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PubMed1989

Contracture and change in membrane potential produced by sodium removal in the dog trachea and bronchiole.

Mechanical responses and changes in membrane potential induced by Na removal were investigated in dog tracheal and bronchiolar smooth muscles. In both muscles, reduction of the external Na concentration ([Na]o) to less than 70 mM produced a sustained contracture, dose dependently. The relative amplitude of the Na-free contracture was greater than that induced by excess [K]o in the trachealis. Readmission of 1-10 mM Na, after exposure to Na-free solution, relaxed the contracture evoked by Na removal, and the degree of relaxation was dependent on [Na] readmitted. In the absence of both Na and Ca, some tension remained, and readmission of Ca increased the muscle tone. Even after pretreatment with Ca-free ethylene glycol-bis (beta-aminoethylether)-N,N,N,N'-tetraacetic acid- (0.2 mM) containing solution for 30 min, removal of Na caused some mechanical response in both muscles. D 600 (10(-7) to 10(-4) M), a blocker of voltage-dependent Ca2+ influx, suppressed the response to Na removal, but 10(-4) M D 600 did not completely block the contracture. Na removal depolarized the smooth muscle membrane to a greater extent in the bronchiole than in the trachealis. It was concluded that an increase in Ca permeability across the membrane and inhibition of the Na-Ca exchange mechanism in the absence of Na are responsible for the generation of Na-free contracture in both muscles.

Animals↗
PubMed1990

Correlation between cytosolic free calcium, contracture, ATP, and irreversible ischemic injury in perfused rat heart.

The relations between ATP depletion, increased cytosolic free calcium concentration [( Cai]), contracture development, and lethal myocardial ischemic injury, as evaluated by enzyme release, were examined using 19F nuclear magnetic resonance to measure [Cai] in 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N',N'-tetraacetic acid (5F-BAPTA)-loaded perfused rat hearts. Total ischemia at 37 degrees C was induced in beating hearts, potassium-arrested hearts, magnesium-arrested hearts, and hearts pretreated with 0.9 microM diltiazem to reduce but not abolish contractility. In the beating hearts, time-averaged [Cai], which is intermediate between the systolic and the basal [Cai], was 544 +/- 74 nM. In contrast, in the potassium- and magnesium-arrested hearts, the time-averaged values are lower than in beating hearts (352 +/- 88 nM for potassium arrest, 143 +/- 22 nM for magnesium arrest). During ischemia, ATP depletion, contracture, and a rise in [Cai] are delayed by cardiac arrest, but all occur more rapidly in the potassium-arrested hearts than in the magnesium-arrested hearts. The diltiazem-treated hearts were generally similar to the magnesium-arrested hearts in their response to ischemia. Under all conditions, contracture development was initiated after tissue ATP had fallen to less than 50% of control; invariably, there was a progressive rise in [Cai] during and following contracture development. Reperfusion with oxygenated perfusate shortly after peak contracture development resulted in a return of [Cai] to its preischemic level, resynthesis of creatine phosphate, no significant enzyme release, and no substantial loss of 5F-BAPTA from the heart. The data demonstrate that an increase in [Cai] precedes lethal myocardial ischemic injury. This rise in [Cai] may accelerate the depletion of cellular ATP and may directly contribute to the development of lethal ischemic cell injury.

Adenosine Triphosphate↗
PubMed1995

Volkmann's ischemic contracture of the foot and ankle: evaluation and treatment of established deformity.

Fibrotic contracture of skeletal muscle can follow weeks or months after the severe ischemic insult of compartment syndrome. Commonly known as Volkmann's ischemic contracture, the affected limb often becomes dysfunctional and painful, and may lose sensibility. The pathogenesis of the muscle contracture includes prolonged ischemia, myonecrosis, fibroblastic proliferation, contraction of the cicatrix, and myotendinous adhesion formation. Resultant shortening or overpull of involved muscles leads to stiffness and deformity. Simultaneously, nerve injury from initial ischemia or subsequent soft tissue fibrotic compression leads to muscle paresis or paralysis of the involved compartment and of those muscles more distally innervated. The resultant deformity is thus a combination of varying degrees of contracture and weakness depending on which muscles and nerves are affected. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by many factors, including: (1) which leg compartment, if any, has been affected and to what degree extrinsic flexor or extensor overpull is exhibited, (2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles (3) which foot compartment, if any, has been affected and to what degree intrinsic overpull is exhibited, and (4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Therefore, a variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Treatment is based on an appreciation of the pathoanatomy of the deformity. Nonoperative therapy is aimed at obtaining or preserving joint mobility, increasing strength, and providing corrective bracing and accommodative footwear. Operative management is usually reserved for treatment of residual nerve compression or severe and problematic deformities. Established surgical protocols are performed in a stepwise fashion, to include: (1) release of residual or secondary nerve compression, (2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy, (3) tendon transfers or arthrodesis to increase function, and (4) ostectomy or amputation for severe, refractory deformities.

