency ◽  
Skeletal Muscle Contraction ◽  
Train Duration ◽  
Arteriolar Vasodilation ◽  
40 Hz

To test the hypothesis that the vasodilator complement that produces arteriolar vasodilation during muscle contraction depends on both stimulus and contraction frequency, we stimulated four to five skeletal muscle fibers in the anesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibers. Diameter was measured before, during, and after 2 min of skeletal muscle contraction stimulated over a range of stimulus frequencies [4, 20, and 40 Hz; 15 contractions/min (cpm), 250 ms train duration] and a range of contraction frequencies (6, 15, and 60 cpm; 20 Hz stimulus frequency, 250 ms train duration). Muscle fibers were stimulated in the absence and presence of an inhibitor of adenosine receptors [10−6 M xanthine amine congener (XAC)], an ATP-dependent potassium (K+) channel inhibitor (10−5 M glibenclamide), an inhibitor of a source of K+ by inhibition of voltage-dependent K+ channels [3 × 10−4 M 3,4-diaminopyridine (DAP)], and an inhibitor of nitric oxide synthase [10−6 M NG-nitro-l-arginine methyl ester (l-NAME) + 10−7 S-nitroso- N-acetylpenicillamine (a nitric oxide donor)]. l-NAME inhibited the dilations at all stimulus frequencies and contraction frequencies except 60 cpm. XAC inhibited the dilations at all contraction frequencies and stimulus frequencies except 40 Hz. Glibenclamide inhibited all dilations at all stimulus and contraction frequencies, and DAP did not inhibit dilations at any stimulus frequencies while attenuating dilation at a contraction frequency of 60 cpm only. Our data show that the complement of dilators responsible for the vasodilations induced by skeletal muscle contraction differed depending on the stimulus and contraction frequency; therefore, both are important determinants of the dilators involved in the processes of arteriolar vasodilation associated with active hyperemia.

scholarly journals In Vivo Fatigue Reduces In Vitro Performance In Human Skeletal Muscle Fibers

2021 ◽  
Vol 53 (8S) ◽  
pp. 110-111
Author(s):  
Austin W. Ricci ◽  
Scott J. Mongold ◽  
Grace E. Privett ◽  
Karen W. Needham ◽  
Damien M. Callahan
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Muscle Fibers ◽  
Skeletal Muscle Fibers ◽  
In Vitro Performance

Diaphragmatic lymphatic vessel behavior during local skeletal muscle contraction

2015 ◽  
Vol 308 (3) ◽  
pp. H193-H205 ◽  
Author(s):  
Andrea Moriondo ◽  
Eleonora Solari ◽  
Cristiana Marcozzi ◽  
Daniela Negrini
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Lymphatic Vessel ◽  
Muscle Fibers ◽  
Video Recording ◽  
Three Dimensional ◽  
Longitudinal Axis ◽  
Vessel Diameter ◽  
Skeletal Muscle Contraction ◽  
Lymphatic Network

The mechanism through which the stresses developed in the diaphragmatic tissue during skeletal muscle contraction sustain local lymphatic function was studied in 10 deeply anesthetized, tracheotomized adult Wistar rats whose diaphragm was exposed after thoracotomy. To evaluate the direct effect of skeletal muscle contraction on the hydraulic intraluminal lymphatic pressures (Plymph) and lymphatic vessel geometry, the maximal contraction of diaphragmatic fibers adjacent to a lymphatic vessel was elicited by injection of 9.2 nl of 1 M KCl solution among diaphragmatic fibers while Plymph was recorded through micropuncture and vessel geometry via stereomicroscopy video recording. In lymphatics oriented perpendicularly to the longitudinal axis of muscle fibers and located at <300 μm from KCl injection, vessel diameter at maximal skeletal muscle contraction ( Dmc) decreased to 61.3 ± 1.4% of the precontraction value [resting diameter ( Drest)]; however, if injection was at >900 μm from the vessel, Dmc enlarged to 131.1 ± 2.3% of Drest. In vessels parallel to muscle fibers, Dmc increased to 122.8 ± 2.9% of Drest. During contraction, Plymph decreased as much as 22.5 ± 2.6 cmH2O in all submesothelial superficial vessels, whereas it increased by 10.7 ± 5.1 cmH2O in deeper vessels running perpendicular to contracting muscle fibers. Hence, the three-dimensional arrangement of the diaphragmatic lymphatic network seems to be finalized to efficiently exploit the stresses exerted by muscle fibers during the contracting inspiratory phase to promote lymph formation in superficial submesothelial lymphatics and its further propulsion in deeper intramuscular vessels.

