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At least 91 records · Page 5Linked to original sources
PubMed1975

Acid-base changes and excitation-contraction coupling in rabbit myocardium. I. Effects on isometric tension development at different contraction frequencies.

The effects of changes in acid-base parameters on the active force of isolated rabbit papillary muscles were studied at contraction frequencies of 12, 60 and 120/min. When extracellular pH was lowered from 7.4 to 7.0 and 6.7 in a bathing solution buffered with 10 mM histidine, the active force decreased at all contraction frequencies studied. After parallel increases of HCO3-minus concentration (up to 47 mM) and PCO2 at a constant extracellular pH of 7.4 the active force of the muscle increased at low and decreased at high contraction frequencies. None of these effects can be attributed to catecholamine release or to altered extracellular concentration of ionized calcium. The inotropic effects produced by bicarbonate were not reproducible by methyl sulfate (47 mM) or propionate (47 mM). It is concluded that: 1. a lowering of the extracellular pH has a negative inotropic effect at all frequencies, 2. HCO3-minus has a positive inotropic effect that is most pronounced at low contraction frequencies and 3. CO2 has a negative inotropic effect exceeding that produced by the mere reduction in extracellular pH. The cellular mechanisms involved in the various inotropic effects are discussed.

Animals↗
PubMed2001

Cardiac excitation-contraction coupling: role of membrane potential in regulation of contraction.

The steps that couple depolarization of the cardiac cell membrane to initiation of contraction remain controversial. Depolarization triggers a rise in intracellular free Ca(2+) which activates contractile myofilaments. Most of this Ca(2+) is released from the sarcoplasmic reticulum (SR). Two fundamentally different mechanisms have been proposed for SR Ca(2+) release: Ca(2+)-induced Ca(2+) release (CICR) and a voltage-sensitive release mechanism (VSRM). Both mechanisms operate in the same cell and may contribute to contraction. CICR couples the release of SR Ca(2+) closely to the magnitude of the L-type Ca(2+) current. In contrast, the VSRM is graded by membrane potential rather than Ca(2+) current. The electrophysiological and pharmacological characteristics of the VSRM are strikingly different from CICR. Furthermore, the VSRM is strongly modulated by phosphorylation and provides a new regulatory mechanism for cardiac contraction. The VSRM is depressed in heart failure and may play an important role in contractile dysfunction. This review explores the operation and characteristics of the VSRM and CICR and discusses the impact of the VSRM on our understanding of cardiac excitation-contraction coupling.

Animals↗
PubMed1976

Length-induced changes in activation during contraction. A study of mechanical oscillations in strontium-mediated contractions of cat and frog heart muscle.

The plateau phase of prolonged Sr-mediated contractions of preparations of cat and frog heart muscle was used to study the transient response to abrupt changes in load or length. An oscillatory response (total amplitude equal to or less than 5% Lmax) was obtained. Isotonic oscillations were less damped than their isometric counterparts, implying positive feedback and thus a causal role of the perturbation in length. Oscillation frequency was 2-3 HZ at 29 degrees C (Q 10, 2-3); it could be increased by epinephrine or caffeine, independently of their effects on extent of shortening; it otherwise changed as a generally constant function of the length at which the oscillation occurred, whether this was altered by changes in extracellular [Sr], frequency of contraction, or load (independent of the direction and magnitude of the preceding load step). Similar oscillatory responses were induced during Sr- or Ca-mediated contractures. Cat muscles showed an additional slower component to the oscillatory response. Transient augmentation of the velocity-length relationship after abrupt reduction in load, previously described for twitch contractions under certain conditions, appears to be analogous to the first phase of the oscillatory response studied here. Our findings indicate that the oscillation is not attributable to any mechanism intrinsic to myofilament interaction, but rather that it involves length-induced changes in the level of activation, probably mediated by Ca2+ or Sr2+. We conclude that length influences the level of activation during contraction of heart muscle.

Action Potentials↗
PubMed1981

Calcium ion-insensitive contraction of glycerinated porcine cardiac muscle fibers by Mg-inosine triphosphate. ITP as a tool to dissociate the contraction mechanism from the regulatory mechanism.