Ankle Joint↗
PubMedDate not supplied

Muscle contractures and adenosine triphosphate depletion in porcine malignant hyperthermia.

This study compares several methods for diagnosing susceptibility to malignant hyperthermia, using two groups of Poland China swine narrowly defined as genetically susceptible or normal (five pigs each) depending respectively on their response to halothane or to halothane and succinylcholine. Vastus medialis muscle biopsies were excised under thiopental-N2O-O2 anesthesia and used for examination of (1) contracture responses to halothane, (2) contracture responses to caffeine and halothane-caffeine, and (3) adenosine triphosphate (ATP) depletion with and without halothane. All studies were performed in organ baths at 37 C. Halothane alone produced contractures in two susceptible and one normal preparation; caffeine always produced a contracture at lower concentrations in susceptible muscle; caffeine-halothane contractures in susceptible muscle occurred at lower mean caffeine concentrations, but there was some overlap of individual values; mean ATP depletion was greater in susceptible muscle, but with considerable overlap. Comparisons with the findings of others were hampered by use of absolute rather than comparative values for tension, e.g., grams, rather than grams per cross-sectional area or fraction of peak tension. Examination of the complete dose-response curve provided the best comparative information and caffeine was the consistent predictor of susceptibility.

Adenosine Triphosphate↗
PubMed1991

Effects of neuroleptic agents on rat skeletal muscle contracture in vitro.

The purpose of this investigation was to examine and compare the effects of both in vivo pretreatment and in vitro treatment with the neuroleptic agents droperidol, haloperidol, and trifluoperazine on skeletal muscle contracture using an in vitro model. Strips of normal rat diaphragm were challenged with succinylcholine and halothane (halothane: 1% and 3%) subsequent to either in vitro administration (10-100 microM) or in vivo pretreatment (0.35-2.80 mg/kg) with droperidol, haloperidol, or trifluoperazine. After equilibration, maximum increases in tension were recorded and mean data analyzed by analysis of variance (P less than 0.05). When either droperidol or trifluoperazine was administered in vivo, contracture values after exposure to succinylcholine and halothane were significantly decreased. After in vivo pretreatment with haloperidol or in vitro administration of droperidol, succinylcholine-induced contractures were significantly reduced; contractures subsequently induced by halothane did not significantly differ from that of controls. In vitro treatment with haloperidol and trifluoperazine, however, produced significant increases in tension in muscles exposed to succinylcholine and halothane. This study provides evidence that droperidol may be considered a safe anesthetic adjunct in malignant hyperthermia-susceptible patients, and, additionally, that caution should be exercised when interpreting results from studies in which contracture testing is performed on muscle from patients treated with neuroleptic agents.

Animals↗
PubMed1993

Muscle contracture and twitch depression induced by arsenite in the mouse phrenic nerve-diaphragm.

The purpose of this investigation was to explore the possible mechanism of muscle contracture and twitch depression induced by arsenite in the mouse diaphragm. Arsenite-contracture was dependent on extracellular Ca2+; both EGTA and Ca(2+)-channel blockers (nifedipine and verapamil) inhibited arsenite-contracture. However, the activators caffeine and ryanodine and the inhibitor ruthenium red of the Ca2+ releasing channel of sarcoplasmic reticulum (SR) all exerted a profound inhibitory action on arsenite-contracture. Neither the Ca(2+)-release nor the Ca(2+)-ATPase activity of SR. were affected by 50 microM arsenite. These findings indicate a possibility that arsenite induced muscle contracture by enhancing Ca(2+)-entry which further induced Ca(2+)-release from SR. Moreover, the possible mechanism of twitch blockade induced by arsenite was studied by an electrophysiological technique. The frequency of miniature endplate potential (m.e.p.p.) was initially increased but eventually abolished by arsenite, while the amplitude of m.e.p.p. remained unaffected and that of endplate potential rapidly declined. It is considered that arsenite increased the spontaneous release of transmitter by enhancing Ca2+ entry into the nerve terminal and inhibited the evoked transmitter release possibly by acting at a certain site which governs transmitter release.

