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PubMed1977

Chloride-induced contraction in a skinned fiber of toad striated muscle.

Cl- -induced contraction was studied in a skinned fiber dissected from toad sartorius muscle. When K-methanesulphonate in a relaxing solution was replaced isotonically with KCl, the skinned fiber contracted due to 'depolarization'-induced Ca++ release on the SR. Contraction was induced by superfusing the fiber with solutions containing different concentrations of Cl-. In the presence of 2 mM EGTA, the Cl- -induced contraction developed when the relaxing solution was replaced by a Cl- solution which contained up to 20 mM Cl-, while contraction started at 15 mM-Cl- in the presence of 0.5 mM EGTA. The peak tension of the Cl- -induced contraction depended on Cl- concentration without obeying the all-or-none law. When the fiber was treated with 1.5 mM caffeine, the threshold for the Cl- -induced contraction was significantly lowered. In spite of previous application of Cl- at different concentrations below 80 mM, the skinned fiber contracted by sudden increase in Cl- concentration, and the tension versus Cl- concentration curve revealed almost the same shape as that in a fiber equilibrated with Cl- -free solution. This suggests that the SR membrane is repolarized after transient depolarization caused by elevation of Cl- concentration.

Animals↗
PubMed1991

Dynamic performance of a load-moving skeletal muscle.

The dynamic response of the tibialis anterior muscle of the cat was determined while it was subjected to sinusoidally varying orderly stimulation of motor units and to different isotonic loads in the range of 14-85% of the maximal isometric force. The dynamic response consisted of three major components: the displacement gain, the displacement attenuation, and a pure time delay. The displacement gain was dependent on the passive load applied to the muscle and the active force generated during contraction, which could be determined from the length-tension relationships and the corresponding shortening velocity. In general, the load displacement decreased as the load mass increased from 25 to 85% of the maximal isometric force. For loads less than 25% of the maximal isometric force, slight decrease in displacement was consistently observed. The displacement attenuation was dependent on the contraction frequency but uniform for all the load masses applied to the muscle. A pure time delay of 5 ms was present and accounted for various physiological processes such as conduction time in nerve and muscle, neuromuscular junction transmission, and excitation-contraction coupling. A quantitative equation was developed to describe the muscle's dynamic response under isotonic conditions and for a wide range of loads for use in various applications.

Animals↗
PubMed1980

Effects of estradiol-17 beta on the membrane response and K-contracture in the uterine longitudinal muscle of ovariectomized rats studied in combination with the Mn action.

The membrane potential was about --50mV, and the spontaneous membrane activity was composed of an irregular discharge of action potentials in the longitudinal muscle of the ovariectomized rat uterus. The membrane potential was increased slightly, and repetitive spike potentials were generated on a plateau potential in uteri of ovariectomized rats injected daily with 5 microgram estradiol benzoate, until the steady effect was built up in 3--4 days. The phasic contraction resulted in a relaxation upon exposure to the isotonic K solution containing 2.2 mM Ca, then a tonic contraction developed in ovariectomized uterus. The phasic contraction decayed slightly and it proceeded into a tonic contraction in estrogen-treated uteri. The amplitude of the tonic contraction became larger when the external Ca concentration was raised, and the dose-response relationship shifted to the lower range of the external Ca concentration in the estrogen-treated uterus. In the Ca-depleted solution, the tonic contraction subsided and a contraction was generated when Mn was applied. The change in the configuration of the K-contractures depending on the estrogenic treatment was ascribed to an increase in the Ca influx upon K-depolarization forming greater tonic contraction.

Animals↗
PubMed1975

Time course of mechanical activity in mammalian cardiac muscle: dependence on species, loading, and displacement.

