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 415 records · Page 23Linked to original sources
PubMed2005

Induction of contracture and extracellular Ca2+ influx in cardiac muscle by sanguinarine: a study on cardiotoxicity of sanguinarine.

In this study, the toxic effect of sanguinarine (SANG) on heart was studied with isolated cardiac muscle strip isolated from Wistar rat. SANG induced positive inotropic action followed by contracture on the left ventricle and both atria strips. In addition, SANG dose-dependently inhibited spontaneous beat of the right atrium. SANG-induced contracture was completely suppressed by pretreatment with La3+ or in a Ca2+ free Tyrode solution containing 2.5 mM EGTA. Incubating isolated cardiomyocytes with SANG enhanced the 45Ca2+ influx, which could be inhibited by pretreatment with La3+. However, the SANG-induced 45Ca2+ influx could not be inhibited by pretreatment with other Ca2+ channel blockers, such as nifedipine, verapamil, diltiazem, nickel and manganese, and amiloride. Although antioxidants can inhibit the SANG-induced lipid peroxidation, they could not prevent the SANG-induced contracture. N-acetylcysteine and dithiothreitol, the sulfhydryl reducing agents, were shown to be effective in preventing the SANG-induced contracture. These data suggested that the SANG-induced contracture is caused by the influx of extracellular Ca2+ through a La3+-sensitive Ca2+ channel.

Alkaloids↗
PubMed1992

Protective effect of bepridil against veratrine-induced contracture in rat atria.

In isolated stimulated rat atria, superfusion with veratrine caused a marked contracture (VIC) which was absent in calcium-free medium and which was inhibited by tetrodotoxin (IC50VIC of 1.38 microM). Lowering the extracellular calcium concentration from 2.5 to 0.5 or 0.1 mM reduced the veratrine-induced contracture and delayed its onset. Superfusion of bepridil (1-10 microM) for 60 min before and during veratrine exposure markedly slowed the onset of contracture, reduced the maximum response (IC50VIC = 2.11 microM) and facilitated recovery upon washout of the alkaloid. The direct negative inotropic effect (NIE) of bepridil (IC50NIE = 10.96 microM) resulted in an VIC/NIE ratio of 5.19 for this drug. The protective effects of bepridil were rate-independent and were not modified by the presence of atropine (1.4 microM) and propranolol (0.3 microM) in the medium. Diltiazem, verapamil and nifedipine only reduced veratrine-induced contracture at concentrations much higher than those producing a negative inotropic effect, giving them negative NIE/VIC ratios of 0.31, 0.08 and 0.08 respectively. Like bepridil, flunarizine had a positive NIE/VIC ratio (15.87, IC50VIC = 3.71 microM). The lack of effect of the quaternary derivative of bepridil CERM 11888 indicated that intracellular sites of action may be involved in the activity of bepridil on veratrine-induced contracture. Given that veratrine-induced changes may mimic some of the pathological changes occurring in ischaemia, the results suggest that bepridil and flunarizine may be more effective than L-type, slow calcium ion-channel blockers in protecting against calcium overload during ischaemia and reperfusion injury.

Animals↗
PubMed1994

Potentiation by metal ions of ryanodine contracture of the mouse diaphragm.

