Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CONTRACTURE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,315 records · Page 73Linked to original sources
PubMed1973

The effects of temperature and metabolic inhibitors on the spontaneous relaxation of the potassium contracture of the heart of the frog Rana pipiens.

1. The spontaneous relaxation of the potassium contracture and the relaxation induced by the removal of extracellular calcium or the restoration of the original potassium concentration, in the frog heart, show a strong dependence on temperature.2. The energy of activation of the later exponential phase of the spontaneous relaxation is 10.43 kcal mole(-1), a value close to that reported for the binding of calcium ions by isolated sarcoplasmic reticulum, but larger than that for the calcium efflux from mammalian heart.3. The use of metabolic inhibitors shows that relaxation can be sustained when glycolysis is poisoned, but the disruption of oxidative phosphorylation slows relaxation.4. Poisoning of both glycolysis and oxidative phosphorylation blocks all but the small initial part of the spontaneous relaxation of the potassium contracture and also interferes with relaxation induced by other means.5. The results are considered to favour the existence, in frog heart, of an active intracellular relaxing system which uses ATP as its substrate to lower the sarcoplasmic calcium concentration. This system is likely to be the sarcoplasmic reticulum but the mitochondria could also be involved.

Adenosine Triphosphate↗
PubMed1976

The effect of caffeine and tetracaine on the time course of potassium contractures of single muscle fibres.

1. The time course of potassium contractures can be significantly prolonged by low concentrations of caffeine. 2. This effect of caffeine is not due to impairment of the fibre relaxing system. 3. Under conditions were contractile repriming is delayed (low temperature) an extra amount of activator can be released by caffeine, in addition to that released by potassium. 4. The source of this extra amount of activator is intracellular since its release can be shown in a O calcium EGTA medium. 5. Local anaesthetics, tetracaine, and to a lesser extent procaine, affect the release of contractile activator, without impairing the contractile machinery itself. 6. The results of the present paper support the view that the time course of potassium contracture is controlled by a membrane mechanism which is activated upon depolarization and later inactivates with time. 7. The effect of caffeine and local anaesthetics can be explained by assuming that the former prolongs the inactivation time course while the latter shortens it.

Animals↗
PubMed1981

The tension-depolarization relationship of frog atrial trabeculae as determined by potassium contractures.

1. In the presence of extracellular Na ions K contractures evoked from isolated frog atrial trabeculae show an initial phasic and a subsequent tonic contractile response. 2. The phasic response shows a steep dependence on membrane potential, persists in Na-free fluid, but is blocked by Mn ions, D600 and tetracaine. It has an indirect dependence on the [Ca]0 and would seem to be associated with both the secondary inward current and the release of Ca2+ from intracellular stores. 3. The tonic component of the K contracture is unaffected by D600 or tetracaine, shows a shallow dependence on membrane potential but is absent in Na-free fluid. Its tension-depolarization curve is immediately affected by alteration of either the [Ca]0 or the [Na]0. The form of the tension-depolarization relationship and the effects of [Ca]0 and [Na]0 are consistent with the strength of the tonic tension being determined by a 3Na+ for 1Ca2+ exchange across the cell membrane. 4. The results agree well with those obtained previously with voltage-clamp experiments on the same tissue, and may also help with the interpretation of Ca-flux experiments.

Animals↗
PubMed1988

Mechanism of contracture on cooling of caffeine-treated frog skeletal muscle fibres.

1. In order to clarify the mechanism of contracture on cooling of caffeine-treated intact muscle fibres, the temperature dependence of a calcium (Ca2+) release mechanism, 'Ca2+-induced Ca2+ release', of the sarcoplasmic reticulum (SR) was examined in skinned frog muscle fibres. 2. Skinned fibres in a solution containing 1.2 mM-caffeine and 0.7 mM-EGTA (Mg2+, 1.5 mM, Mg-ATP, 3.5 mM, pH 7), contracted on cooling (from 22 to 2 degrees C) due to Ca2+ release from the SR. 3. The rate of Ca2+ release from skinned fibre SR in a medium which contained Ca2+ ions (with 10 mM-EGTA) and no ATP salts, was determined under various conditions using the 'caffeine method.' 4. In the absence of Mg2+ ions, adenine nucleotides and caffeine, the rates at room temperature (21-22 degrees C) were 3-4 times greater than those at a lower temperature (1.5-3 degrees C), at any concentrations of Ca2+ ions external to the SR. 5. In the presence of Mg2+ ions (1.5 mM) and beta,gamma-methylene ATP (1 mM), the effect of temperature on the rates disappeared in Ca2+-containing media, although the effect remained in Ca2+-free medium. 6. When caffeine (1.2 mM), which is a potentiator of the Ca2+-induced Ca2+ release, was added to the test medium with Mg2+ and beta,gamma-methylene ATP, the resulting potentiating effect was several times greater than that at lower temperature. 7. In order to examine the temperature dependence of the Ca2+ pump activity of the SR, the initial rate of Ca2+ uptake by the empty SR was determined under various conditions in the presence of Mg2+ ions (1.5 mM) and Mg-ATP (3.5 mM). The Q10 of the pump activity was around 2.0 at the Ca2+ ion concentrations examined (less than 10(-6) M). 8. A numerical model based on the results obtained, together with some reasonable assumptions, suggested that both suppression of the Ca2+ pump and enhancement of the Ca2+ release contribute to the cooling contracture of caffeinized fibres.

