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PubMed1988

Distribution of vascular resistance in terminal arteriolar networks of cat sartorius muscle.

Morphometric information on the terminal arteriolar networks (n = 10) in cat sartorius muscle [Koller et al., Am. J. Physiol. 253 (Heart Circ. Physiol. 22): H154-H164, 1987] is utilized in the calculations of distribution of vascular hindrance throughout the networks. These networks have tree-type geometry, i.e., they do not contain closed loops. The results are discussed in terms of simulated flow distribution. The flow calculations are based on the exact geometry of the arteriolar networks (the control and dilated diameter and the length of each vascular segment) and on assumed values of postarteriolar resistances. Three cases of postarteriolar resistances are considered: zero, constant, and randomly distributed. With zero postarteriolar resistances, the distribution of flow in the terminal arteriolar segments would be highly heterogenous. The simulated flow in each terminal segment is determined primarily by the number of bifurcations on the pathway leading to the terminal segment, with a slight compensation for the length of the pathways. The coefficient of variation of flow in the control state, CV(Qc), would be close to the value in the dilated state, CV(Qd). When each of the terminal segments is connected to a constant postarteriolar resistance, the CV's in both states decrease. The coefficient of variation in the dilated state becomes significantly smaller than in the control state. When postarteriolar resistances are randomly distributed, both CV's increase, and their values become closer to each other. These results suggest that postarteriolar resistances may play a very important role in distribution of flow in the microvascular network. This study formulates a framework for the quantification of the effect of arteriolar dilation on flow redistribution in the network.

Animals↗

PubMedDate not supplied

Morphometric analysis of the anastomosing arteriolar network in cat sartorius muscle.

Topological and geometrical characteristics of the anastomotic arteriolar network in cat sartorius muscle were studied. The vessels were dilated and filled with gelatin-ink solution and the muscle cleared with methylsalicylate. The analysis was done on 11 muscles and included 2297 vascular segments and 772 vascular loops classified according to their position within the network. On average, each muscle had 644 transverse arterioles arising from the anastomotic vessels. The length of vascular segments close to feeding arteries was greater than those located in the central region, while the number of transverse arterioles per unit length of arcade vessel showed an opposite tendency. Most vessel orders had similar diameters, except for the segments at the periphery of the muscle, which were significantly larger. No correlation was found between vessel length and diameter. Vascular loops located in the central part of the network were smaller, as assessed by area, perimeter, number of segments, segment length and number of branches. The variability of the parameters between muscles was smaller than variability within each muscle. We concluded that, in addition to the parameters previously reported, quantitative descriptions of anastomotic networks may be enhanced by considering certain topological aspects of microvessels. The separation of segments and loops according to the position in the network may reveal differences between muscles of different sizes and functions which would not be detected if the vessels were considered as a single group.

Animals↗

PubMed1975

Sarcotubular anomalous rectification of frog sartorius muscle.

The membrane site responsible for anomalous rectification was determined in frog sartorius muscle fibers. The total current-voltage relation of glycerol-treated fibers which represents mainly the properties of the sarcolemma was linear for membrane potentials between about -90 and -50 mV. Thus moderate depolarization-induced anomalous rectification in intact fibers represents a property of the sarcotubular system. The absence of slow hyperpolarization in glycerol-treated fibers was caused by the abolition of early conductance increase, and the sarcotubular system is responsible for the inward rectifier. Picrotoxin selectively inhibited both moderate depolarization-induced anomalous rectification and hyperpolarization-induced early conductance increase. This suggests that the same component in the sarcotubular system is responsible for these conductance changes. The inhibition with picrotoxin of moderate depolarization-induced anomalous rectification suggests the possibility that it is caused by an electrogenic effect rather than a decrease in K conductance. A sarcolemmal hyperpolarization-activated slow conductance increase was revealed.

Animals↗

PubMed1983

[Mediator secretion in the proximal and distal portions of a nerve ending of the sartorius muscle in the frog].

