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PubMed1981

Potassium contracture in the tonic bundle isolated from the enlarged flexor carpi radialis muscle of the frog.

The flexor carpi radialis muscle (FCRM) of the frog was divided into phasic and tonic bundles, and the properties of the potassium contracture in the tonic bundle were examined. The potassium contracture was tonic and the contracture induced by K higher than 75 mM consisted of the initial phasic component and of the following sustained component. Both components were abolished by the transverse tubule disruption. The curve relating the peak tension to the log[K]o (activation curve) started at about 15 mM K and reached maximum at about 75 mM K. By reducing [Ca]o, the activation curve shifted downward at higher [K]o, being little affected near the mechanical threshold. The time course of inactivation induced by 20 mM K was slow and monophasic, and was markedly accelerated by reducing [Ca]o. The spontaneous relaxation of the contracture induced by high K was little affected by reducing [ca]o.

Animals↗
PubMed1988

Effects of external sodium removal on the contracture of frog skeletal muscle.

Effects of removal of the external sodium on the contractility of the frog's skeletal muscle were studied. Sodium-free solution, replaced by choline, strongly augmented the twitch tension before it abolished the action potential. A similar marked potentiation was also observed in the sustained contracture induced by a small depolarization under the current-clamped condition where generation of conductive action potential was blocked. On the other hand, the maximum contracture induced either by electrical stimulation or by high potassium solution was not modified by lowering the external sodium concentration. Furthermore, contraction threshold measured on the electrically induced contracture was shifted to more negative value of the membrane potential. Caffeine contracture, examined by a short-term application of 5 mM caffeine, was first inhibited by sodium-free solution but afterwards restored or even augmented during the sodium-free perfusion. From these observations it is concluded that a removal of external sodium lowered the mechanical threshold of the muscle by affecting some step of the coupling process at the T-SR junction without affecting the contractile machinery.

Animals↗
PubMed1990

Multiple congenital contractures (MCC) and cleft palate induced in goats by ingestion of piperidine alkaloid-containing plants: reduction in fetal movement as the probable cause.

Fetal movement, observed by ultrasound imaging, was significantly reduced (P less than or equal to 0.001) in pregnant goats gavaged with Conium seed and Nicotiana glauca and temporarily reduced with fresh Conium plant. Conium seed and Nicotiana glauca induced cleft palate and multiple congenital contractures in 100% of the kids born to pregnant goats gavaged with these plants. Multiple congenital contractures included torticollis, scoliosis, lordosis, arthrogryposis, rib cage anomalies, over extension, and flexure and rigidity of the joints. However, in goats gavaged with fresh Conium plant, fetal movement was inhibited for only about 5 hours after each individual dosage and gradually returned to control levels 12 hours after dosing. Fetal malformations in this group were limited from modest to moderate contractures of the front limbs, which resolved by 8-10 weeks post partum. No cleft palates were induced. Fetal movement was not inhibited in goats fed Lupinus caudatus and no cleft palates or multiple congenital contractures were induced in their offspring. The duration of the reduction in fetal movement appears to be an important factor in the severity and permanence of the deformities, particularly with cleft palate, spinal column defects, and severe joint deviation and fixation.

Abnormalities, Drug-Induced↗
PubMed1975

K+ and Mg-2+ net fluxes in relation to zero [Ca-2+] perfusion and subsequent cardiac contracture.

Following within 45 sec after the development of contracture induced by restoring normal ionic composition perfusion conditions after a 12 min period of mechanical arrest in the rabbit heart caused by zero [Ca-2+] perfusion, there is an explosive efflux of K+ and Mg-2+. After shorter periods of Ca-2+-lack arrest, the restoration of [Ca-2+] to normal causes recovery of rhythmic contraction and no K+ efflux. The K+ and Mg-2+ effuxes are ascribed to the effects of the contracture itself and not simply to the loss of Ca-2+ during zero [Ca-2+] arrest nor to the restoration of normal perfusate [Ca-2+], except insofar as the latter operates to induce the contracture. It is suggested that cell membrane permeability progressively increases during zero [Ca-2+] arrest and that an abnormally large influx of Ca-2+ after restoration of normal perfusate [Ca-2+] induces the contracture.