Animals↗
PubMed1999

Relaxing action of sodium nitroprusside independent of membrane potential in the CCh-induced contracture of the guinea pig stomach muscle.

Carbachol (CCh, 10(-6) M) induced biphasic contraction of longitudinal muscle of the guinea pig stomach, consisting of rapid phasic contraction and contracture. The contracture was almost completely inhibited by sodium nitroprusside (SNP, 10(-6) M) and S-nitroso-N-acetyl penicillamine (SNAP, 10(-6) M). A membrane permeable analogue of cyclic GMP, 8Br-cGMP (10(-4) M), also inhibited the CCh induced contracture. Although a heme site inhibitor of nitric oxide-sensitive guanylyl cyclase, 1-H-[1, 2, 4] oxadiazolo-[4, 3 a]quinoxalin-1-one (ODQ; 10(-6) M), reduced the inhibitory action of SNP, it did not affect the inhibitory action of 8Br-cGMP, indicating that the effect of SNP was developed via cyclic GMP production in the presence of D600. Charybdotoxin (10(-7) M), an inhibitor of Ca2+ activated K+ channel, did not influence on the CCh induced contracture. On the other hand, CCh induced a depolarization of the longitudinal muscle cell membrane (from -60 mV to -45 mV) in the presence of 10(-6) M D600, but SNP did not affect the depolarization. These results suggest that in the presence of D600 SNP induces relaxation of CCh induced contracture of the longitudinal muscle of the guinea pig stomach via cyclic GMP but not membrane potential dependent mechanism.

Animals↗
PubMed1997

Effect of trolox C on cardiac contracture induced by hydrogen peroxide.

Hydrogen peroxide (H2O2) perfused into the aorta of the isolated rat heart induces a positive inotropic effect, with cardiac arrhythmia such as extrasystolic potentiation or cardiac contractures, depending on the dose. The last effect is similar to the "stone heart" observed in reperfusion injury and may be ascribed to lipoperoxidation (LPO) of the membrane lipids, to protein damage, to reduction of the ATP level, to enzymatic alterations and to cardioactive compounds liberated by LPO. These effects may result in calcium overload of the cardiac fibers and contracture ("stone heart"). Hearts from male Wistar rats (300-350 g) were perfused at 31 degrees C with Tyrode, 0.2 mM trolox C, 256 mM H2O2 or trolox C + H2O2. Cardiac contractures (baseline elevation of the myograms obtained) were observed when hearts were perfused with H2O2 (Tyrode: 5.9 +/- 3.2; H2O2: 60.5 +/- 13.9% of the initial value); perfusion with H2O2 increased the LPO of rat heart homogenates measured by chemiluminescence (Tyrode: 3,199 +/- 259; H2O2: 5,304 +/- 133 cps mg protein-1 60 min-1), oxygen uptake (Tyrode: 0.44 +/- 0.1; H2O2: 3.2 +/- 0.8 nmol min-1 mg protein-1) and malonaldehyde (TBARS) formation (Tyrode: 0.12 +/- 0; H2O2: 0.37 +/- 0.1 nmol/ml). Previous perfusion with 0.2 mM trolox C reduced the LPO (chemiluminescence: 4,098 +/- 531), oxygen uptake (0.51 +/- 0) and TBARS (0.13 +/- 0) but did not prevent the H2O2-induced contractures (33.3 +/- 16%). ATP (Tyrode: 2.84 +/- 0; H2O2: 0.57 +/- 0) and glycogen levels (Tyrode: 0.46 +/- 0; H2O2: 0.26 +/- 0) were reduced by H2O2. Trolox did not prevent these effects (ATP: 0.84 +/- 0 and glycogen: 0.27 +/- 0). Trolox C is known to be more effective than alpha-tocopherol or gamma-tocopherol in reducing LPO though it lacks the phytol portion of vitamin E to be fixed to the cell membranes. Trolox C, unlike vitamin A, did not prevent the glycogen reduction induced by H2O2. Trolox C induced a positive chronotropic effect that resulted in higher energy consumption. The reduction of energy level seemed to be more important than LPO in the mechanism of H2O2-induced contracture.

Animals↗
PubMed1977

On the roles of calcium ion during potassium induced contracture in the smooth muscle cells of the rabbit main pulmonary artery.