The contraction of cardiac muscle that has been treated with glycerol requires Ca2+ (pCa 8-5), when MgATP is used as a substrate. In contrast, this preparation contracts, even in the absence of Ca2+ (pCa 8-10), when ATP is replaced by ITP. Ca2+ dependency was not observed after increasing free Ca2+ concentrations from pCa 8.0 to 5.0, or after increasing MgITP concentration from 5 to 80 mM. On the other hand, rabbit skeletal muscle fiber treated by the same method as cardiac muscle demonstrates Ca2+ dependency in the presence of both MgITP and MgATP, although this Ca2+ regulation is less in the presence of MgITP. Loss of Ca2+ dependency was confirmed by the finding that, in contrast to ATPase, the ITPase activity of cardiac myofibrils was not dependent on Ca2+ concentrations. Furthermore, the very fast tension responses (quick phases) following quick stretch and quick release were missing in MgITP, and the contractions were similar to rigor. These were not rigor however, because phosphate liberation from ITP continued, and muscle shortening occurred in MgITP. These findings suggest that MgITP dissociates the contraction mechanism from the regulatory mechanism, modulating the regulatory properties of cardiac muscle fiber.

Adenosine Triphosphatases↗
PubMed1990

The clinical information system contract process--contract philosophy and management: Part III.

The first two installments in this series dealt with contract negotiation methodology and contract contents. This final segment deals with subjects that all too often overlooked, but which are just as important as the first two. They are important because the attitude with which parties enter contractual arrangements largely determines the parties' future relationship and the management of contracts large determines whether the contract is successful.

Clinical Medicine↗
PubMed1978

[Effect of neural regulation on the fluctuations in the intervals between cardiac contractions and the force of the contractions].

Statistical analysis of the cardiac rhythm according to the R--R intervals and the force of contractions according to their amplitude was undertaken. The variation coefficient (N%) reflecting the degree of irregularity of intervals between the contractions and the force of contractions during maximum cardiac hyperfunction induced by clamping the aorta for 30 sec was determined. Vagotomy led to a decrease in the irregularity for cardiac rhythm and force of cardiac contractions.

Animals↗
PubMed1990

[Muscle contraction headache and posture--with special reference to ischemic contraction of the posterior neck muscles].

Cause of muscle contraction headache (MCH) results from sustained contraction of scalp and posterior neck muscles. Recently, we published an effect of posture on the etiology of MCH. According to our data, head bending posture seems to be one of the main causes of sustained contraction of the posterior neck muscles. Wolff presented a hypothesis of ischemic contraction of these muscles as a cause of pain. However, about the blood flow of scalp or posterior neck muscles, only two reports were published so far. These two papers failed to demonstrate a reduction of blood flow in MCH patients, and neglected the effect of posture. The purpose of this report is to examine a change of blood flow of posterior neck muscles with the change of posture. A total of 40 patients with MCH were studied using laser doppler blood flow meter. Needle shaped probe with a diameter of 0.55 mm was inserted 15 mm into the posterior neck muscle. The angle between orbito-meatal line and horizontal plane were measured using a light helmet with goniometer. Surface EMG of the posterior neck muscles was recorded at the same time. In the case of controls who do not experience headache, the amplitude of EMG increases slightly with the bending posture (40 microV with OM line 20 degrees upward from the horizontal plane, 46 microV with OM line horizontal, and 52 microV when 30 degrees downward). In reverse to the increase of the EMG activity, blood flow of the neck muscles decreases (12 ml/100 g/min with OM line 20 degrees upward, 10.8 with OM line horizontal, 7.6 at 10 degrees down, 4.6 at 20 degrees down, and 4.1 at 30 degrees down).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Patterns of uterine contractions and prolonged uterine activity using three methods of breast stimulation for contraction stress tests.

The contraction patterns in 378 breast-stimulated contraction stress tests administered to 213 women are described. The subjects were assigned sequentially to one of four intervention groups: bilateral manual breast massage, unilateral pump stimulation, heating pad stimulation, and placebo. There was a marked increase in the proportion of tests with three to four contractions in 5-minute intervals after the interventions occurred. Twenty-five percent of all tests showed prolonged uterine activity, occurring most frequently in women with postdate gestations using manual massage or breast pump stimulation. The duration of prolonged contractions ranged from 1.5-8 minutes, with 19% lasting from 4.5-8 minutes. There was no difference in the incidence of fetal heart rate abnormalities between tests with and without prolonged uterine activity, and no late decelerations occurred in tests with tachysystole.