Animals↗
PubMed1998

A multiaxial constitutive law for mammalian left ventricular myocardium in steady-state barium contracture or tetanus.

The constitutive law of the material comprising any structure is essential for mechanical analysis since this law enables calculation of the stresses from the deformations and vice versa. To date, there is no constitutive law for actively contracting myocardial tissue. Using 2,3-butanedione monoxime to protect the myocardium from mechanical trauma, we subjected thin midwall slices of rabbit myocardium to multiaxial stretching first in the passive state and then during steady-state barium contracture or during tetani in ryanodine-loaded tissue. Assuming transverse isotropy in both the passive and active conditions, we used our previously described methods (Humphrey et al., 1990a) to obtain both passive and active constitutive laws. The major results of this study are: (1) This is the first multiaxial constitutive law for actively contracting mammalian myocardium. (2) The functional forms of the constitutive law for barium contracture and ryanodine-induced tetani are the same but differ from those in the passive state. Hence, one cannot simply substitute differing values for the coefficients of the passive law to describe the active tissue properties. (3) There are significant stresses developed in the cross-fiber direction (more than 40 percent of those in the fiber direction) that cannot be attributed to either deformation effects or nonparallel muscle fibers. These results provide the foundation for future mechanical analyses of the heart.

Animals↗
PubMed1987

Stimulation frequency and external ionic composition control the repriming of caffeine-induced contractures in frog skeletal muscle.

The effect of stimulation rate and of external ionic composition on the repriming period of contractures induced by 6 mM caffeine was tested on isolated skeletal muscle fibres of the frog (Rana ridibunda). The repriming period, which was 11.2 +/- 0.1 min (mean +/- SEM, n = 9) on quiescent fibres, was shortened in fibres stimulated at a frequency ranging from 3 to 12 min-1 (optimal rate, 8 min-1; full repriming 5.7 +/- 0.2 min; n = 10). A 10-fold increase in the extracellular calcium concentration shortened the repriming period on both stimulated and quiescent fibres, whereas decreasing external calcium (1/10) delayed it. In a Na+-free solution (Li+ substituted) the repriming period of stimulated fibres was markedly delayed (14 min), whereas quiescent fibres never recover more than 10% of their ability to develop subsequent caffeine contractures. In contrast, with a 35% Na solution, the repriming period was greatly shortened (stimulated, 5.4 +/- 0.2 min, n = 7; quiescent, 6.2 +/- 0.5 min, n = 8). It is concluded that repriming depends on three mechanisms that seem to refill a calcium store and trigger recovery: the slow inward calcium current, a Na+-Ca2+ exchange, and perhaps a passive Ca2 influx.

Animals↗
PubMed1989

Caffeine treatment inhibits drug-induced calcium release from sarcoplasmic reticulum and caffeine contracture but not tetanus in frog skeletal muscle.

Effects of pretreatment with caffeine on Ca2+ release induced by caffeine, thymol, quercetin, or p-chloromercuriphenylsulfonic acid (pCMPS) from the heavy fraction of sarcoplasmic reticulum (SR) were studied and compared with those effects on caffeine contracture and tetanus tension in single fibers of frog skeletal muscle. Caffeine (1-5 mM) did induce transient Ca2+ release from SR vesicles, but subsequent further addition of caffeine (10 mM, final concentration) induced little Ca2+ release. Ca2+ release induced by thymol, quercetin, or pCMPS was also inhibited by pretreatment with caffeine. In single muscle fibers, pretreatment with caffeine (1-5 mM) partially reduced the contracture induced by 10 mM caffeine. However, tetanus tension was almost maximally induced by electrical stimulus in caffeine-treated fibers. These results indicate that SR, which becomes less sensitive to caffeine, thymol, quercetin, or pCMPS by pretreatment with caffeine, can still respond to a physiological signal transmitted from transverse tubules.