The half decay time of the K-induced contracture of rabbit main pulmonary artery following pretreatment with Ca-free EGTA containing solution was 110 sec. A Ca-free K-solution did not generate contraction while noradrenaline, acetylcholine and prostaglandin F2alpha-containing solution did evoke contracture. The decays of the chemically induced mechanical response in Ca-free solution against the exposure times could be classified into three components (2 min, 28 min and over 100 min, respectively). When the membrane depolarization produced by excess K+ was simulated in Krebs solution by application of current, the generated mechanical response was smaller than that produced by 118 mM K+. When the membrane potential was clamped at the resting level before, during and after application of the excess K+, and excess K+ still evoked contracture. The amplitudes of contracture depended on [K]o. The effects of various [K]o on the length constant of the tissue were also observed in relation to the clamping condition. It is postulated that the mechanical response of the pulmonary artery induced by excess K is mainly due to influx of Ca++ and the depolarization plays only a minor role. This means that release of stored Ca by depolarization is not an essential factor in generation of K-induced contracture in this tissue.

Acetylcholine↗
PubMed1985

Rapid cooling contracture in frog striated muscles treated with chlorpromazine and haloperidol.

Rapid cooling contracture (RCC) was observed in frog toe muscles pretreated with caffeine, chlorpromazine (CPZ), or haloperidol (HPD). During rapid cooling contracture in the presence of caffeine (caffeine-RCC) tension developed to more than 0.8 of the maximum tetanic tension (P0). CPZ inhibited twitch but induced rapid cooling contracture (CPZ-RCC) between 50 and 150 microM; the tension saturated at the level of 0.75 P0 at 100 microM. HPD also inhibited twitch and induced rapid cooling contracture (HPD-RCC) at concentrations greater than 25 microM; the maximum tension was 0.25 P0. In the presence of dantrolene (10 microM), the tension during CPZ-RCC was reduced by 40%. Procaine (0.25%) reduced the CPZ-RCC tension by as much as 60%. These results suggest that CPZ and HPD induced rapid cooling contracture by reducing Ca2+-accumulation in sarcoplasmic reticulum.

Animals↗
PubMed1991

Adrenergic modulation of the K+ contractures in tonic skeletal muscle fibers of the frog.

The effects of adrenaline and isoprenaline on K+ contractures of curarized tonic skeletal fibers were investigated. The K+ contractures of tonic fibers have a peak tension followed by a sustained tension. The peak tension and total tension (the tension-time integral--area--of K+ contractures) were increased by adrenaline and isoprenaline. The resting potential of tonic skeletal fibers were unaffected by adrenaline. The calcium channel blocker (cadmium and nifedipine) greatly blocked the effects of adrenaline on the peak and total tension of K+ contractures. On the other hand, the peak and sustained tensions of K+ contractures were greatly reduced in Ca(2+)-free solution, but, the peak tension recovered when the fibers were pre-incubated in adrenaline. It is proposed that adrenergic modulation of tension in tonic skeletal muscle fibers could be related with the modulation of Ca2+ channels and/or Ca2+ release from the sarcoplasmic reticulum.

Animals↗
PubMed1992

An analysis of post-contracture potentiation in frog twitch skeletal muscle.

Post-tetanic potentiation (PTP) was mimicked by post-contracture potentiation (PCP) in the twitch muscle of frog. A marked PCP was observed in small bundles of semitendinosus muscle in tetrodotoxin (TTX)-containing solution under current clamp condition. Contractures were induced by a constant depolarizing current pulse of 1 s every 5 min. Each contracture (C) was preceded and followed by a twitch-corresponding short contracture, T1 and T2, with an interval of 2 s. The ratio of twitch height, T2/T1, was measured and compared under various conditions. In TTX-containing Ringer solution, T2/T1 depended on magnitude of both T and C. When T2/T1 was plotted against C/T1 a quasi-linear relationship was found. The slope of the curve was 0.076 and was found to decrease when the duration of T was increased to 1 s. In TTX-containing solution, addition of 2 mM Ba2+ or 1 mM caffeine potentiated T as well as C but decreased T2/T1 markedly. Similar effects were observed when Na+ was replaced with TEA+ or when bath temperature was lowered from 20 to 8 degrees C. In all cases T2/T1 vs. C/T1 curve was shifted to the left and downwards. It was considered that these results could be attributable to an elevation of the resting Ca2+ concentration in the sarcoplasm. Thus the phenomenon of PCP probably reflects the time course of Ca2+ transients in the conditioning contracture C.

Action Potentials↗
PubMedDate not supplied

Joint contractures in patients with juvenile diabetes and their siblings.

