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PubMed1988

Sodium-depletion-induced contractures in isolated rat vas deferens: possible role of endogenous catecholamines.

The mechanism involved in the development of contracture in an isolated smooth muscle in Na+-depleted saline solution is not clearly understood. Whereas most of the reported studies attribute it to direct myogenic action of Na+ depletion, a few suggested the contracture to be an indirect mechanism through the release of the neurotransmitter from presynaptic nerve endings. The present study employed rat vas deferens and it showed that the slowly developing contracture in Na+-depleted saline solution was blocked by prior treatment with in vitro prazosin and in vivo reserpine. Prior exposure of the tissue to verapamil caused the development of rhythmic contractions in Na+-free medium and these rhythmic contractions were blocked by prazosin. Exposure of the tissue to a Ca2+-free solution abolished the contractures induced by Na+-free solution. Na+-depletion increased the sensitivity of the vas deferens to exogenous noradrenaline. It is concluded that the contractures induced by Na+ depletion result from the stimulation of postjunctional alpha-adrenoceptors by endogenously released catecholamines from the adrenergic nerve terminals innervating the vas deferens smooth muscle. Further, these contractures result from an influx of extracellular Ca2+ through both voltage-dependent and receptor-operated calcium channels.

Animals↗
PubMed1988

Caffeine contracture in guinea-pig ventricular muscle and the effect of extracellular sodium ions.

1. The mechanisms underlying the virtual absence of caffeine contracture in guinea-pig heart in a Na+-rich external solution were reinvestigated in small (50-120 microns thick) bundles of intact and skinned papillary muscle fibres. 2. In Na+-free solution, the peak tension of 30 mM-caffeine contracture corresponded to the maximum tension of the skinned fibres, and was independent of changes in [Ca2+]o and [K+]o. In the presence of external Na+, the peak tension, which was at most several per cent of the maximum, was affected by [Ca2+]o, [Na+]o and [K+]o, and enhanced by Mn2+ and Ni2+. 3. In the absence of Ca2+, replacement of Na+ with K+ allowed caffeine to evoke a large contracture, showing that there was sufficient calcium stored in the cells under Na+-rich conditions. After treatment with 30 mM-caffeine in the Na+-rich, Ca2+-free solution, and upon replacement of all Na+ with Li+, caffeine was still able to produce a large contracture, which was dependent upon Ca2+ pre-loading of the cells before the first caffeine treatment and upon the subsequent duration in the Na+-free solution. 4. Replacement of Li+ with Na+ during the contracture led to rapid relaxation which was delayed by an increase in [Ca2+]o, depolarization by K+, and addition of La3+ and Mn2+. After Na+-induced complete relaxation in the absence of Ca2+, upon removal of the drugs and Na+, subsequent application of caffeine to the cells evoked a large contracture without Ca2+ reloading. 5. In the skinned fibres, 30 mM-caffeine increased the Ca2+ sensitivity of the contractile system and depressed the maximum tension. An increase in Na+ from 8.4 to 58.4 mM altered neither Ca2+ sensitivity nor the rate of tension development in the absence or presence of caffeine. 6. Increase in Na+ affected neither the rate nor the amount of Ca2+ uptake by the sarcoplasmic reticulum (SR) in the absence or presence of caffeine. Increasing Na+ slightly inhibited the caffeine-induced Ca2+ release from the SR, but more than 10 mM-caffeine produced SR Ca2+ depletion. 7. In the presence of a strong Ca2+ buffer, the steady level of Ca2+ uptake by the SR with 1 mM-caffeine was equal to the amount of Ca2+ remaining in the SR just after the application of caffeine, indicating that Ca2+ release was not inactivated.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1979

The effects of temperature, local anaesthetics, pH, divalent cations, and group-specific reagents on repriming and repolarization-induced contractures in frog skeletal muscle.

Contractures appear during repolarization of frog toe muscles in media containing perchlorate in place of chloride. These contractures were suppressed or delayed by certain procedures which retard the repriming of K contractures, i.e., by sufficient reduction in temperature or by alkaline pH in solutions lacking divalent cations. They also were greatly reduced without interference with repriming after treatment with a reagent which selectively modifies free amino groups. In the presence of appropriate concentrations of procaine, repriming was markedly impaired with only a small reduction in the amplitude of repolarization-induced contractures. Small contractures were produced during repolarization in chloride solutions in the presence of 10 mM procaine at pH 8.0. None of these procedures affected the changes produced by perchlorate solutions in the potential dependence and the time course of K contractures. The results support the view that activation and inactivation of contraction following depolarization are separate potential dependent processes. Tension appears to develop during repolarization when the reversal of inactivation occurs before the reversal of activation is completed, both steps being necessary to recover the reprimed resting state.