Animals↗
PubMedDate not supplied

[The prevention of the development of myocardial contracture in the "calcium paradox" by action on Na-Ca metabolism].

The effect of artificial high sodium gradient on the rate of the myocardium contracture development during "calcium paradox" was studied in the experiments on the isolated heart of Langendorf-perfused rats. It is stated that artificial creation of a high sodium gradient decreases the rate of the myocardium contracture development. Exogenous nucleotides, activators of Na, K-ATPase, and their precursors intensified the protective action of the hypersodium medium. Phosphocreatine (100 mmol/l) had no protective effect during the "calcium paradox". However, under conditions of the high sodium gradient phosphocreatine efficiently prevented development of the contracture during the "calcium paradox". It is important to note that under analogous conditions creation of high osmosity of the solution adding 12 mmol/l of saccharose does not protect the heart from development of the myocardium contracture.

Animals↗
PubMed2004

[Dependence of myocardial contracture on energy resources during the calcium paradox].

Perfusion of the rat isolated hearts with calcium-free and calcium containing solution revealed a complex and deep myocardial damage called the calcium paradox. The reperfusion of the rat heart with calcium rich media resulted in myoglobin loss from the heart, significant decreasing of ATP and phosphocreatine level, complete uncoupling of respiration and phosphorylation in mitochondria, occurrence of myocardial contracture. Decreasing of sodium level to 30 mM--80 mM in calcium free media exacerbates the heart damage due to the calcium paradox with absence of contracture. Addition of phosphocreatine (1 mM, 5 mM, 10 mM) evoked some restoration of ATP contents in the tissue with appearance of significant contracture. Phosphocreatine exacerbated the loss of myoglobin from the heart subjected to the calcium paradox. A discrepancy between myocardial contracture and degree of cellular damage has been observed during the calcium paradox.

Animals↗
PubMed2006

[Mini-invasive distraction technique for treatment of severe ankle and foot deformities secondary to ischemic contracture of the leg].

OBJECTIVE: To explore the Ilizarov mini-invasive distraction technique for the treatment of severer ankle and foot deformities secondary to ischemic contracture of the leg. METHODS: Based on the tension-stress low of Ilizarov, a serial of adjustable three dimensions external distractive instrument was developed in our department. From April 2002 to March 2004, 8 patients with ankle and foot deformities secondary to ischemic contracture of the leg induced by trauma and fracture were treated with the distractive instrument. Of them, 4 patient were male and 4 female, aged from 13 to 31 years with an average of 23 years. Five affected legs were in the left and 3 in the right. Preoperative abnormal style included talipes equines in 6 feet and equinovarus in 2 feet, with extensive scar contracture in the legs. Five patients suffered from failure of soft tissue release before, two patients with severe bony deformity of the feet were underwent limited foot triple osteotomy in this department before the distractive correction. The distraction was begun from 7 d after operation and distractive time from 29 to 60 d with an average 46 d. RESULTS: All of the 8 patients were followed up from 10 months to 29 months, with an average of 13 months. All of deformities in the feet were corrected satisfactorily, full feet contacted with the ground in stand or walking and achieved with good function. No complication, such as pin tract infection, skin necrosis and neurovascular injury was occurred in this group. CONCLUSIONS: Mini-invasive distraction technique for treatment of severe ankle and foot deformity secondary to ischemic contracture of the leg is safe and mini-injury, it is also an effective approach for the treatment of various kinds of rigid foot anomaly.

Adolescent↗
PubMed1990

Effects of the calcium antagonist, TMB-8 on halothane and on caffeine contractures of malignant hyperthermia susceptible skeletal muscle.