In experiments on neuromuscular preparations of the frog sartorius muscle the evoked transmitter release was investigated by extracellular recording. A decrease of the evoked transmitter release from proximal to distal parts of nerve terminals was observed related to a decrease in probability of transmitter quantum release. The terminal part of synapse showed smaller sensitivity to an increase in extracellular Ca2+ concentration as compared with the proximal part, smaller facilitation of transmitter release at double and repetitive stimulation, deeper and more quickly developing depression. A conclusion is made that these peculiarities of the transmitter release in the terminal parts of the synapse are due to smaller transmitter reserve and smaller permeability of the presynaptic membrane to Ca2+ ions.

Animals↗

PubMed1978

The effect of veratrine on 24Na uptake by frog sartorius muscle in hypertonic media.

The effect of veratrine on 24Na uptake by sartorius muscles incubated in hypertonic media has been studied. 1. 0.1 mM veratrine increases 24Na uptake in muscles incubated even in different hypertonic solutions (normal Ringer + 300 mM sucrose or glucose or 150 mM NaCl). 2. 0.05 mM curare inhibits the 24Na uptake increasing effect of veratrine in hypertonic solution 3. 0.1 mM ouabain, whether in isotonic or hypertonic solution, does not influence the resting 24Na uptake, and does not decrease the 24Na uptake increasing effect of veratrine in isotonic media; however, in hypertonic solution it inhibits the 24Na uptake increasing effect. 4, 5 X 10(-8) M tetrodotoxin blocks completely the 24Na uptake enhancing effect of veratrine both in isotonic and in hypertonic Ringer's solution. 5. It is suggested that the sites of action of the 24Na uptake increasing effect of veratrine are the neural structures in muscle, in hypertonic media.

Animals↗

PubMed1984

[Arterial supply of the sartorius muscle].

According to dissections of 40 specimen we received an impression of the arterial supply of the sartorius muscle. The results were as following that the sartorius is supplied by 2-4 arteries, occasionally up to 9, which originate from the middle and distal third of the femoral artery. As a result of the dissections we may state that the sartorius receives an adequate supply, when only the proximal or distal artery remains intact. Because of the above, the sartorius is suitable as a proximally or distally based flap in plastic surgery of the abdominal wall and as covering of bone defects of the hip, femur and knee.

Femoral Artery↗

PubMed1967

Quinine and caffeine effects on 45Ca movements in frog sartorius muscle.

1 mM caffeine, which produces only twitch potentiation and not contracture in frog sartorius muscle, increases both the uptake and release of (45)Ca in this muscle by about 50 %, thus acting like higher, contracture-producing concentrations but less intensely. Quinine increases the rate of release of (45)Ca from frog sartorius but not from the Achilles tendon. The thresholds for the quinine effect on (45)Ca release and contracture tension are about 0.1 and 0.5 mM, respectively, at pH 7.1. Quinine (2 mM) also doubles the uptake of (45)Ca by normally polarized muscle. However, there are variable effects of quinine upon (45)Ca uptake in potassium-depolarized muscle. Quinine (2 mM), increases the Ca, Na, and water content of muscle while decreasing the K content. Both caffeine (1 mM) and quinine (2 mM) act to release (45)Ca from muscles that have been washed in Ringer's solution from which Ca was omitted and to which EDTA (5 mM) was added. These results, correlated with those of others, indicate that a basic effect of caffeine and quinine on muscle is to directly release activator Ca(2+) from the sarcoplasmic reticulum in proportion to the drug concentration. The drugs may also enhance the depolarization-induced Ca release caused by extra K(+) or an action potential. In respect to the myoplasmic Ca(2+) released by direct action of the drugs, a relatively high concentration is required to activate even only threshold contracture, but a much lower concentration, added to that released during excitation-contraction coupling, is associated with the condition causing considerable twitch potentiation.

Action Potentials↗

PubMed1989

Changes in thick filament structure during compression of the filament lattice in relaxed frog sartorius muscle.