scholarly journals Effects of dihydropyridine receptor II-III loop peptides on Ca2+ release in skinned skeletal muscle fibers

2000 ◽  
Vol 279 (4) ◽  
pp. C891-C905 ◽  
Author(s):  
Graham D. Lamb ◽  
Roque El-Hayek ◽  
Noriaki Ikemoto ◽  
D. George Stephenson
Keyword(s):  
Skeletal Muscle ◽  
Direct Action ◽  
Muscle Fibers ◽  
Dihydropyridine Receptor ◽  
Intracellular Loop ◽  
Release Channel ◽  
Voltage Sensors ◽  
Skeletal Muscle Fibers ◽  
Peptide Segments

In skeletal muscle fibers, the intracellular loop between domains II and III of the α1-subunit of the dihydropyridine receptor (DHPR) may directly activate the adjacent Ca2+ release channel in the sarcoplasmic reticulum. We examined the effects of synthetic peptide segments of this loop on Ca2+ release in mechanically skinned skeletal muscle fibers with functional excitation-contraction coupling. In rat fibers at physiological Mg2+ concentration ([Mg2+]; 1 mM), a 20-residue skeletal muscle DHPR peptide [AS(20); Thr671-Leu690; 30 μM], shown previously to induce Ca2+ release in a triad preparation, caused only small spontaneous force responses in ∼40% of fibers, although it potentiated responses to depolarization and caffeine in all fibers. The COOH-terminal half of AS(20)[AS(10)] induced much larger spontaneous responses but also caused substantial inhibition of Ca2+release to both depolarization and caffeine. Both peptides induced or potentiated Ca2+ release even when the voltage sensors were inactivated, indicating direct action on the Ca2+ release channels. The corresponding 20-residue cardiac DHPR peptide [AC(20); Thr793-Ala812] was ineffective, but its COOH-terminal half [AC(10)] had effects similar to AS(20). In the presence of lower [Mg2+] (0.2 mM), exposure to either AS(20) or AC(10) (30 μM) induced substantial Ca2+ release. Peptide CS (100 μM), a loop segment reported to inhibit Ca2+ release in triads, caused partial inhibition of depolarization-induced Ca2+ release. In toad fibers, each of the A peptides had effects similar to or greater than those in rat fibers. These findings suggest that the A and C regions of the skeletal DHPR II-III loop may have important roles in vivo.

scholarly journals Contraction and AICAR Stimulate IL-6 Vesicle Depletion From Skeletal Muscle Fibers In Vivo

Diabetes ◽  
2013 ◽  
Vol 62 (9) ◽  
pp. 3081-3092 ◽  
Author(s):  
Hans P.M.M. Lauritzen ◽  
Josef Brandauer ◽  
Peter Schjerling ◽  
Ho-Jin Koh ◽  
Jonas T. Treebak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Skeletal Muscle Fibers

scholarly journals Mesenteric lymph flow in adult and aged rats

2011 ◽  
Vol 301 (5) ◽  
pp. H1828-H1840 ◽  
Author(s):  
Tony J. Akl ◽  
Takashi Nagai ◽  
Gerard L. Coté ◽  
Anatoliy A. Gashev
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Ex Vivo ◽  
Lymphatic Vessels ◽  
Lymph Flow ◽  
Contraction Frequency ◽  
Stress Load ◽  
Wall Shear ◽  
Contractile Characteristics

The objective of study was to evaluate the aging-associated changes, contractile characteristics of mesenteric lymphatic vessels (MLV), and lymph flow in vivo in male 9- and 24-mo-old Fischer-344 rats. Lymphatic diameter, contraction amplitude, contraction frequency, and fractional pump flow, lymph flow velocity, wall shear stress, and minute active wall shear stress load were determined in MLV in vivo before and after Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME) application at 100 μM. The active pumping of the aged rat MLV in vivo was found to be severely depleted, predominantly through the aging-associated decrease in lymphatic contractile frequency. Such changes correlate with enlargement of aged MLV, which experienced much lower minute active shear stress load than adult vessels. At the same time, pumping in aged MLV in vivo may be rapidly increased back to levels of adult vessels predominantly through the increase in contraction frequency induced by nitric oxide (NO) elimination. Findings support the idea that in aged tissues surrounding the aged MLV, the additional source of some yet unlinked lymphatic contraction-stimulatory metabolites is counterbalanced or blocked by NO release. The comparative analysis of the control data obtained from experiments with both adult and aged MLV in vivo and from isolated vessel-based studies clearly demonstrated that ex vivo isolated lymphatic vessels exhibit identical contractile characteristics to lymphatic vessels in vivo.

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