We have found that animal species is of great importance when mechanics of contraction are analyzed in mammalian cardiac muscle. Mechanics of contraction have been studied comparatively in the isolated papillary muscles of the rat, cat, and rabbit under control conditions and following alterations of loading and inotropic interventions. The time course of the shortening ability measured in terms of the velocity of shortening at constant contractile element length and load following quick releases to preload peaked at 20, 30, and 70% of time to peak force (TPF) in the rat, cat, and rabbit, respectively, and declined more slowly in the rabbit. The shortening ability peaked progressively later in contraction at increasing loads in the cat, but not in the rabbit. Shortening ability measured after releases to zero load or after imposing "load clamps" of variable magnitude and duration reached the maximum much later in the rabbit than in the cat. The contractile response to changes of the contraction mode from isometric to isotonic was different in cat and rabbit. Upon increase in the stimulation rate from 6 to 60/min, force increased to a greater extent in the rabbit than in the cat, while TPF did not decrease in the rabbit as seen in the cat. Caffeine (10mM) increased developed force more in the rabbit than in the cat, while even 1 mM caffeine decreased force in the rat. The onset of the shortening ability was greatly delayed by caffeine in the cat and rat but not in the rabbit. Afterloaded force-peak velocity relations were curvilinear in the cat and rat; these relations approached linearity in the rabbit in the control state, and in both cat and rabbit in the presence of caffeine. The differences in the mechanics of contraction, in the contractile response to alterations in loading, and to caffeine in the ventricular muscle of the rat, cat, and rabbit are viewed as indicators of differences in excitation-contraction coupling of ventricular cardiac muscle from these different mammalian species.

Animals↗
PubMed1993

Mechanism of the contractile response to platelet-activating factor (PAF) of the rat stomach fundus. I. PAF-induced contractile response and calcium mobilization.

1. Platelet-activating factor (PAF) caused contraction of the rat stomach fundus in a concentration-dependent manner in the presence of atropine, guanethidine, chlorpheniramine, methylsergide, indomethacin, nordihydroguaiaretic acid and tetrodotoxin. 2. PAF produced phasic contraction followed by tonic contraction. The PAF-induced tonic contraction was significantly reduced by treatment with CV-6209, an antagonist of PAF, but phasic contraction induced by PAF was rather resistant to CV-6209. 3. The contraction induced by PAF was markedly reduced when tissues were previously exposed to PAF (desensitization). 4. Nicardipine reduced the PAF-induced phasic contraction but not of the tonic contraction. 5. PAF-induced contractions were almost abolished in Ca(2+)-free medium. 6. The Ca(2+)-contraction in Ca(2+)-free solution was significantly augmented by PAF, whereas the Ca(2+)-contraction in Ca(2+)-free, isotonic high K+ (60 mM) medium was unaffected by PAF. 7. These results suggest that PAF-induced contractile response in the rat stomach fundus is due to an influx of Ca2+ through voltage-dependent Ca(2+)-channels (VDC) and receptor-operated Ca(2+)-channels (ROC). It is further suggested that PAF may depolarize the stomach fundus and this depolarization may open the VDC, whereas PAF may not act directly on the VDC.

Animals↗
PubMed1988

Regulation of glycerinated smooth muscle contraction and relaxation by myosin phosphorylation.

Regulation of isometric force maintenance, isotonic shortening velocity, and muscle stiffness by myosin phosphorylation was examined during both contraction and relaxation of chemically permeabilized (glycerinated) rat uterine smooth muscle. Phosphorylation of the 20,000-Da light chain of myosin (LC20) was manipulated by varying the calcium activity of the bathing solution or by thiophosphorylation of LC20 in the presence of ATP gamma S. With saturating calcium and calmodulin, LC20 phosphorylation was 0.43 mol PO4/mol LC20. This increased to 0.92-0.96 mol PO4/mol LC20 on addition of ATP gamma S. Over the entire range of phosphorylation, there was a significant (P less than 0.001) linear correlation between force and phosphorylation. Stiffness increased monotonically with increasing force; however, the relationship was nonlinear, with stiffness increasing faster at lower levels of activation. Force, stiffness, shortening velocity, and LC20 phosphorylation were compared at identical calcium activities during steady-state conditions of partial contraction and partial relaxation. The ratio of the value of each parameter measured during relaxation to that measured during contraction was 1.11 for force, 1.09 for stiffness, 1.01 for shortening velocity, and 0.83 for LC20 phosphorylation. These results support the hypothesis that contraction and relaxation in glycerinated rat uterine muscle are regulated primarily by phosphorylation and dephosphorylation of LC20.

Adenosine Triphosphate↗
PubMed1999

Calcium currents during contraction and shortening in enzymatically isolated murine skeletal muscle fibres.