4-Chloromercuribenzenesulfonate↗
PubMed1999

Severe Contractures of the Proximal Interphalangeal Joint in Dupuytren's Disease:Value of Capsuloligamentous Release.

A retrospective review of severe flexion contractures (60 degrees or more), involving 51 proximal interphalangeal joints in 40 patients with Dupuytren's disease, was performed. Thirty-two joints underwent aponeurectomy alone, 19 joints additional capsuloligamentous release. Mean follow-up was 12 months. No statistically significant difference was seen in the percentage of contracture correction in the capsulotomy group compared with the noncapsulotomy group.

Journal Article↗
PubMed1997

beta-Adrenergic modulation of Ba2+ currents and K+ contractures in frog slow skeletal muscle fibers.

beta-Adrenergic modulation of the Ba2+ current (IBa) and K+ contracture in slow skeletal muscle fibers of the frog (Rana pipiens) were investigated in intact fibers with the three-microelectrode voltage-clamp technique and isometric tension measurements. Application of epinephrine (10(-6) to 10(-5) M) to the bath increased the amplitude of IBa. This increase was blocked by the beta-antagonist propranolol (3 microM), and a similar increase was observed with the beta-specific agonist isoproterenol (1 microM). Thus the epinephrine effect was mediated mainly by beta-adrenergic receptors. External application of permeable 8-bromoadenosine 3',5'-cyclic monophosphate (0.5 mM) increased the amplitude of both IBa and K+ contractures. The present results suggest that beta-adrenergic modulation of IBa in slow skeletal muscle fibers could reflect a modulation of Ca2+ channels via adenosine 3',5'-cyclic monophosphate (cAMP). cAMP (0.5 mM) also potentiated the K(+)-evoked tension in these slow fibers. The physiological contribution made by the modulation of slow skeletal muscle Ca2+ channels to the increase in tension is still not completely understood.

Adrenergic beta-Agonists↗
PubMed1980

Transient tension responses of heart muscle in Ba2+ contracture to step length changes.

To characterize mechanical properties of activated heart muscle, kitten papillary muscles in Ba2+ contracture were stretched or released stepwise, and the transient tension responses were analyzed. Various amplitudes of step length change (0.1-1.0% of Lmax) were tested from different initial lengths and at different temperatures. The tension response to either stretch or release showed four different phases, which were nearly symmetric when the input length change was 0.1% of Lmax. When the length changes was 1%, the second phase of stretch response became shorter, whereas that of release became longer. The third phase of stretch response was prolonged, whereas that of release response became obscure. The peak tension (F1) in the first phase was linearly related to the amplitude, whereas those in the second and third phase were not. Increasing temperature markedly decreased F1 and shortened the second and third phase independently of initial muscle length. These results were consistent with those properties of heart muscle in Ba2+ contracture previously characterized with sinusoidal length changes.

Animals↗
PubMed1989

Rapid cooling contractures as an index of sarcoplasmic reticulum calcium content in rabbit ventricular myocytes.

Rapid cooling contractures (RCCs) were used to assess changes in sarcoplasmic reticulum (SR) Ca content in both isolated rabbit ventricular myocytes and multicellular preparations. The main difference observed between these preparations was the magnitude of RCCs relative to twitches, apparently due to differences in measured parameters, i.e., unloaded shortening vs. isometric tension. When multicellular preparations were unloaded, RCC shortening was similar to that observed in myocytes. RCC magnitude decreased as the time between the last electrical stimulation and the RCC was increased (rest decay). RCC rest decay closely paralleled that of postrest twitches, suggesting that SR Ca loss is responsible for this process. Paired RCC experiments were used to investigate RCC relaxation and rest decay. When a second RCC (RCC2) was induced immediately after the first (RCC1), a large contracture was still observed (RCC2/RCC1 x 100 = 77.8 +/- 7.3%, mean +/- SD), indicating that the SR resequestered the majority of Ca on rewarming. This fraction was increased (to 92.9 +/- 5.5%) if Na and Ca-free solution was used during RCCs and rewarming, indicating that Na-Ca exchange also contributes to RCC relaxation. Increasing the interval between paired RCCs led to a decrease in RCC2, analogous to rest decay. This rest decay was abolished by inhibiting Na-Ca exchange, indicating that SR Ca loss during rest is mediated primarily by this process. RCCs were abolished by 10 mM caffeine. Ryanodine (1 microM) greatly accelerated RCC rest decay but had less effect on RCCs generated immediately after a train of stimulation. This accelerated rest decay was also dependent on Na-Ca exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Cellular functions of diabetic cardiomyocytes: contractility, rapid-cooling contracture, and ryanodine binding.