Action Potentials↗
PubMed1984

A comparison of the effects of cationic, anionic, and neutral amphipathic agents on the contractile behaviour of frog skeletal muscle. II. Amplitude of depolarization and repolarization-induced contractures.

Sufficiently high concentrations of cationic (n-alkyl trimethylammonium) or neutral (n-alkanols) amphipathic agents reduced the amplitude of maximum K contractures of frog toe muscles, an effect which was antagonized by reduced temperature, by the presence of perchlorate anions, or (to a lesser extent) by an increased concentration of divalent cations. Enhancement of the similar effect of tetracaine was prominent only with alkyl trimethylammonium compounds. Enhancement of the depressant effect of acidity (pH 5.0) was observed with octyl trimethylammonium and octanol but not with octanesulfonate or butanol. Partial restoration of potassium contractures in media lacking divalent cations was produced by octane- or nonane-sulfonate and by propanol but not by octyl trimethylammonium or octanol. The alkyl sulfonates differed from the other agents studied in producing tonic contractures at concentration which did not reduce maximum K-contracture tension. The alkyl sulfonates also differed from other amphipaths of similar size in their ability to elicit small repolarization-induced contractures in the absence of perchlorate, although this property also was shared by small alkanols. Sufficient concentrations of all amphipaths reduced the amplitude of repolarization-induced contractures in the presence of perchlorate. The intensity of the effects of these agents on contractile function usually was proportional to the size of their apolar group, and with ionic apmphipaths such effects were apparent only with compounds having hydrocarbon chains containing eight or more carbon atoms. These experiments indicate that hydrophobic interactions in the external lamina of the sarcolemma can influence the potential-dependent control of contractile function in skeletal muscle, presumably by effects on the conformational transitions of integral membrane proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Iodoacetate-induced skeletal muscle contracture: changes in ADP, calcium, phosphate, and pH.

The effects of iodoacetic acid (IAA) and ischemic contraction were studied in rat extensor digitorum longus muscles. Ischemic stimulation of IAA-treated muscles produced contracture. We measured total muscle water content, distribution of water between intracellular and extracellular spaces, creatine concentration ([Cr]), creatine phosphate concentration ([PCr]), [ATP], [Pi], intracellular pH, and intracellular Ca2+ concentration ([Ca2+]i) at the onset of contracture. [ADP] was calculated from the equilibrium of the creatine kinase reaction using the measured values of [ATP], [PCr], [Cr], and pH. At the onset of contracture there was a 75% reduction of [PCr], a 12-fold increase in [ADP], and an 11-fold increase in [Ca2+]i compared with unstimulated IAA-treated muscles. [ATP] was not depleted at contracture compared with unstimulated IAA-treated muscles, and [Pi] increased less in muscles at contracture compared with stimulated control muscles. The persistent tension in contractures probably resulted from increased [Ca2+]i combined with increased myofibrillar Ca2+ sensitivity due to elevated [ADP] and relatively reduced intracellular acidification and [Pi].

Adenosine Diphosphate↗
PubMed1977

Determinants of hypoxic and posthypoxic myocardial contracture.

The relationship between contracture (a rise in resting tension at constant length) and contractile activity was studied in isometric rat trabeculae carneae and cat right ventricular papillary muscles. Muscles at Lmax were paced at 12/min in solutions equilibrated at 29 degrees C with 95% O2-5% CO2. In rat myocardium, exposure to 60 min hypoxia (95% N2-5% CO2) at alkalotic pH produced contracture. In cat myocardium contracture was produced by the combination of exposure to digitalis and the recovery from hypoxia. Delayed relaxation was not responsible for the rise in resting tension in either preparation. In muscles not paced during hypoxia, contracture appeared despite total absence of contractile activity. Exposure to low calcium or acidosis reversed or prevented the rise in resting tension. Thus, contracture can be: 1) dynamic, reversible, and modified by factors which affect intracellular calcium availability; 2) independent of contractile activity and apparent activity of the relaxing system; and 3) distinct from delayed or incomplete relaxation. The extent of contracture during the recovery from hypoxia is not simply the function of the level of contractile activity during hypoxia but appears related to calcium availability at a critical time.