1. Calcium currents (ICa) were monitored in enzymatically isolated murine toe muscle fibres using the two-microelectrode voltage-clamp technique. ICa was recorded (i) in hypertonic solution to suppress contraction, and (ii) in actively shortening fibres in isotonic solution. 2. In hypertonic solution the threshold potential for ICa was about -30 mV for both 2 and 10 mM external Ca2+ solution. Maximum peak currents measured -12.6 +/- 2.3 nA (mean +/- s.d.; n = 4) in 2 mM Ca2+ and -65 +/- 15 nA (n = 7) in 10 mM Ca2+. The time to peak (TTP) ICa was 96 +/- 22 ms (n = 4) in 2 mM Ca2+ and 132 +/- 13 ms (n = 7) in 10 mM Ca2+. The exponential decay of ICa was similar in 2 and 10 mM Ca2+ with rate constants (tau-1(V)) of 3.7 s-1 (2 mM) and 3.8 s-1 (10 mM) at +10 mV. 3. ICa in isotonic 10 mM Ca2+ solution was recorded by inserting the micropipettes exactly opposite to each other close to the centre of mass of the fibre where negligible contraction-induced movement occurs. 4. In isotonic 10 mM Ca2+ solution ICa had a smaller peak amplitude (-45 +/- 5 nA; n = 7) and faster TTP (82.8 +/- 22.1 ms; n = 7) than in hypertonic solution. The exponential decay of ICa showed a significantly larger tau-1(V) of 6.4 s-1 at +10 mV (P < 0.03). 5. To test for calcium depletion, extracellular Ca2+ was buffered by malic acid in isotonic solution to 9 mM. The decay of ICa had a time constant of 348 +/- 175 ms (n = 14) vs. 107 +/- 24 ms (n = 12; P < 0.001) at 0 mV in unbuffered 10 mM Ca2+ solution. 6. We conclude that calcium depletion from the transverse tubular system contributes significantly to the decay of calcium currents in murine toe muscle fibres under hypertonic as well as isotonic conditions. In the latter, depletion is even more prominent.

Animals↗
PubMedDate not supplied

Chronic implantation of a skeletal muscle energy convertor for cardiac assist devices: a preliminary report.

An efficient energy convertor capable of driving a variety of cardiac assist devices is being developed in goats. Muscle work in a linear configuration is converted to hydraulic energy and transmitted to an external test system that controls muscle loads during shortening contractions. This investigation focuses on the variation of muscle characteristics and optimal power output during muscle conditioning. The energy convertor was mounted on the rib cage, the latissimus dorsi insertion reattached to the device, and percutaneous hydraulic lines exited near the spine. Following device, stimulator, and intramuscular electrode implantation, a progressive conditioning protocol was initiated. Weekly biomechanical muscle characterization was performed in the conscious animal, with single twitch and tetanic contractions performed under isometric and isotonic conditions. The characterization data provide a measure of available power, as well as inputs, for a computer simulation that predicts optimal muscle power output and operating conditions. These ongoing implants provide insight into the available muscle power and suggest an implantable energy convertor is feasible. Development of an energy convertor is an important step toward tether free skeletal muscle powered cardiac assist. These studies will be expanded in number and duration to further investigate the effects of conditioning and identify improvements in device development.

Animals↗
PubMed1998

The contractile apparatus of airway smooth muscle. Biophysics and biochemistry.

Qualitatively the mechanical, structural, and biochemical properties of airway smooth muscles resemble those of all other smooth muscle. However, one important distinguishing feature of airway smooth muscle is that the major portion of isotonic shortening is completed within the first 3 s in a muscle whose contraction is 10 s. This indicates the importance of focusing on the changes that occur in these 3 s and also the limiting role of the maximum velocity of shortening in determining shortening data. There is evidence that the maximum capacity and velocity of shortening in human bronchial smooth muscle from patients with asthma are significantly greater than those obtained from healthy siblings. In the demonstration in which cells in culture are arrested by withdrawing all fetal calf serum, the cells alter their phenotype to cells that are very long (more than 200 micrometers) and shorten twice as much as cells freshly isolated when the tissue is new. Speculatively, if such cells developed in vivo they could account for the increased contractility of asthmatic airway smooth muscle. These cultured cells could also be excellent models for study of airway smooth muscle contractility.

Animals↗
PubMed1972

Biophysical effects of adrenaline on the smooth muscle of the rabbit common carotid artery.