The aim of this study was to elucidate the possible mechanism of the potentiating action of metal ions (Cu2+, Hg2+, Ag+ and SeO3(2-)) on the ryanodine-induced contracture of the mouse diaphragm. The ryanodine contracture in the quiescent muscle could be augmented by either electrical stimulation or pretreatment with high K+ of the diaphragm. Lowering the external Ca2+ concentration from 2.5 mM to 1 microM or the addition of 7 microM d-tubocurarine, which abolished the muscle excitability by blocking the receptors of acetylcholine, markedly attenuated the ryanodine contracture. Application of Cu2+, Hg2+, Ag+ and SeO3(2-) but not Ni2+ and Co2+, to quiescent muscle restored the ryanodine contracture. The potentiating effects of Hg2+, Ag+ and high K+ were dependent on the presence of external Ca2+ (2.5 mM) and intact transverse tubular systems but the effects of Cu2+ and SeO3(2-) were not. Treatment with 1 mM dithiothreitol 10 min after the application of metal ions and then subsequent addition of ryanodine abolished the potentiating effects of Hg2+ and Ag+ but not those of Cu2+ and SeO3(2-). Although ryanodine by itself had no effect on 45Ca2+ uptake by the mouse diaphragm, it significantly potentiated the increased 45Ca2+ uptake elicited by Cu2+ and Hg2+. Further elucidation of the interaction between metal ions and ryanodine on the outer sarcolemma showed that all of these metal ions, including the inactive Co2+ and Ni2+, not only decreased the membrane potential but also altered the membrane input resistance, effects which were not correlated with the potentiating effects of the metal ions on the ryanodine contracture.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Potassium and caffeine contractures in limb muscles of normal and dystrophic (C57 BL/6J dy2J/dy2J) mice.

The strength of contractures, produced by 15 to 146 mM [K]0 (as L-glutamate), was measured in isolated small bundles of muscle fibers from the fast-twitch extensor digitorum longus and from the slow-twitch soleus of normal and dystrophic (C57 BL/6J dy2J/dy2J) mice. The analysis of the relation between the maximal amplitude of the contracture vs the membrane potential and the time constant of relaxation of the K-contractures has shown that dystrophy induced an attenuation of the differences between fast- and slow-twitch muscles. The repriming of K-contractures was more affected by changes in [Ca]0 in normal soleus than in normal extensor digitorum longus and this difference was unaffected by dystrophy. For both types of muscles, the ability of caffeine to produce contractures was reduced in dystrophic muscle and this modification was not related to a change in the fiber typing.

Animals↗
PubMed1991

Effects of 2,3-butanedione monoxime (BDM) on contracture and injury of isolated rat myocytes following metabolic inhibition and ischemia.

The relationship between myocardial cell contracture and injury during total metabolic inhibition (amylobarbital and iodoacetic acid) and ischemia was examined, using 5-50 mM butanedione monoxime (BDM) as an inhibitor of contracture. BDM had no apparent effect on control myocytes during 180 min incubations, but inhibited contracture following anoxia or ischemia in a dose-dependent fashion, as directly quantitated by length/width ratios. Cellular ATP levels decreased at a similar rate in the absence or presence of BDM, following metabolic inhibition. BDM-mediated inhibition of contracture was associated with accelerated cell injury, as defined by: the uptake of an extracellular marker (trypan blue) by the cardiomyocytes, by direct analysis of myoglobin released into the supernatant and by ultrastructural demonstration of defects in sarcolemmal membrane integrity. Calcium was not required for BDM's enhancement of injury, in that cells incubated in calcium free-EGTA buffer showed a similar BDM-mediated acceleration of injury. In the presence or absence of calcium, enhancement of injury was more marked in cells osmotically stressed with a brief incubation in hypotonic buffer, than in cells resuspended in isotonic media. It is concluded that BDM enhances development of osmotic fragility of inhibited or ischemic cardiomyocytes and that contracture is not a necessary contributing factor to myocardial cell death.

Adenosine Triphosphate↗
PubMed1987

Effects of resting membrane potential and intactness of the T-tubules on caffeine contractures in rat skeletal muscle.

We have studied the effects of changes in the resting membrane potential (Vm) and T-tubules on caffeine contracture (25 mM) elicited in rat soleus muscle in vitro at 34 degrees C. In high [K]o (30-140 mM, [K]o X [Cl]o constant) caffeine contractures were reduced by about 40-50% and had a faster time course than in normal Krebs ([K]o = 5 mM). Detubulation of the muscles by an osmotic treatment produces a reduction of about 30% in the caffeine contracture tension. Our results with high K solutions suggest a reduced sensitivity of the myofibrils to calcium released by caffeine. The effects of detubulation on caffeine contracture suggest that caffeine may have a direct effect on sarcolemma in addition to its well known action on the sarcoplasmic reticulum (SR). However, a depletion of the calcium content in the SR of depolarized muscle fibres as well as an anatomical damage produced by the osmotic treatment can not be ruled out as an explanation for the reduced caffeine contracture.