Acidosis↗
PubMed1990

Metabolic and functional consequences of barium-induced contracture in rabbit myocardium.

Barium contracture tonically activates myocardium while preserving cellular integrity. We studied the metabolic and mechanical consequences of sustained Ba2+ contracture. We measured the time course of phosphocreatine (PCr), ATP, Pi, total phosphate, and intracellular pH via 31P nuclear magnetic resonance (NMR) in isolated, isovolumic rabbit hearts. For mechanical studies, we measured force transients and dynamic stiffness in excised rabbit right ventricular papillary muscles at different elapsed times in Ba2+ contracture. In the perfused hearts, PCr fell steadily to 20% of control after 60 min. ATP remained constant for approximately 25 min then fell to 25% by 60 min. Pi rose to 200% within 15 min and then remained unchanged, whereas total phosphate dropped steadily to 50% of control by 60 min. Myocardial O2 consumption remained near control for 30 min and then declined to 50% by 60 min. Consistent with ATP and O2 consumption measurements, mechanical responses were unchanged for approximately the first half hour. Because of the elevated Pi, however, myofilament kinetics may have been accelerated compared with the control metabolic state. After the initial period of stable contracture, the gradual alteration of mechanical behavior exhibited a progressive trend toward more rigor-like characteristics. In summary, myocardium in Ba2+ contracture is metabolically and mechanically stable for approximately 30 min but begins to degrade thereafter. When compared with other tonic states of activation, Ba2+ contracture appears to be less demanding energetically.

Animals↗
PubMed1991

Ischemic contracture begins when anaerobic glycolysis stops: a 31P-NMR study of isolated rat hearts.

The relationships among myocardial ATP, intracellular pH, and ischemic contracture in Langendorff-perfused rat hearts were investigated by 31P nuclear magnetic resonance spectroscopy during total global normothermic ischemia while the left ventricular pressure was recorded continuously via an intraventricular balloon. Glucose-perfused hearts (n = 63) were divided into five groups based on the time of onset of contracture (TOC), and three other groups of hearts were treated to vary the ischemic glycogen availability. ATP levels, which showed no evidence of accelerated ATP depletion during contracture, were significant and variable at TOC. Intracellular pH initially declined and then leveled off at TOC, with lower final pH in hearts with later TOC. We conclude that contracture began when anaerobic glycolysis (and thus glycolytic ATP synthesis) stopped. These results, though consistent with the concept that ischemic contracture in normal hearts results from rigor bond formation due to low ATP levels at the myofibrils, suggest that TOC is more closely related to glycolytic ATP production than to total cellular ATP content, thus providing evidence of some degree of subcellular compartmentation or metabolite channeling. In glycolytically inhibited hearts, the quite early contracture may have a Ca2+ component.

Anaerobiosis↗
PubMed1975

Contractures in partially depolarized muscle treated with caffeine or nitrate.

Frog toe muscles partially depolarized with a subcontracture concentration (15 or 20mM) of K+ rapidly developed tension when exposed to 1 mM caffeine, which alone did not cause contracture. This action resulted from a lowering of the mechanical threshold by the caffeine and thus was similar to that caused by replacement of Cl- with NO3-. Maximal tension was the same in the caffeine and NO3- media but took much longer to develop in the former. Equilibrating the muscles with caffeine for 60 s (the time calculated for complete diffusion) did not reduce contraction time significantly. However, prolonging the exposure of muscles to caffeine beyond this time enhanced the drug's capacity to potentiate both the twitch and 30 mM K+ contractures and shortened the contraction time of the contractures. Toe muscles that had undergone a contracture in 100 mM K+ and were recovering in 15 mM K+-Ringer generated tension in the presence of 1 mM caffeine or NO3- but only after enough repolarization had been achieved so that a response to a second challenge with 100 mM K+ could be demonstrated. Although prolonged immersion in the K+-enriched recovery solution caused a disappearance of sensitivity to a test depolarization, addition of 1 mM caffeine or replacement of Cl- with NO3- promptly evoked a contracture. These results imply a reversible step in the recovery process that is both potential and time dependent. Since application of 5 mM caffeine to either normally polarized or depolarized muscles always immediately causes contracture, more than one site of action for caffeine is indicated. After disruption of the transverse tubules, partially depolarized muscles showed no response to NO3- or 1 mM caffeine but contracted vigorously when exposed to 5 mM caffeine.