Effects of adrenaline on the smooth muscle of the rabbit common carotid artery were studied by the partitional chamber method. The experiments on excitation-contraction coupling were carried out in isotonic Krebs solution; the other experiments were carried out in hypertonic Krebs solution. Adrenaline (10(-7) g/ml) caused rhythmical electrical and mechanical activity of arterial strips in isotonic Krebs solution. By addition of adrenaline (10(-5) g/ml), the membrane was depolarized by about 10 mv and the amplitude of the electrotonic potential was decreased by 40-50% of the control in hypertonic Krebs solution. Present experimental results suggest that the depolarization of the membrane and the decrease of the amplitude of the electrotonic potential in the artery are due to the increase of Na and Cl conductance. Contraction appeared in all preparations exposed to 10(-8) g/ml adrenaline; at that concentration membrane potential and membrane resistance showed little or no change.

Animals↗
PubMed2004

Experimental muscle pain reduces initial motor unit discharge rates during sustained submaximal contractions.

The aim of this human study was to investigate the effect of experimentally induced muscle pain on the modifications of motor unit discharge rate during sustained, constant-force contractions. Intramuscular and multichannel surface electromyographic (EMG) signals were collected from the right and left tibialis anterior muscle of 11 volunteers. The subjects performed two 4-min-long isometric contractions at 25% of the maximal dorsiflexion torque, separated by a 20-min rest. Before the beginning of the second contraction, hypertonic (painful; right leg) or isotonic (nonpainful; left leg) saline was injected into the tibialis anterior. Pain intensity scores did not change significantly in the first 150 s of the painful contraction. Exerted torque and its coefficient of variation were the same for the painful and nonpainful contractions. Motor unit discharge rate was higher in the beginning of the nonpainful contraction than the painful contraction on the right side [means +/- SE, 11.3 +/- 0.2 vs. 10.6 +/- 0.2 pulses/s (pps); P < 0.01] whereas it was the same for the two contractions on the left side (11.6 +/- 0.2 vs. 11.5 +/- 0.2 pps). The decrease in discharge rate in 4 min was smaller for the painful (0.4 +/- 0.1 pps) than for the control contractions (1.3 +/- 0.1 pps). Initial value and decrease in motor unit conduction velocity were not different in the four contractions (right leg, 4.0 +/- 0.1 m/s with decrease of 0.6 +/- 0.1 m/s in 4 min; left leg, 4.1 +/- 0.1 m/s with 0.7 +/- 0.1 m/s decrease). In conclusion, stimulation of nociceptive afferents by injection of hypertonic saline did not alter motor unit conduction velocity but reduced the initial motor unit discharge rates and the difference between initial and final discharge rates during sustained contraction.

Adult↗
PubMed2004

[Effects of fatigue on the characteristics of cat gastrocnemius muscle contraction and elongation in response to changes of the controlled load].

Spreading of fatigue-related effects from active to inactive parts in the cat gastrocnemius muscle was studied. Fatiguing contractions of a part of gastrocnemius muscle were evoked through stimulation of the cut ventral root (VR) S1 with rate 50 s(-1) during 20 s followed by 10 s of rest, over 10-30 min (CFS). To test activation of a non-active part of this muscle the distributed stimulation of dissected VR L7 with rate of 10 s(-1) per filament was applied. After achieving by the muscle a steady-state level of isometric contraction, a quick transition to isotonic condition was produced. Transient responses of shortening and lengthening were analyzed in terms of the two-component model including the fast inertialess and slow aperiodic components. Test duration was 12 s, time intervals between tests consisted of 3 min. CFS reduced isometric force of the tested part of muscle as well as the velocity of shortening and lengthening. The muscle lengthening had been slowing down with development of the fatigue effects; the final steady value of the muscle length in transients was reduced, while weight of the inertialess component increased. Slowing of shortening was accompanied by reduction of the final length amplitude and the time constants of aperiodic component were increased. We suppose that diffusion of metabolites from active to inactive muscle fibers was the major reason for contractility deterioration.

Animals↗
PubMed2005

Experimental muscle pain decreases voluntary EMG activity but does not affect the muscle potential evoked by transcutaneous electrical stimulation.