Animals↗
PubMed1995

Acetylcholine contractures of skeletal muscles: inhibition by chlorpromazine and diltiazem.

The maximum contractures evoked by 100 microM ACh of mouse soleus muscles denervated for 3-7 days are completely inhibited by a 10 min exposure to 100 microM chlorpromazine (CP). Recovery on washout of CP takes more than 1 hr to complete. ACh evoked contractures are also inhibited by diltiazem (D); washout of D is immediately followed by recovery. Electrically evoked twitches and K evoked contractures are largely unaffected by CP, caffeine evoked contractures are decreased but not abolished. Fast mouse and (non-denervated) frog tonic muscles behave similarly. Depolarization by ACh and ACh-evoked whole cell currents show enhanced desensitization at low, and block at high [CP] and [D]; more than 50% recovery is achieved by less than 1 min washout of CP and D. Currents carried by Na+ and Mg2+ ions behave similarly. It is concluded that activation of ACh evoked contractures may be blocked by CP independent of ionic currents through nicotinic ACh receptors and that it depends on intracellular processes linked to these receptors.

Acetylcholine↗
PubMed1987

The role of acetylcholine in tetraethylammonium induced contractures of the chick biventer cervicis muscle in the presence of lidocaine.

Lidocaine (0.92 mM) potentiated tetraethylammonium (TEA, 0.6-6 mM) induced contractures of the chick biventer cervicis muscle (BVC) in vitro. The dose ratio for TEA (EC50 in lidocaine/EC50 control) was 1.16 X 10(-3). Lidocaine (0.92 mM) blocked nerve and muscle action potentials in the BVC preparation, blocked slow fibre MEPPS, and blocked indirectly elicited muscle contraction. Lidocaine (0.92 mM) non-competitively blocked acetylcholine (ACh) induced contractures of the chick BVC. Gallamine competitively blocked ACh contractures (pA2 6.53) but produced only a relatively weak non-competitive block of TEA induced contractures in lidocaine. TEA induced contractures of the chick BVC in the presence of lidocaine probably do not involve ACh.

Acetylcholine↗
PubMed1987

L-glutamate and potassium-induced contractures in denervated cockroach muscles.

1. The effects of denervation on the mechanical responses to various concentrations of L-glutamate in retractor unguis muscle of cockroach (Perilpaneta americana) was examined, comparing them with contractures induced by high potassium saline. 2. The dose-response curve was shifted to the lower concentrations of L-glutamate after 9 days of denervation. 3. Following a transient increase in the maximum contracture tension, it decreased with days after denervation and reached a constant level by several days. However, from 16 to 20 days after denervation, the tension ratios of the maximum glutamate to potassium contractures were significantly higher than that of the innervated muscles. 4. A sustained contracture was observed on and after treatment of L-glutamate in the denervated muscle. Pretreatment of the muscle by concanavalin A facilitated to induce L-glutamate contracture. 5. It was suggested that the sensitivity of the muscle membrane to L-glutamate was increased in the denervated muscle.

Animals↗
PubMed2006

Botulinum toxin A for treating muscular contractures in cephalic tetanus.

OBJECTIVE: This study reports the use of botulinum toxin for treatment of muscle contractures in a patient with cephalic tetanus. METHOD: Case report. RESULTS: An 80-year-old woman was diagnosed with cephalic tetanus, with contractures of the masseter, sternocleidomastoid, trapezius, and levator scapulae muscles. After one month of conventional treatment good recovery was observed, but with persistence of the contractures of the sternocleidomastoid, trapezius and levator scapulae. These contractures were treated with botulinum toxin A (75IU in the right sternocleidomastoid, 25IU in the right trapezius; one month later 50IU in the left levator scapulae, 50IU in the right levator scapulae, 75IU in the left sternocleidomastoid; two months later 25IU in the left trapezius). Full recovery was observed. CONCLUSIONS: Local infiltration with botulinum toxin A appears to be an effective treatment for persistent muscle contracture in cephalic tetanus.