This investigation sought to determine if the Ca2+ antagonist, TMB-8, alters the contracture responses of malignant hyperthermia susceptible (MHS) skeletal muscle to halothane and to caffeine. Muscle fiber bundles were excised from both MHS and normal pigs and exposed to TMB-8 (100 microM), halothane (3%) and caffeine (0.5-8.0 mM), administered alone and in combination. TMB-8 depressed tension developed during isometric twitches in both MHS and normal muscle but had no effect on resting tension (RT). Halothane, however, increased RT in MHS but not in normal muscle. TMB-8 failed to reduce the halothane contracture of MHS muscle but hastened its onset. Caffeine concentrations of greater than or equal to 2 mM increased RT in MHS whereas only 8 mM evoked contracture of normal muscle. These effects were also unaltered by TMB-8. Results suggest that TMB-8 does not inhibit halothane nor caffeine contractures of MHS muscle.

Animals↗
PubMed1989

[Clinical implications of enhanced caffeine contracture in malignant hyperthermia (MH) and Duchenne muscular dystrophy (DMD)].

The caffeine contracture response was studied on the skinned muscle fiber in patients with MH episodes or with DMD. An abnormally enhanced caffeine contracture was observed in 12 out of 14 subjects with MH episodes and 11 out of 13 patients with DMD. The extent of abnormality was almost the same in both group of patients. Ca-induced Ca release (CICR) of the sarcoplasmic reticulum was also analyzed on the same specimens. CICR was increased in 3 out of 4 cases with MH episodes, but it was decreased or unchanged in 4 patients with DMD. It was suggested that the mechanism of abnormal caffeine contracture might not be the same between MH and DMD. Thus, adverse anesthetic reactions, which are occasionally reported in DMD, could be different from genuine MH in its pathophysiology. However, before concluding this issue, further studies seem necessary concerning the molecular mechanism of abnormal Ca release. In the meantime, studies of caffeine contracture on the skinned fiber are helpful as one of predictive tests of MH and related disorders.

Adolescent↗
PubMed1989

Mechanism of protective effects of Ca++ channel blockers on energy deprivation contracture in cultured ventricular myocytes.

To examine mechanisms of the protective effects of Ca++ channel blockers on energy deprivation contracture, we measured cystolic calcium ion concentration ([Ca++]i) (Indo-1 fluorescence), development of contracture (video motion detector) and ATP contents during exposure of cultured chick embryo ventricular cells to 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG). The time periods required for [Ca++]i to reach 50% of [Ca++]i transient ([Ca++]i-50) and contracture were determined after exposure to 1) CN + 2-DG alone, 2) CN + 2-DG simultaneous with 1 microM verapamil (V-sim) and 3) verapamil followed by CN + 2-DG (V-pre). Time periods required to reach [Ca++]i-50 under these conditions were 4.2 +/- 0.4 min (CN + 2-DG alone), 3.8 +/- 0.4 min (NS vs. CN + 2-DG alone) (V-sim) and 6.4 +/- 1.1 min (P less than .05 vs. CN + 2-DG alone) (V-pre), respectively. Time periods required for contracture development were 4.4 +/- 0.3 min (CN + 2-DG alone), 4.4 +/- 0.6 min (NS vs. CN + 2-DG alone) (V-sim) and 9.3 +/- 1.2 min (P less than .05 vs. CN + 2-DG alone) (V-pre). Three minutes after metabolic inhibition, ATP contents declined from 32.3 +/- 0.7 nmol/mg of protein to 4.2 +/- 1.0 in CN + 2-DG alone, to 4.5 +/- 0.9 (NS vs. CN + 2-DG alone) with V-sim and to 8.3 +/- 2.2 (P less than .05 vs. CN + 2-DG alone) with V-pre.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1988

Volkmann's ischemic contracture. A case report.

A case is presented illustrating some of the basic principles in the development and repair of Volkmann's ischemic contracture following a supracondylar fracture. The etiology, initial signs, prevention, and possible treatments of the contracture are discussed. Early fasciotomy is the best treatment for impending contracture, while neurolysis with infarct excision, a flexor pronator slide, and tendon transfer can return much function following established contracture of the forearm.

Child↗
PubMed1988

Pyridostigmine-induced decrement in skeletal muscle contracture is not augmented by soman.