Action Potentials↗
PubMed1998

Effect of reactive oxygen species on K+ contractures in the rat diaphragm.

Reactive oxygen species (ROS) are postulated to alter low-frequency contractility of the unfatigued and fatigued diaphragm. It has been proposed that ROS affect contractility through changes in membrane excitability and excitation-contraction coupling. If this hypothesis is true, then ROS should alter depolarization-dependent K+ contractures. Xanthine oxidase (0.01 U/ml) + hypoxanthine (1 mM) were used as a source of superoxide anion eliciting oxidative stress on diaphragm fiber bundles in vitro. Diaphragm fiber bundles from 4-mo-old Fischer 344 rats were extracted and immediately placed in Krebs solution bubbled with 95% O2-5% CO2. After 10 min of equilibration, a K+ contracture (Pre; 135 mM KCl) was induced. Fiber bundles were assigned to the following treatment groups: normal Krebs-Ringer (KR; Con) and the xanthine oxidase system (XO) in KR solution. After 15 min of treatment exposure, a second (Post) K+ contracture was elicited. Mean time-to-peak tension for contractures was significantly decreased in Post vs. Pre (16.0 +/- 0.7 vs. 19.8 +/- 1.0 s) with XO; no change was noted with Con. Furthermore, peak contracture tension was significantly higher (31.5%) in the XO group Post compared with Pre; again, no significant change was found with KR. The relaxation phase was also altered with XO but not with KR. Additional experiments were conducted with application of 1 mM hypoxanthine, with results similar to the Con group. We conclude that the application of ROS altered the dynamics of K+ contractures in the rat diaphragm, indicating changes in voltage-dependent excitation-contraction coupling.

Animals↗
PubMed2004

Alteration of cyclopiazonic acid-mediated contracture of mouse diaphragm after denervation.

As a major Ca(2+) source for muscle contraction, the sarcoplasmic reticulum (SR) of skeletal muscle maintains its Ca(2+) content by uptake of myoplasmic Ca(2+) and by replenishment with extracellular Ca(2+). Since transection of motor nerve alters the functions of SR Ca(2+) pump and sarcolemma ion channels, this study explored the effect of denervation on the contracture evoked by cyclopiazonic acid (CPA), an inhibitor of SR Ca(2+) pump. In innervated hemidiaphragm, CPA elicited a bimodal elevation of muscle tone, which was dependent on extracellular Ca(2+) and differentially inhibited by pretreatment with 2-aminoethoxydiphenylborane (APB) and U73122. Activation of muscle Na(+) channels to simulate denervation-induced membrane depolarization did not change the contracture profile. After denervation for 5-14 days when the contracture induced by caffeine was not yet depressed, CPA elicited only APB-sensitive monophasic contracture. Stimulation of ATP-regulated K(+) channels with lemakalim hyperpolarized muscle membrane and attenuated CPA contracture in denervated, but not innervated, hemidiaphragm. The effects of lemakalim were antagonized by glybenclamide. It is inferred that the bimodal CPA contracture is resulted from distinct recruitments of Ca(2+) entry and that denervation alters the voltage dependence and down-regulates CPA-mediated Ca(2+) influx.

Action Potentials↗
PubMed1976

High-potassium induced contracture in guinea pig ureter.

Some characteristic properties of guinea pig ureter in high-K induced contracture were studied. The contracture was composed of three contraction components, quick-phasic, slow transient, and substained states. The height of the second component decreased with time when the preparation was immersed in high-K solution. This was observed during a brief washing treatment with normal Tyrode solution applied at varius times after immersion in high-K solution. When the brief washing treatment was applied after 30 min, a contracture composed of the first and the third components was observed. Similar results were obtained in Ca-induced contracture of K-depolarized preparations. Fluctuations of tension were observed in the course of the contracture. The fluctuations could be evoked by various types treatments and were observed to have some relationship to extracellular Ca. It was indicated that extracellular Ca has an important role in the initiation of each component of the contracture and that the role of Ca is controlled by the cell membrane.

Animals↗
PubMed1978

The role of membrane electrical activities and extracellular calcium in high-K-induced contracture of guinea pig ureter.