Aged, 80 and over↗
PubMed2004

Gastrocnemius and soleus lengths in cerebral palsy equinus gait--differences between children with and without static contracture and effects of gastrocnemius recession.

Equinus gait is one of the most common abnormalities in children with cerebral palsy. Although it is generally assumed that the calf muscles are abnormally short in equinus gait, no studies have been done to confirm that the muscles are short and that this shortness contributes to the equinus. This study used musculoskeletal modeling combined with computerized gait analysis to examine medial gastrocnemius (MGAS), lateral gastrocnemius (LGAS), and soleus (SOL) musculotendinous lengths during equinus gait in children with cerebral palsy. All three muscles were abnormally short during equinus gait whether or not the children had equinus contractures (P < or = 0.005). Children with static contractures had shorter maximum static MGAS and LGAS lengths than children with dynamic equinus (P < or = 0.002). The children with static contractures had ratios of peak dynamic length to maximum static length close to 1.0 for MGAS and LGAS (1.005 +/- 0.015) but lower ratios for SOL (0.984 +/- 0.024). For the children with static contracture, these ratios did not change significantly after gastrocnemius recession (P > or = 0.14) because both static and dynamic lengths increased postoperatively (P < or = 0.04). These results support the current clinical understanding of the role of calf "tightness" in equinus gait, including the appropriateness and effectiveness of gastrocnemius recession for children with equinus contracture.

Ankle Joint↗
PubMed1991

[Ryanodine-induced contractures for the diagnosis of malignant hyperthermia susceptibility].

The halothane-caffeine contracture test is presently the most well-established method for identification of malignant hyperthermia susceptibility (MHS) or non-susceptibility (MHN). However, 10-20% of the patients tested are classified as equivocal (MHE), i.e. their susceptibility remains uncertain. A genetic disorder of the calcium releasing ryanodine receptor has been postulated recently. Therefore, 12 patients were tested in addition to the protocol of the European Malignant Hyperthermia Group (EMHG) for dose- and time-dependent contracture after ryanodine application. In this study, contracture of 0.2g appeared significantly earlier in MHS patients (17.5 +/- 1.7 min; n = 5) during cumulative ryanodine exposition (0.4-0.8-1.6-10.0 mumol/l) than in MHN (38.2 +/- 5.4 min; n = 5). A significant difference between MHS (10.0 +/- 1.7 min; n = 6) and MHN (19.8 +/- 0.6 min; n = 3) was also seen after bolus application of ryanodine (10.0 mumol/l). One patient classified as MHE according to the EMHG protocol, manifested as MHN after the ryanodine contracture test. This study supports previous work suggesting the ryanodine contracture test as an improvement in the in-vitro diagnosis of MH susceptibility.

Adolescent↗
PubMed1990

Halothane cooling contractures of skinned mammalian muscle fibers.

The effects of halothane or cooling on Ca2(+)-activated tensions and on the uptake and release of Ca2+ by the sarcoplasmic reticulum were investigated in chemically skinned fibers of the extensor digitorum longus muscle of adult rabbits. At 22 degrees C, halothane (greater than 0.46 mM) induced Ca2+ release from the SR of Ca2(+)-loaded skinned fibers that resulted in transient tensions. Higher concentrations of halothane (greater than 4.65 mM) reduced the steady-state accumulation of Ca2+ in the SR at 22 degrees C. Cooling (to less than 10 degrees C) elicited transient contractures (cooling-induced contractures [CC]) in Ca2(+)-loaded skinned fibers, despite the fact that the tensions elicited by adding Ca2+ to the bath were depressed at these low temperatures. The skinned fibers did not develop CCs at 12-16 degrees C. Halothane cooling contractures could be elicited at these temperatures by exposing the fibers to halothane concentrations that failed to elicit Ca2+ release at 22 degrees C. The halothane cooling contractures were blocked by procaine but not by lidocaine. It was concluded that these contractures resulted from a synergistic interaction between halothane and cooling that stimulates Ca2+ release from, and reduces Ca2+ uptake by, the sarcoplasmic reticulum.