Adolescent↗
PubMed1980

Reversible phosphorylation and dephosphorylation of the 20,000-dalton light chain of myosin during the contraction-relaxation-contraction cycle of arterial smooth muscle.

The myosin light chain of intact arterial smooth muscle displayed a cyclic phosphorylation-dephosphorylation and rephosphorylation in consort with contraction, followed by relaxation, followed by a second contraction of the muscle. Application of pharmacological contractile agonists and antagonists of vascular smooth muscle revealed that the level of light chain phosphorylation is related to the contractile state of the muscle. The central role of Ca2+ in regulation of light chain phosphorylation was shown by the effect of ethylene glycol bis(beta-aminoethyl ether)N,N,N',N'-tetraacetic acid (EGTA) in inhibiting contraction and light chain phosphorylation and in inducing relaxation and light chain dephosphorylation. Furthermore, studies with antipsychotic drugs, inhibitors of calmodulin, suggested that the Ca2+-dependent regulatory protein is intimately involved in both light chain phosphorylation and contraction of intact smooth muscle. In addition to the myosin light chain, several other proteins were also found to be phosphorylated in intact smooth muscle.

Animals↗
PubMed1994

Pertussis toxin blocks M2 muscarinic receptor-mediated effects on contraction and cyclic AMP in the guinea pig ileum, but not M3-mediated contractions and phosphoinositide hydrolysis.

The effects of pertussis toxin on muscarinic receptor-induced contractions of the isolated guinea pig ileum were investigated. In control tissues, isoproterenol (1 microM) only slightly inhibited contractions in response to oxotremorine-M; however, in pertussis toxin-treated tissues, isoproterenol exhibited an enhanced inhibition of the concentration-effect curve. Under basal conditions, pertussis toxin had no dampening effect on oxotremorine-M-induced contractions. When ilea were precontracted with histamine (1 microM) and then relaxed back to base line using forskolin (10 microM) before contractile responses to oxotremorine-M were measured, pertussis toxin shifted the concentration-effect curve to oxotremorine-M by a 6.1-fold increase in the EC50 value. Ilea were then incubated with [N-(2-chloroethyl)-4-piperidinyl diphenylacetate] (40 nM; 1 hr) in the presence of [[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5,11- dihydro-6H-pyrido[2,3b][1,4]benzodiazepine-6-one (1 microM) to selectively inactivate the M3 muscarinic receptors. Under these conditions, pertussis toxin blocked the concentration-effect curve to oxotremorine-M by a 30-fold increase in the EC50 value. Prior treatment of guinea pigs in vivo with pertussis toxin diminished the labeling of a 41-kDa protein in membranes suspensions of the longitudinal muscle incubated with [32P]nicotinamide adenine dinucleotide] and pertussis toxin. This ADP-ribosylation caused a functional uncoupling of the G protein from its receptor as indicated by radioligand-binding studies and second messenger assays. Our results verify that the M2 muscarinic acetylcholine receptor, like the M3 receptor, can elicit contractions of the guinea pig ileum and that the mechanism of this action involves inhibition of adenylate cyclase.

Adenosine Diphosphate Ribose↗
PubMed2002

Contraction-mediated pinocytosis of RGD-peptide by dermal fibroblasts: inhibition of matrix attachment blocks contraction and disrupts microfilament organisation.

Force generation in collagen and matrix contraction are basic functions of fibroblasts and important elements of tissue repair. Cell-matrix attachment is critical to this contraction, involving RGD-binding integrins. We have investigated how this process operates, in terms of force generation (in the Culture Force Monitor) and cytoskeletal structure, using a synthetic RGD-decapeptide. The RGD-peptide blocked force generation over the first 6 h, followed by near complete recovery by 20 h. However, dose response was complex indicating multiple processes were operating. Analysis of cytoskeletal structure after treatment with RGD-peptide indicated major disruption with condensed aggregates of actin and microtubular fragmentation. Fluorescent labeling and tracking of the RGD-peptide demonstrated intracellular uptake into discrete cytoplasmic aggregates. Critically, these RGD-peptide pools co-localised with the condensed actin microfilament aggregates. It is concluded that RGD-peptide uptake was by a form of contraction-mediated pinocytosis, resulting from mechanical tension applied to the untethered RGD-peptide-integrin, as contractile microfilament were assembled. These findings emphasize the importance of sound mechanical attachment of ligand-occupied integrins (e.g., to extracellular matrix) for normal cytoskeletal function. Conversely, this aspect of unrestrained cytoskeletal contraction may have important pathogenic and therapeutic applications.