To study the mechanisms of cardiac dysfunction in experimental diabetes, adult rat cardiomyocyte shortening (measured with a video edge-detector system), the sarcoplasmic reticulum (SR) Ca2+ content [assessed by rapid-cooling contracture (RCC) and caffeine contracture (CC)] was examined. Ryanodine binding to the SR Ca(2+)-release channel of myocardium homogenate was also studied. Myocytes from diabetic rats showed depressed shortening (44% decrease compared with controls), reduced maximum rates of shortening and relengthening (58 and 56% decrease, respectively), and prolonged time to peak shortening (47% increase). RCCs and CCs from diabetic cells were 68 and 75% of the control values, respectively. Most of these cardiomyocyte abnormalities were corrected by daily insulin treatment in the diabetic rats. Ryanodine binding parameters indicated that the number of high-affinity binding sites was decreased in diabetic hearts. These data suggest that changes in contractile parameters as measured in diabetic myocytes are in good agreement with data obtained from intact heart or cardiac tissue preparations. Decreased SR Ca2+ content and reduced ryanodine binding sites indicate that the SR functions of storage and release of Ca2+ were depressed. This consequently may cause depressed contraction in diabetic hearts.

Animals↗
PubMed1999

Diacylglycerol delays pH(i) overshoot after reperfusion and attenuates contracture in isolated, paced myocytes.

Although protein kinase C (PKC) plays a pivotal role in ischemic preconditioning, it is not clear what the end effector is that protects the myocardium. In isolated, paced (1.25 Hz, 36-37 degrees C) adult rat cardiomyocytes, the effects of PKC preactivation by diacylglycerol on cell motion, intracellular Ca(2+) concentration ([Ca(2+)](i); indo 1), and intracellular pH (pH(i); seminaphthorhodafluor-1) during simulated ischemia-reperfusion (I/R) were investigated. The degree of reperfusion-induced contracture was significantly attenuated in the myocytes pretreated with 10 microM 1, 2-dioctanoyl-sn-glycerol (DOG; n = 19) compared with the untreated myocytes (n = 23, P < 0.02). There were no differences in twitch amplitude, end-diastolic [Ca(2+)](i), or peak-systolic [Ca(2+)](i) during I/R between the DOG-pretreated and untreated myocytes. Although there were no differences in pH(i) during ischemia, the pH(i) overshoot during reperfusion was significantly delayed in the DOG-pretreated myocytes compared with the untreated myocytes (n = 17 for each, P < 0.01). Chelerythrine completely abolished the favorable effects of DOG on the reperfusion-induced contracture and the pH(i) overshoot. These data suggest that diacylglycerol attenuates I/R injury in isolated, paced cardiomyocytes, which may be related to the slower pH(i) overshoot during reperfusion.

Alkaloids↗
PubMed1978

Dynamic stiffness of cat heart muscle in Ba2+-induced contracture.

We analyzed mechanical properties of kitten papillary muscles both at rest and in Ba2+ contracture by the frequency response method. The muscle length was perturbed sinusoidally, with an amplitude less than 0.3% of Lmax over a frequency range from 0.1 to 60 Hz to determine the dynamic stiffness, F(omega)/L(omega), in which F(omega) = amplitude of the force response wave, L(omega) = amplitude of sinusoidal length wave, and omega = frequency, and the phase shift of F(omega) relative to L(omega). In resting muscles, the dynamic stiffness increased minutely with increasing frequency and the phase relation showed a small lead over the entire frequency range. In muscles in contracture at low temperature (22-24 degrees C), the stiffness first decreased with increasing frequency from about 0.2 to 1 Hz, then increased with a slope of 10-fold/decade, and finally plateaued over the range above 8 Hz. The phase relation showed a small lag between 0.3 and 0.5 Hz, but a clear lead of up to 60 degrees between 0.8 and 16 Hz. With an increase in temperature to 36 degrees C, the peculiar decrease in stiffness and the phase lag in the low frequency region decreased in size and shifted to a higher frequency region (about 4 Hz). These findings led us to two alternative, approximate analogues, which are similar to but simpler than that previously proposed for a twitching papillary muscle.

Animals↗
PubMed1979

Contractures and increase in internal longitudianl resistance of cow ventricular muscle induced by hypoxia.