Action Potentials↗
PubMed1992

Effect of Bay K 8644 on the magnitude of isoflurane and halothane contracture of skeletal muscle from patients susceptible to malignant hyperthermia.

Isoflurane has a lesser ability than halothane to induce contracture in malignant hyperthermia (MH) muscle in vitro. This does not necessarily imply that isoflurane is not as potent an MH trigger as halothane in vivo. A hypothesis was tested that in vitro treatment with Bay K 8644, an activator of both the dihydropyridine receptors as well as the sodium channels of the T-tubules, potentiates isoflurane-induced MH-susceptible skeletal muscle contracture. In addition to the usual halothane-caffeine test, other muscle bundles were exposed to 10 microM Bay K 8644-halothane and equipotent anesthetic concentrations (expressed in multiple minimum alveolar concentration [MAC]) of isoflurane either alone or combined with Bay K 8644. In 14 MH-susceptible muscle bundles, the mean maximum contracture induced by 2 MAC isoflurane was 0.20 +/- 0.22 g (mean +/- SD), and this value was significantly less than that obtained with 2 MAC halothane (0.68 +/- 0.40 g). Bay K 8644 did not induce muscle contracture on its own but consistently enhanced both the 0.5 MAC isoflurane and halothane to the same maximal isometric tension (1.09 +/- 0.35 g and 1.11 +/- 0.37 g, respectively). Such an effect was not observed in the MH-nonsusceptible group. Under the conditions of this in vitro study, 0.5 MAC isoflurane appears to be as potent as halothane in inducing muscle contracture in skeletal muscle bundles from individuals susceptible to MH.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1981

Effect of implant location on compressibility and capsule formation around miniprostheses in rats, and experimental capsule contracture.

Our study of experimental contracture in rats confirms the existence in laboratory animals of a phenomenon very much like human capsule contracture. The ultrastructural features of capsules in rats are essentially identical to those for humans and rabbits. Macrophages with silicon-containing material were present. Star-shaped myofibroblasts with extended processes appeared in contracted and noncontracted capsules. The myofibroblasts contained bundles of 60 to 80 A microfilaments with included dense bodies, convoluted nuclei, and extensive peripheral vesiculation. The myofibroblasts tended to be associated with more extensive ground substance and smaller diameter extracellular fibrils than were normal synthetic fibroblasts. The incidence of contracture was similar for implants beneath different amounts of overlying soft tissue dorsally and sternally, while compressibility and subjective softness were greater for implants beneath lesser amounts of overlying tissue. A greater mass of capsule formed beneath the heavier covering, however, suggesting that in clinical experience, cosmetically more acceptable results from submuscular prosthesis placement are probably due to a padding effect. Capsule glycosaminoglycans were primarily hyaluronic acid and dermatan sulfate. The occurrence of myofibroblasts in these capsules at a relatively late period (26 weeks) implicates myofibroblasts in the contracture mechanism, but details are still unknown. Contracture is a property of the capsule tissue; preliminary observations suggest that its occurrence is independent of species, anatomical site, surgical procedure, presence of extruded gel, presence of myofibroblasts, capsule thickness, or protein, collagen, or glycosaminoglycan composition. Cells within the capsule were geometrically asymmetrical, being extremely flattened in the plane parallel to the prosthesis surface.

Animals↗
PubMed2001

Amp 579 reduces contracture and limits infarction in rabbit heart by activating adenosine A2 receptors.