Previous studies have reported that pyridostigmine induces a decrement in contractile force generated during tetanic stimulation of skeletal muscle. Although our studies suggested that pyridostigmine affected release of transmitter from the motor nerve terminal, we could not exclude the possibility that the drug's action was due to depolarization blockade of the muscle brought on by excessive transmitter in the synaptic cleft. The purpose of this study was to determine whether the effect of combined treatment with pyridostigmine and an irreversible cholinesterase inhibitor (soman) would potentiate the decrement in muscle contracture observed with pyridostigmine alone. As reported previously, pyridostigmine (25 mg/kg) significantly reduced muscle contracture during tetanic stimulation (20-100 Hz), and soman (0.075 mg/kg) increased muscle contracture. Combined treatment with pyridostigmine and soman produced a decrease in muscle contracture equivalent to the effect of pyridostigmine alone. Since there was no evidence of depolarization blockade of the muscle despite aggressive treatment with two cholinesterase inhibitors, these results support the view that pyridostigmine has a significant presynaptic action to decrease neurotransmitter release. This action opposes the drug's inhibition of cholinesterase, and the net effect of combined treatment with pyridostigmine and soman is a muscle response which is largely unchanged from the effect of pyridostigmine alone.

Acetylcholinesterase↗
PubMed1987

Reversible inhibition of acetylcholine contracture of molluscan smooth muscle by heavy metals: correlation to Ca++ and metal content.

The present study examined the effects of three heavy metals on the acetylcholine (ACh) contracture and Ca++ kinetics of the anterior byssus retractor muscle of Mytilus edulis. An isolated tissue bioassay using anterior byssus retractor muscle was prepared according to standard procedures and the isometric tension produced in response to ACh was measured. Ten millimolar Ni++, Co++ or Cd++ reduced the maximum contracture response to ACh in zero-Ca medium in a time-dependent manner. The inhibition was reversed upon restoration of medium containing 10 mM Ca++. The loss (and re-establishment) of contracture response to ACh corresponded to the influx (and efflux) of the heavy metal ions opposite to the direction of Ca++ flow. These results are consistent with the concept that the loss of the ACh contracture response is attributable to the displacement of tissue Ca++ from release sites by heavy metals.

Acetylcholine↗
PubMed1986

Halothane-cooling contractures of mammalian muscles.

Mouse soleus and extensor digitorum longus muscles exposed to halothane concentrations (0.3-2.0%) that, at room temperature, have no effect on either resting or twitch tension, develop transient contractures when cooled to 2-10 degrees C. The halothane-cooling contractures (HCC) are reproducible and their amplitudes can be graded by both the halothane concentration and the temperature of cooling. Under identical conditions the HCC is significantly larger in soleus as compared to extensor digitorum longus muscles. The maximal HCC in soleus muscles (1-2% halothane, 2 degrees C) reaches 42% of the tetanic tension recorded at 24 degrees C; in extensor digitorum longus the maximum is 12% of tetanic tension. This difference is ascribed to the predominance of slow-twitch fibers in the soleus muscle. Neither membrane depolarization with high [K]0 solutions nor a short (2 min) exposure to Ca-free media inhibits the HCC. The contractures are depressed, however, when the muscles are preequilibrated for 30 min with Ca-free solutions; under these conditions, the muscle twitches and the caffeine-cooling contractures are also depressed. These effects are ascribed to partial depletion of the Ca content of the sarcoplasmic reticulum. The HCC is abolished by 4 mM procaine, partially inhibited by 4 to 10 mM procainamide and potentiated by 4 mM lidocaine, but it is not significantly affected by dantrolene (40 microM). It is proposed that the HCC results from synergistic interaction of halothane and low temperature inhibiting Ca-sequestration by the sarcoplasmic reticulum of the muscle fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Local↗
PubMed1984

Sodium withdrawal contractures in rat slow twitch skeletal muscle.