Actin Cytoskeleton↗
PubMed1993

Age-related changes in collagen gel contraction by cultured human lung fibroblasts resulting in cross-over of contraction curves between young and aged cells.

We examined the effects of population doubling levels on collagen gel contraction by human lung fibroblasts (TIG-1). The sizes of gels at day 4 of culture, when the number of cells was the same as the initial number, were smaller with young cells than with aged cells. Therefore, retractive force had decreased with in vitro cellular aging. On the other hand, the lag time until gel contraction began became shorter with aging, resulting in the cross-over of contraction curves of young and aged cells. Morphological changes, such as pseudopodia protrusion, were suppressed in collagen gel. The surrounding collagen fibrils prevented young cells from moving more than aged cells. The weakened omnidirectional interaction with collagen fibrils on the entire surface of aged cells might result in an earlier occurrence of morphological change and, thereby, gel contraction.

Cell Division↗
PubMed1987

Caldesmon regulates the three-dimensional contraction (myosin-dependent contraction of the actin binding protein-induced actin gel).

We managed to develop a three-dimensional contractile model system using gizzard smooth muscle contractile elements. Phosphorylation of myosin was prerequisite for contraction. A high Mr actin-binding protein (ABP, or filamin), which cross-links actin filaments into a three-dimensional meshwork, was an essential factor for the three-dimensional contraction. Caldesmon suppressed contraction through the inhibition of the actin-ABP and actin-myosin interactions. Further, it was found that calmodulin could overcome the inhibitory effects of caldesmon on the above interactions, resulting in contraction. The possibility of this contractile model system being applied to nonmuscle contractile event is also discussed.

Actins↗
PubMed1998

Use of novel urodynamic parameters, detrusor contraction duration and detrusor contraction index, in men with lower urinary tract symptoms.

The aim of this study was to correlate the results of the urodynamic measures, detrusor contraction duration (DCD) and detrusor contraction index (DCI), with voiding symptoms in untreated men with lower urinary tract symptoms (LUTS) and in men treated with doxazosin. Ninety-one men with untreated LUTS underwent urodynamic evaluation. DCD (duration of detrusor contraction in seconds), DCI (interval, in seconds, that urine is passed divided by the total duration of the bladder contraction), and standard urodynamic measures of obstruction were determined. The urodynamic findings were correlated with the severity of voiding symptoms as assessed by the International Prostate Symptom Score (I-PSS). Fifty of these men were treated subsequently with 4 mg of doxazosin for 3 months and then underwent repeat urodynamic evaluation, in which changes in symptom score and urodynamic results were analyzed. DCD was the only urodynamic measure that correlated significantly with the I-PSS results in untreated patients. Although DCD, detrusor pressure at maximum flow, and the Abrams-Griffiths number decreased in men treated with doxazosin, only DCI and symptom score improved significantly after treatment for 3 months. No urodynamic parameter was useful in predicting the likelihood of a favorable response to treatment with doxazosin. DCD and DCI may be useful urodynamic measures in untreated men with LUTS and in those treated with doxazosin. Further study of these parameters is warranted.

Adrenergic alpha-Antagonists↗
PubMed1979

Role of calcium and cyclic adenosine 3':5' monophosphate in regulating smooth muscle contraction. Mechanisms of excitation-contraction coupling in smooth muscle.