To determine the mechanism by which AMP 579, an adenosine A1/A2 agonist, administered at reperfusion protects ischemic myocardium, buffer-perfused rabbit hearts were subjected to 30 min of global ischemia and 2 h of reperfusion. AMP 579 (500 nM) was included in the reperfusate for the first 70 min. Average left ventricular diastolic pressure during reperfusion in hearts receiving AMP 579 was lower than that in control hearts (17.9 +/- 2.4 vs. 39.0 +/- 6.5 mm Hg, p < 0.05), indicating attenuation of contracture. Left ventricular developed pressure and coronary flow during reperfusion were also significantly improved with AMP 579 treatment. AMP 579's anti-contracture effect was blocked by the adenosine A2-receptor antagonist 8-(3-chlorostyryl)caffeine (CSC), but not by the A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). CSC, but not DPCPX, also blocked AMP 579's ability to preserve developed pressure and coronary flow in these hearts. AMP 579 significantly reduced infarction in isolated hearts subjected to regional ischemia. The anti-infarct effect again was abolished by CSC but not by DPCPX. Finally, we tested whether 5'-(N-ethylcarboxamido)adenosine (NECA), another A1/A2 agonist, also administered for the initial 70 min of reperfusion, could duplicate the anti-infarct effect of AMP 579. One-hundred-nanomolar NECA duplicated the protection, but neither 50 nM CGS21680, a selective A2 agonist, nor 100 microM adenosine was protective. Therefore, AMP 579 given at reperfusion reduces contracture and infarction. Anti-contracture and anti-infarct effects require the adenosine A2, but not the A1, receptor suggesting that prevention of contracture and tissue salvage are mechanistically related. Not all A2 agonists were able to duplicate the anti-infarct effect, suggesting something unique about AMP579.

Animals↗
PubMed1984

Volkmann's contracture of the extraocular muscles following blowout fracture.

In the past decade there has been considerable controversy over the surgical indications for treatment of blowout fractures of the orbit. It has been well recognized that some fracture patients develop an ischemic contracture of the inferior rectus muscle. We have found that a Volkmann's type of contracture of the inferior rectus muscle does exist and is similar to that found in the distal extremities. A specific group of fracture patients is at greater risk for development of a contracture. Elderly patients, hypotensive patients, patients with small fractures, and those with high inferior rectus compartment pressures are more prone to developing a contracted extraocular muscle. We have measured compartment pressures in 18 patients who were surgical candidates following orbital fracture. Our conclusions indicate that surgical intervention following blowout fractures in these high-risk patients may be more prudent than medical management. Patients with persistent diplopia due to a contracted inferior rectus are extremely difficult to treat many months after fracture. We still believe it prudent to surgically repair orbital fractures in patients with diplopia, enophthalmos, and a risk for muscle contracture. The documentation of this additional sequela of unrepaired fractures lends more strength to this belief. There is no evidence to indicate that a Volkmann's contracture would be possible after early repair of a blowout fracture.

Adolescent↗
PubMed1985

The incidence of experimental contracture varies with the source of the prosthesis.

Nominally equivalent gel-filled miniprostheses supplied by three different manufacturers were placed subcutaneously in rats under identical conditions in a double-blind comparison. The incidence of experimental contracture, defined by grossly visibly asymmetrical distortion of the implant, was 0, 9, and 91 percent for the different manufacturers, consistent with previous observations. Differences among the different implants with respect to the density of the fibrillar capsule structure, the cellularity, and the amount of extruded gel did not correlate with the incidence of contracture. Contracture rate was inversely proportional to the relative degree of filling of the prostheses, as reflected in deviations from the nominal hemispherical shape, and to the viscosity of the gel filling. For implants of the same type, the incidence of contracture was higher when the prosthesis was underfilled. Contracted capsules were more fibrous and contained more cells with microfilament bundles. It is concluded that the physical and geometric properties of silicone implants are critical in the expression of contracture and that these properties vary significantly among prosthesis manufacturers.

Animals↗