Equatorial X-ray diffraction patterns from relaxed, chemically-skinned frog sartorius muscles under a range of external osmotic pressures from 0 to 290 torr have been analysed and compared to the pattern from the relaxed intact muscle. Lattice spacings and electron density diagrams were determined as a function of external pressure. Reflection intensities, averaged over small ranges of pressures, were determined out to the 4,0 reflection; phases for the first five orders were established as ++--+ over the whole pressure range. As external pressure was increased, lattice spacing decreased, as did full width at half maximum density for both thick and thin filaments. Most of the lattice spacing and thick filament compression occurred at low pressure, whereas thin filaments were compressed proportionally to pressure over the whole pressure range. These conclusions were confirmed by fitting cylindrical models for filament density to the X-ray diffraction patterns. Axially-projected electron density across the A-band filament lattice showed that in relaxed muscle the thick filament projections (myosin heads) are concentrated in regions between adjacent thick filaments, as far as possible from the thin filaments, and they tend to become pushed against the thick filament backbone as the lattice is compressed. Both thick and thin filament axes can be displaced randomly from their lattice positions; on average this displacement is about twice as great for the thin filaments, accounting for their larger projected size as compared to isolated thin filaments and for their apparent decrease in diameter as the lattice is compressed.

Absorptiometry, Photon↗

PubMed1984

Effect of veratridine on membrane potential of sartorius muscle from Rana pipiens.

The effect of veratridine on the membrane potential of sartorius muscles from Rana pipiens was studied. Membrane potential (Vm) was measured in Ringer solutions containing 2.5, 10, 30, 75, and 190 mM K+ in the absence and presence of veratridine. The product [K]o[Cl]o was kept at 300 mM2 to maintain Donnan equilibrium. External Na+ was lowered to 10 mM. Ouabain (100 microM) was present in all solutions. Vm vs. log [K]o curves were fit using the Goldman-Hodgkin-Katz equation with a single free parameter, alpha = PNa/PK (permeability ratio of Na to K). Veratridine (100 microM) causes alpha to increase 12.6 +/- 1.2-fold (n = 9), from 0.146 to 1.657. The effect of veratridine on Vm is dose dependent and reversible, with a time constant for washout of 40 min. The depolarization produced by veratridine is prevented by tetrodotoxin and by Mg, is sensitive to external Na concentration, and is insensitive to curare.

Animals↗

PubMed1980

Ionic mechanism of the resting membrane depolarization of frog sartorius muscle induced by dimorpholamine.

Ionic mechanism of the resting membrane depolarization of frog sartorius muscle induced by dimorpholamine was studied in a variety of ionic conditions. The resting membrane was depolarized in a dose-dependent manner reaching a maximum with a dose of 6 X 10(-5) M. The amount of the depolarization (1.4 mV) was suppressed with doses over 10(-4) M. This dose-dependent response was accompanied by change in the membrane conductance. The chloride conductance was increased by 16% and the potassium conductance by 7%, however the sodium conductance did not significantly change with a dose of 2 X 10(-5) M. The slight depolarization induced by the drug was well explained by the changes in the ionic conductance. The effects of these actions on the membrane action potentials were simulated, suggesting that this drug possesses the nature of a stimulant on excitable membranes yet does not produce any appreciable depolarization blockade.

Animals↗

PubMed1976

Effect of hypocalcic media on chemical sensitivity of toad sartorius muscle.

Membrane potential and spike activity were recorded through intracellular electrodes from toad sartorius muscles superfused in Krebs solution. When this was replaced by a hypocalcic medium (1/20 of normal Krebs Ca2+ concentration), muscles showed extrajunctional sensitivity to acetylcholine, histamine and noradrenaline applied iontophoretically. Normal sensitivity was restored when muscles were bathed in normal calcium media. Changes in chemical excitability of the fibers immersed in hypocalcic solution were related to decreased input membrane resistance. These observations emphasize the role played by Ca2+ on electrical stability and chemical sensitivity of skeletal muscle membrane.

Animals↗

PubMed1976

Aerobic recovery metabolism following a single isometric tetanus in frog sartorius muscle at 0 degrees C.