This study was performed to determine whether hypoxia in glucose-free solutions can increase the electrical resistance of intercellular junctions in ventricular muscle. Internal longitudinal resistance (Ri), mechanical tension, and transmembrane action potentials were measured simultaneously in cow ventricular trabeculae. The mean control value of Ri was 265 +/- 38 omegacm (mean +/- SE) at 34 degrees C. After 1 hour of hypoxia in glucose-free Tyrode's solution, it had increased by 300 +/- 41% (n = 11, P less than 0.001). The rise in Ri was closely related to the increase in resting tension (contracture). These effects were more pronounced during a second exposure to hypoxia and were potentiated by application of epinephrine, by increasing extracellular calcium concentration, and by increasing frequency of stimulation. Addition of glucose (50 mM) provided some protection against hypoxia. It is inferred that the increase in Ri is entirely due to the increase in the resistance of intercellular junctions (electrical uncoupling). Intracellular calcium may be responsible for both the contracture and the uncoupling.

Animals↗
PubMed2006

Surgical correction of unsuccessful derotational humeral osteotomy in obstetric brachial plexus palsy: evidence of the significance of scapular deformity in the pathophysiology of the medial rotation contracture.

BACKGROUND: The current method of treatment for persistent internal rotation due to the medial rotation contracture in patients with obstetric brachial plexus injury is humeral derotational osteotomy. While this procedure places the arm in a more functional position, it does not attend to the abnormal glenohumeral joint. Poor positioning of the humeral head secondary to elevation and rotation of the scapula and elongated acromion impingement causes functional limitations which are not addressed by derotation of the humerus. Progressive dislocation, caused by the abnormal positioning and shape of the scapula and clavicle, needs to be treated more directly. METHODS: Four patients with Scapular Hypoplasia, Elevation And Rotation (SHEAR) deformity who had undergone unsuccessful humeral osteotomies to treat internal rotation underwent acromion and clavicular osteotomy, ostectomy of the superomedial border of the scapula and posterior capsulorrhaphy in order to relieve the torsion developed in the acromio-clavicular triangle by persistent asymmetric muscle action and medial rotation contracture. RESULTS: Clinical examination shows significant improvement in the functional movement possible for these four children as assessed by the modified Mallet scoring, definitely improving on what was achieved by humeral osteotomy. CONCLUSION: These results reveal the importance of recognizing the presence of scapular hypoplasia, elevation and rotation deformity before deciding on a treatment plan. The Triangle Tilt procedure aims to relieve the forces acting on the shoulder joint and improve the situation of the humeral head in the glenoid. Improvement in glenohumeral positioning should allow for better functional movements of the shoulder, which was seen in all four patients. These dramatic improvements were only possible once the glenohumeral deformity was directly addressed surgically.

Journal Article↗
PubMed1988

Early-onset benign autosomal dominant limb-girdle myopathy with contractures (Bethlem myopathy).

We report a large French-Canadian kindred with 33 affected members in six generations showing early-onset autosomal dominant limb-girdle myopathy and contractures. This myopathy is unique because of its benign course, with many members only minimally impaired even in old age. Examination of affected members revealed mild to moderate proximal weakness and wasting. Contractures were observed at the elbows and ankles in all, while in some they were more widespread. Serum CK was either normal or slightly raised, and electrodiagnostic studies suggested a primary myopathy. Muscle biopsy revealed nonspecific features of a myopathy without fiber necrosis or regeneration. Cardiac involvement was absent clinically in all patients and at autopsy in two affected individuals. The similarities between four previously reported families and our own establishes this myopathy as a distinct clinicogenetic entity, for which we propose the name "Bethlem myopathy."

Adolescent↗
PubMed1992

Is resting membrane potential a possible indicator of viability of muscle bundles used in the in vitro caffeine contracture test?

In 22 patients susceptible to and 34 patients not susceptible to malignant hyperthermia, we examined which muscle conditions may influence the degree of sensitivity of skeletal muscle to the in vitro caffeine contracture test: predrug resting membrane potential, predrug twitch tension, and maximum contracture induced by 32 mM caffeine in two caffeine tests performed respectively at 30 and 75 min after biopsy. No differences in the measured variables were observed between the first and the second caffeine tests in the 34 patients susceptible to malignant hyperthermia. The first caffeine test was found to be positive in all of the 22 patients susceptible to malignant hyperthermia. However, in eight patients, the second caffeine test was negative and the muscle fibers were found to be significantly depolarized. Resting membrane potential was -73.4 +/- 7.9 mV before the first caffeine test and -65.8 +/- 8.8 mV before the second test. We suggest that when time-induced partial depolarization of malignant hyperthermia-susceptible fibers occurs, fibers may become less sensitive to caffeine.

Caffeine↗