Contractile responses due to alterations in [Na+]o have been investigated in fast (iliacus) and slow (soleus) twitch muscles of the rat. On exposure to a Na-free solution, the soleus in contrast to the iliacus cells, generated contractile responses without depolarizing the surface membrane. Following glycerol treatment, the twitch and a part of the Na-withdrawal contracture were abolished. The amplitude of the remaining contracture was between 5 and 50% of the original response and the time to peak was 0.4 to 2 times longer. In intact and detubulated preparations, the amplitude of the zero-Na contracture was modified by changes in [Ca2+]o and a linear relationship was found if the reciprocal of tension was plotted against 1/square root[Ca2+]o. In intact and detubulated fibres, a steep dependence of the Na-withdrawal contracture on [Na+]o was found and [Na+]o which induced the half maximal response at each [Ca2+]o was the same, the responses were inhibited by Mg-ions in a competitive way. It is assumed that the activator Ca is triggered at the tubular and sarcolemmal membrane level by lowering [Na+]o and that a calcium-induced calcium release mechanism at the S.R. level may also be involved.

Animals↗
PubMed1980

K and Ca in muscle mechanics, II. K-contracture.

K-rich solution, the isotony of which corresponds to normal Ringer's solution, was used in our experiments: 4.59 g KCl + 40.5 g saccharose, 1000 ml bidistilled water. Freshly prepared living muscles of Rana esculenta (m. sartorius, m. iliofibularis, m. peroneus, m. tibialis, m. gastrocnemius, m. semimembranosus) got into K-contracture in this solution, but they relaxed within some minutes. In muscles of dead frog (which canno tbe stimulated with 110 V a.c.) the K-rich solution did not elicit contracture, i.e. on the one hand K-contracture could be observed only in living muscle and on the other hand, the muscles did not lose their excitability after the K-contracture had ceased (a.c. 2V).

Animals↗
PubMedDate not supplied

Mechanism of cardiac contracture during anoxic arrest using cardiopulmonary by-pass.

Cardiac contracture during anoxic cardiac arrest might result from a reduction in the adenosine triphosphate or from an accumulation of cytoplasmic calcium. The present study was undertaken to test the hypothesis that the accumulation of cytoplasmic calcium is a factor in the anoxic myocardial contracture in a setting similar to that used during cardiac surgery, using cardiopulmonary bypass. Anoxic cardiac arrest was produced for 30 and 60 minutes in 7 dogs each, by clamping the ascending aorta, using cardiopulmonary bypass. At the end of anoxic period, aorta was declamped for reperfusion of the heart for 30 minutes of termination of anoxic cardiac arrest. Total tissue and intracellular electrolytes were determined before and at various intervals (0, 5, 15, 30 minutes) after termination of anoxic cardiac arrest. Thirty minutes of anoxic cardiac arrest produced a significant decrease in the mean aortic and left ventricular systolic pressures, and left ventricular dp/dt/IIP; and a significant increase in the cardiac index. Total tissue and intracellular Na, Ca, and K did not change significantly at the end of 30 minutes of anoxia and during 30 minutes of reperfusion. Anoxic arrest for 60 minutes resulted in cardiac contracture in all dogs. The total and intracellular Ca decreased significantly at the end of 60 minutes of anoxia and during 30 minutes of reperfusion. Total tissue and intracellular Na, although, did not change during anoxic arrest, it increased significantly at 15 and 30 minutes of reperfusion. Cardiac potassium did not change significantly during the whole period of experiment. These studies suggest that total and intracellular calcium did not increase above the control values during anoxic myocardial contracture in a setting similar to that used during cardiac surgery, using cardiopulmonary bypass.

Animals↗
PubMed1976

[Experiments on the mechanism of action of vascular spasmolytic agents. II. Action of nitroprusside sodium, nitroglycerin, prenylamine and verapamil on the lanthanum contracture of isolated coronary arteries].

On isolated coronary arteries of cattle, lanthanum causes after preceding calcium depletion by EGTA a contracture which is independent of the presence of extracellular calcium. Nitroprusside sodium and nitroglycerol act on this contracture strongly relaxing in the same concentrations that were active on the potassium contracture. In contrast, a very low spasmolytic effect is demonstrable for verapamil on the lanthanum contracture, and prenylamine is without any statistically significant influence. Nitroprusside sodium and nitroglycerol and act by a mechanism entirely different from that of verapamil and prenylamine.

Animals↗