1. Basal and recovery O2 consumption, delatO2, in frog sartorius muscles at 0 degrees C were measured with a polarographic electrode. Reproducible observations were made with the same muscle over many hours. 2. The experimental records had an exponential form except for the early phases of recovery following a single isometric tetanus. Diffusion of O2 within the muscle was adequate to account for this deviation from an exponential time course of recovery. The time constant of the recovery O2 consumption increased with the duration of tetanic stimulation from 5 to 20 sec. 3. Lactate synthesis was measureable in unstimulated aerobic muscles and increased in proportion to total O2 consumption as long as the muscle did not lack O2. The contribution of glycolysis to the total chemical energy production during recovery was 6-9%; for hypoxic muscles it was greater. 4. The resynthesis of phosphorylcreatine and the decrease in inorganic phosphate and free creatine following a tetanus showed an exponential time course similar to recovery O2. Initial concentrations were re-attained within 60 min following a 20 sec tetanus. 5. We conclude that recovery O2 consumpation is a useful and accurate measure of the net chemical energy utilization for a single contraction.

Aerobiosis↗

PubMed1986

Enhancement of the twitch of bull frog sartorius muscle by fluorides.

Effects of 5 kinds of fluorides on the twitch of the sartorius muscle of the bull frog were investigated. All of the fluorides (0.1-2.0 mM) enhanced the twitch evoked by nerve stimulation. The extents of enhancement at 2.0 mM were in the order: stannous fluoride much greater than potassium fluoride greater than sodium silico fluoride greater than sodium fluoride greater than diammine silver fluoride. The extent of each enhancement was larger than that in the case of direct stimulation of the muscle. These findings show that fluorides commonly enhance the twitch of skeletal muscle and that the extent of enhancement is related to the properties of cations included in the fluoride.

Animals↗

PubMed2002

Sartorius muscle afferents influence the amplitude and timing of flexor activity in walking decerebrate cats.

Recent investigations have demonstrated that afferent signals from hindlimb flexor muscles can strongly influence flexor burst activity during walking and during fictive locomotion in decerebrate cats. We have reported previously that modifying afferent feedback from the sartorius (Sart) muscles by assisting or resisting hip flexion has a marked effect on the magnitude and duration of activity in iliopsoas (IP) as well as the sartorius muscles. The objective of the present investigation was to identify the afferents responsible for these effects by examining, in walking decerebrate cats, the influence of electrically stimulating sartorius afferents on burst activity in the IP and tibialis anterior (TA) muscles. Stimulation of the sartorius nerve at group I strength resulted in an increase in the duration of IP and TA bursts and an increase in the magnitude of IP bursts. The effect on burst durations was only observed at stimulus strengths of 1.6 T and higher. At lower stimulus strengths, there was a strong excitatory effect on IP bursts but no effect on TA bursts. Stimulation of the sartorius nerve at group II strength yielded variable results. When group II stimulation was delivered repeatedly during a walking sequence, the initial response was usually a strong inhibition of burst activity in IP and TA followed by a progressive reduction in inhibition and the emergence in IP of an excitatory response. This observation, together with findings of previous studies, suggests the existence of parallel excitatory and inhibitory pathways from sartorius group II afferents to flexor motoneurons. Taken together, these results support an earlier speculation that feedback from large afferents from the sartorius muscles has a strong influence on the generation of flexor burst activity in walking cats.

Afferent Pathways↗

PubMed1988

Synaptic competition and the elimination of polyneuronal innervation following reinnervation of adult frog sartorius muscles.

The elimination of polyneuronal innervation (synapse elimination) that occurs following reinnervation was studied in sartorius muscles of adult Rana pipiens. The percentage of neuromuscular junctions that were polyneuronally innervated declined from 47% at 40-80 days after nerve crush to 22% at greater than 250 days after nerve crush. We measured the size, synaptic strength, and position of competing nerve terminals at identified dually innervated neuromuscular junctions at these two different periods of synapse elimination. Our goal was to determine if any of these parameters play a role in the competition between nerve terminals that ultimately results in the elimination of polyneuronal innervation. Our data support the hypothesis that polyneuronal innervation will persist if competing nerve terminals are of similar synaptic efficacies but will be eliminated if the competing terminals are of different synaptic efficacies. We also tested, but failed to find any evidence, that the spatial proximity of competing nerve terminals at the same synaptic site influences the elimination of polyneuronal innervation.