Six hundred fifteen children (310 with diabetes, 106 nondiabetic siblings, and 199 nonsibling controls) were examined for the presence of joint contractures. Forty children had contractures: 8.4 per cent of those with diabetes and 4.6 per cent of those without diabetes. Contractures were present, however, in 9.4 per cent of nondiabetic siblings, and only 2 per cent of nonsibling controls, suggesting a familial tendency to joint contractures. The older the patient, the more likely he was to have contractures. There was no correlation with sex, race, or age at onset of the disease.

Adolescent↗
PubMed1975

[The effect of hypertonic solutions on contracture of a tonic muscle fiber].

Effect of glycerol, sucrose and NaC1 hypertonic solutions exerted on potassium contracture and resting membrane potential in isolated frog tonic muscle fibres were studied. Sucrose and NaC1 hypertonic solutions induce a stable depolarization and depress potassium contracture, while glycerol results in a transient depolarization followed by recovery of resting membrane potential and contracture reactions. The removal of 400 mM glycerol induces an insignificant depolarization and disappearance of contracture reactions, however, after the removal of sucrose of NaC1 hypertonicity both the parameters tend to restore. The isolated phasic and tonic fibres lose irreversibly potassium contracture reactions after the removal of 100 mM and 400 mM glycerol, respectively, the latter being more resistant to this procedure. Nevertheless it is concluded that the T-system is equally important for excitation--contraction coupling in tonic and in phasic fibres.

Animals↗
PubMed2000

Volkmann's ischemic contracture. Prevention and treatment.

It may be concluded that treatment of patients with Volkmann's ischemic contracture is complicated and depends on a number of different variables. Optimal treatment of an established contracture requires a through examination of the extent of damage of the ischemia, followed by conservative therapy or operation. The most important measures concerning Volkmann's ischemic contracture, however, involve measures to prevent the contracture. It is poignant that very simple measures, such as monitoring high-risk injuries and immediate vascular repair or decompression if symptoms of a compartment syndrome are present, can prevent this disabling condition. The following summaries hopefully provide guidelines for prevention and treatment of Volkmann's ischemic contracture.

Arm↗
PubMed1976

The effect of Ca2+, temperature and sucrose upon potassium contracture of the isolated rat right ventricle.

Potassium (100 mM KC1) contracture of the isolated rat right ventricle was lower in Tyrode solution (37 mM Na) than on substituting sucrose (270 mM) for NaC1 and was biphasic in 70% of the experiments. As in slow (tonic) skeletal muscle, the maximum contracture value persisted as long as a raised KC1 concentration was maintained. Even after complete potassium depolarization it changed when Ca was altered. At 37 degrees C, the second phase of potassium contracture was higher than at 34 degrees C (p less than 0.01). The effect of K+ and Ca2+ was inhibited if the ions were added after adding sucrose to the Tyrode solution. Contracture of the rat ventricle resembled contracture of slow (tonic) skeletal muscle.

Animals↗
PubMedDate not supplied

[Early hypoxic contracture of the myocardium in adult and newborn rats].

The effect of 30 min substrate free hypoxia (H) on isometric tension was studied in isolated myocardium (M) of adult (A) and newborn (N) rats. The perfusion with 50% Na+ H solution caused in AM the development of H contracture which was more than 50% higher than control contracture. H perfusion with 0.1 mM Ca2+, 1.0 mM La3+, and 10.0 mM of caffeine provides the discrimination of control and hypoNa+ contractures. It is assumed that early H contracture in AM is a result of inability of Ca-sequestering system to accumulate intracellular Ca2+ and Ca2+ influxing through the sarcolemma. In myocardium of N rats Na-Ca exchange is proposed as a main source of Ca2+ for H contracture development.

Animals↗
PubMed1992

Na(+)-Ca2+ exchange influences halothane and caffeine contractures of malignant hyperthermic skeletal muscle.

These experiments sought to determine the influence of sarcolemmal Na(+)-Ca2+ exchange on halothane and on caffeine contractures of malignant hyperthermic (MH) skeletal muscle. Fiber bundles excised from MH susceptible pigs (Pietrain) were exposed to halothane (3%) and caffeine (0.5-8.0mM) while Na(+)-Ca2+ exchange was inhibited by reducing extracellular Na+ from 100% to 50, 25 and 0% of control. Halothane contracture magnitude was not altered by 50 or 25% Na+ whereas 0% Na+ increased the contractures by 51%. 0 and 25% Na+ increased the magnitude of caffeine contractures (2-8mM) by 53-176%. These results suggest that external Na+ and the Na(+)-Ca2+ exchange mechanism influences contractures of MH skeletal muscle.

Animals↗