OBJECTIVE: The aim of this human study was to investigate if voluntary EMG activity and supra-maximal M-wave are affected by injection of hypertonic saline to experimentally induce muscle pain. METHODS: Surface EMG signals were recorded with an electrode array from the tibialis anterior muscle of 12 subjects. Two sets of 6 contractions, 3 electrically elicited and 3 voluntary (30% of the maximal force), alternated, were performed with each leg. During the second set of 6 contractions, hypertonic (painful; right leg) or isotonic (non-painful; left leg) saline was injected 3 times (0.2, 0.5, 0.9 ml), separated by 140 s, into the tibialis anterior. RESULTS: In the voluntary contractions, EMG average rectified value (ARV) significantly decreased (mean+/-SE, 13.2 +/- 4.2%) with increasing pain, although the exerted torque was unaltered. Conduction velocity (CV) (4.2 +/- 0.2 and 4.4 +/- 0.3 m/s, right and left leg, respectively) and mean power spectral frequency (MPF) (119.0 +/- 8.4 and 119.5+/-8.9 Hz) were not affected by the injection of hypertonic saline. In the electrically elicited contractions, M-wave CV (4.6 +/- 0.3 and 4.7 +/- 0.2 m/s), ARV (748.6 +/- 101.8 and 822.3 +/- 104.4 microV), and MPF (72.0+/-5.1 and 76.9+/-4.8 Hz) did not change with pain. CONCLUSIONS: Injection of hypertonic saline did not change muscle fiber conduction velocity or impaire neuromuscular transmission. The decrease in voluntary EMG activity with injection of hypertonic saline was thus due to central factors. SIGNIFICANCE: The injection of hypertonic saline provides a model for exciting nociceptive afferents without affecting muscle fiber electrophysiological properties.

Action Potentials↗
PubMed1997

Acetaldehyde depresses shortening and intracellular Ca2+ transients in adult rat ventricular myocytes.

Acetaldehyde (ACA), an ethanol metabolite, exerts both stimulatory and depressive effects on isolated myocardial tissue, but its impact on individual cardiac myocytes is unknown. The purpose of this study was to determine whether ACA-induced myocardial depression is due to an intrinsic alteration of the contractile properties of heart at the cellular level. Mechanical properties of adult rat ventricular myocytes were evaluated using a video edge-detection system. Myocytes were electrically stimulated to contract at 0.5 Hz under isotonic conditions in a physiological buffer containing 1 mM CaCl2. Contractile properties analyzed include: peak twitch amplitude (PTA), time-to-PTA (TPT), time-to-relengthening (TR90) and maximal velocities of shortening and relengthening (+/-dL/dt). Ca2+ transients were measured as fura-2 fluorescence intensity (FFI) changes. ACA (1-30 mM) disproportionately depressed PTA and FFI in a dose-dependent manner, with maximal inhibitions of 57 and 19%, respectively. Neither the durations nor maximal velocities of shortening and relengthening were affected by ACA. The depression of cell shortening by ACA was either attenuated or blocked by BayK 8644 or elevated extracellular Ca2+ (2.7 mM). In addition, ACA also reduced caffeine-induced FFI changes. These results suggest that ACA-induced myocardial depression in multicellular preparations is due to an intrinsic action on individual myocytes. The mechanism underlying ACA-induced myocardial depression may be due, in part, to either reduced Ca2+ entry through voltage-dependent Ca2+ channels and/or depression of sarcoplasmic reticular Ca2+ release.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Effects of CD-349, a dihydropyridine derivative, on contraction induced by vasoactive agents in canine basilar artery after subarachnoid hemorrhage.

We investigated the effects of CD-349, a dihydropyridine derivative, on contraction induced by vasoactive agents in canine basilar artery after subarachnoid hemorrhage (SAH). Ca(2+)-induced contraction of basilar arterial strips preincubated with serotonin (5-HT, 3x10(-6)M) was potentiated in strips from SAH. However, Ca(2+)-induced contraction of arterial strips which were depolarized with isotonic K+ (64mM) was attenuated in strips from SAH. These Ca(2+)-induced contractions of the basilar arteries preincubated with 5-HT and K+ from both control and SAH dogs were significantly inhibited by CD-349 and nicardipine, both dihydropyridine derivatives. 5-HT contracted the basilar arterial strips in a concentration-dependent manner; however, the maximal contraction of the basilar arterial strips to 5-HT was enhanced in SAH. Endothelium-dependent relaxation in response to substance-P was attenuated in SAH when compared to that in control dogs. Early treatment with CD-349 (1 or 2mg/kg/day, i.m.) for 1 week reversed not only the enhanced contraction of the basilar artery in response to 5-HT but also the impairment of endothelium-dependent relaxation in response to substance-P in SAH. It is expected that CD-349 may be a useful agent for the treatment of cerebrovascular diseases such as SAH.

Animals↗