Action Potentials↗

PubMed1963

INHIBITION OF CAFFEINE RIGOR AND RADIOCALCIUM MOVEMENTS BY LOCAL ANESTHETICS IN FROG SARTORIUS MUSCLE.

Local anesthetics have been found to act as competitive inhibitors of caffeine in frog sartorius muscle. They block caffeine-induced rigor and the attendant increase in Ca(45) influx and efflux. Increased net uptake of sodium, loss of potassium, and concurrent increase in oxygen consumption are all effectively blocked by procaine. Evidence is presented that the inhibitory effect of the local anesthetics cannot be explained by the formation of molecular complexes with caffeine. Increased efflux of Ca(45) produced by changing from zero calcium Ringer's to 0.1 mM or 1 mM calcium Ringer's is inhibited by procaine and tetracaine. EDTA-stimulated calcium efflux is not affected by either local anesthetic. Caffeine rigor develops in frog muscle depolarized with KCl or rendered electrically inexcitable by sodium lack. Both the rigor and the increased calcium fluxes are inhibited by local anesthetics in depolarized muscle.

Anesthetics, Local↗

PubMed1973

Electrical properties of toad sartorius muscle fibres in summer and winter.

1. The area and circumference of surface fibres of sartorius muscles were measured from photomicrographs of frozen sections of whole muscles, and compared with the values obtained assuming a circular cross-section. The latter assumption gave an over-estimate of the mean area of 28%, but only a 2% over-estimate of the circumference. In isolated, single fibres, the assumption gave over-estimates of 25 and 6%, of area and circumference respectively.2. The passive electrical properties of fibres were different in summer and winter. The mean internal resistivity, membrane resistance and membrane capacitance were 147 Omega.cm, 7.6 kOmega.cm(2) and 4 muF/cm(2) in summer, and 194 Omega.cm, 3.9 kOmega.cm(2) and 6.7 muF/cm(2) in winter, in fibres of comparable diameters in situ. In single fibres in summer, the mean values were 120 Omega.cm, 8.6 kOmega.cm(2) and 3.6 muF/cm(2).3. In glycerol-treated fibres the mean specific membrane capacitance was 1.0 muF/cm(2) in summer and 2.0 muF/cm(2) in winter. The internal resistivity and specific membrane resistance were 167 Omega.cm and 8.9 kOmega.cm(2) in summer, and 232 Omega.cm and 3.9 kOmega.cm(2) in winter.4. Early after-depolarizations were recorded in glycerol-treated fibres which had a low membrane capacitance, did not twitch and showed little ;creep'. Electron micrographs of glycerol-treated fibres showed disruption of the transverse tubular system and sarcoplasmic reticulum.5. After exposure of muscles to 400 mM urea or acetamide for 1 hr, muscle fibres did not twitch and had a reduced membrane capacitance in Ringer solution.

Acetamides↗

PubMed1981

Effect of acclimation temperature and pH on contraction of frog sartorius muscle.

The effect of acclimation temperature and pH on the isometric twitch and tetanus of sartorius muscle from frog, Rana pipiens, was studied at different experimental temperatures. Seven variables were measured, namely: tension, latent period, time to maximum tension, half-relaxation time, mean rate, maximum rate, and maximum acceleration of tension development. The effect of experimental temperature was similar to that reported in the literature. The effects of acclimation temperature were small and were not compensatory. Different pH's were obtained by varying CO2 in the gas phase, while the HCO3- concentration was kept constant. The main effects of a decrease in pH on the isometric twitch and tetanus were a reduction in tension and rate of tension development and an increase in latent period. A decrease in pH had no effect on the time to maximum tension or the half-relaxation time. Analysis of variance showed that the test temperature had the greatest effect of all three treatments on each variable, the effects of test and acclimation temperature were dependent on neither the test nor the acclimation temperatures. The in vivo relationships between these three treatments are discussed.

Acclimatization↗