Caclium initiates smooth muscle contraction by activating an enzyme, myosin light chain kinase. This enzyme catalyzes the transfer of phosphate from adenosine triphosphate to the 20,000 dalton light chain of myosin. In its phosphorylated form myosin interacts with actin to produce muscle contraction. The mechanism by which calcium activates myosin kinase requires (1) the binding of calcium to a 16,500 dalton calcium-binding protein (calmodulin), and (2) the binding of calmodulin-calcium to a 125,000 dalton catalytic subunit. This two protein complex is the active form of myosin light chain kinase. Smooth muscle relaxation is mediated by cyclic adenosine 3':5' monophosphate (cyclic AMP). One nechanism by which the latter may exert a direct effect on actin-myosin interaction is through the activation of a cyclic AMP-dependent protein kinase that can phosphorylate the 125,000 dalton component of myosin light chain kinase. Phosphorylation of myosin light chain kinase decreases the activity of the enzyme, thus favoring the unphosphorylated form of myosin, which cannot interact with actin to produce smooth muscle contraction.

Actins↗
PubMed1985

Electromechanical changes during electrically induced and maximal voluntary contractions: electrophysiologic responses of different muscle fiber types during stimulated contractions.

The electrophysiologic and mechanical responses of a synergistic muscle group composed of different muscle fiber types were studied with respect to excitation frequency and muscle fatigue in five men. The force and evoked action potentials obtained from surface and intramuscular fine wire electrodes were recorded continuously during stimulated contractions of the gastrocnemius and soleus at 20, 50, and 80 Hz. The stimulus voltage was adjusted so that the force generated by high-frequency tetani (50 and 80 Hz) could initially match the force of maximal voluntary contractions (MVCs). The surface and intramuscular EMG signals were digitized at a sampling rate of 10 kHz with 16-bit fast A/D converters and stored on a floppy disk. The digitized data were then processed for every 5 s to calculate evoked potential amplitude and conduction time using an HP 9836 computer. Results indicated that after 30 s of high-frequency stimulation, significantly less force was generated than after a similar period of MVC. During this period of high-frequency force fatigue, considerably greater force was developed at 20-Hz stimulation. The excessive force loss during high-frequency tetanic contractions was accompanied by a marked reduction in the evoked potential amplitude and conduction time (prolongation of the M wave). The recording of intramuscular evoked potentials showed the gastrocnemius muscle to have greater reductions in these parameters. Our results support the hypothesis that force fatigue during high-frequency stimulation results from failure of electrical propagation due to reduced muscle membrane excitability. The observed muscle-fiber-dependent electrophysiologic responses may suggest that the metabolic profile of muscle fibers plays an important role in regulating the muscle membrane excitability during high-frequency stimulation.

Adult↗
PubMed1985

Electromechanical changes during electrically induced and maximal voluntary contractions: surface and intramuscular EMG responses during sustained maximal voluntary contraction.

Changes in the electrical activity of the human gastrocnemius and soleus muscles during fatiguing maximal plantar flexions were studied with computer-aided EMG frequency power spectral analysis and intramuscular spike amplitude-frequency histogram analysis. In some experiments, brief supramaximal nerve stimulations of 80 Hz were given at 15-s intervals during sustained maximal voluntary contractions (MVCs). Multiple muscle biopsy samples were also obtained from the gastrocnemius muscle for fiber type determination. The surface EMG frequency spectral analysis showed a highly significant reduction in mean power frequency and root mean square EMG amplitude during sustained MVCs. The intramuscular spike amplitude-frequency histograms showed that the gastrocnemius muscle had a progressive reduction in the motor unit discharge frequency, particularly those with a relatively high amplitude, whereas the soleus muscle hardly showed a reduction in motor unit activity. Reduction in motor unit activity was also found to be more pronounced in gastrocnemius muscles with higher proportions of type II fibers. Brief maximal tetanic stimulations initially matching the MVC failed to increase the contraction force. Similarly, the evoked compound mass action potentials showed little change in the amplitude in subjects with different muscle fiber compositions. Results of this study suggest that during sustained MVCs, force fatigue could not be attributed to a failure of muscle membrane electrical propagation; a progressive reduction in motor unit activation does not result in a functional disadvantage, but may optimize excitation-contraction coupling by avoiding a muscle electrical conduction failure; and the extent of the reduction in motor unit activation seems to be muscle-fiber-type-dependent which may account for the reduction in amplitude and frequency of the surface EMG.

Biomechanical Phenomena↗