Electrical and mechanical activities in high-K-induced contracture of guinea pig ureter and taenia coli were studied using the sucrose-gap method. Ureter immersed in high-K solution showed a contracture consisting of three components as well as twitch contractions evoked by a few spikes which were observed during the depolarizing phase. Reapplication of high-K solution after a short washing procedure with normal solution induced a contracture composed of only the first and the third components. No action potential was observed during the course of membrane depolarization by this procedure. High-K-induced contracture was highly sensitive to extracellular Ca: no tension development of the ureter despite the membrane depolarization was observed in Ca-free high-K solution. The addition of Ca to Ca-free high-K solution caused a contracture similar to that by high-K solution in the presence of Ca. Verapamil (10(-5) M) blocked all three components, leaving only slightly depressed twitch contractions initiated by action potentials. The possibility that all of these components of high-K-induced contracture were initiated by influxed Ca from extracellular space was also strengthened.

Animals↗
PubMed1987

Contracture caused by sodium removal in the pregnant rat myometrium.

The contracture produced by removal of the external Na was studied in the pregnant rat myometrium and this was compared with that of the non-pregnant myometrium. The Na-free contracture was small compared with spontaneous phasic contractions in the circular muscle of non-pregnant rat, but the contracture increased during pregnancy. On the other hand, in the longitudinal muscle, the contracture was large in both non-pregnant and pregnant myometria. The change in circular muscle did not seem to result from an increased sensitivity to the external Ca. Since the contracture induced by 40 mM K had properties similar to those of the Na-free contracture, it is likely that weak tension development in non-pregnant circular muscle is either due to a limited Ca influx or due to a low efficiency of the excitation-contraction coupling for the sustained contraction compared with the phasic contraction. A small contraction which was independent of the external Ca was observed in Na-free solution in the both layers of non-pregnant myometrium, but this was not observed in the longitudinal muscle of pregnant myometrium.

Animals↗
PubMed1990

Dihydropyridine calcium channel antagonists block and agonists potentiate high potassium contractures but not twitches in frog skeletal muscle.

The effects of two dihydropyridine calcium channel antagonists (nitrendipine and nifedipine) and two agonists (Bay K8644 and CGP-28392) were tested on high K(+)-induced contractures of frog's toe muscles. All four drugs depressed or blocked maximum contractures induced by 123 mM K+. Agonist effects, i.e., an increase in contracture amplitude, were found with smaller contractures produced by lower high K+ concentrations (i.e., 10, 20, and 25 mM). Bay K8644 produced its maximum agonist effect at 10(-7) M and only depressed contractures with 10(-6) M. CGP-28392 had its greatest agonist effect with 10(-9) M and had only antagonist effects with 10(-7) M or more. Nitrendipine had no agonist effects but nifedipine produced agonist effects with all concentrations tested (10(-9) to 10(-4) M). These results support previous results indicating that these contractures are initiated by extracellular Ca2+ ions entering via the voltage-sensitive, slow calcium channels in the t-tubules. The results obtained in the present study also are consistent with the known pharmacological effects of these drugs on calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2000

[Volkmann's contracture and suprcondylar fractures of the humerus in children].

The most frequent cause of the compartment syndrome with subsequent Volkmann's contracture of the upper extremity in children is a supracondylar fracture of the humerus. Often it is being associated by some with the concurrent injury and obliteration of the brachial artery. In the majority of cases of Volkmann's contracture in children with dislocated supracondylar fractures of the humerus, described in the available literature, the development of Volkmann's contracture was preceded by reduction of the fracture and fixation with bandage or in cast with the elbow in flexion. The aim of this study work was to evaluate the impact of specific methods of treatment on the development of Volkmann's contracture. No Volkmann's contracture was observed in a group of 257 patients with displaced supracondylar fracture of the humerus at the authors department from 1984 till 1999 while 7 children with obliteration of the brachial artery were successfully treated without an operation. The development of Volkmann's contracture can be successfully prevented for patients with the displaced supracondylar fracture of the humerus. Minimal elbow flexion, careful manipulation during closed reduction, stabilisation of fragments by percutaneous pinning and careful clinical follow-up are the crucial factors in the prevention of compartment syndrome in this context.

Child↗
PubMed1975

Porcine malignant hyperthermia: effects of temperature and extracellular calcium concentration on halothane-induced contracture of susceptible skeletal muscle.

Skeletal muscle from malignant hyperthermic (MH) pigs incubated at 37 C in 2.3 mM calcium-Krebs-Ringer solution contracts spontaneously when exposed to halothane. In contrast, halothane did not induce contracture in MH muscle incubated in 2.3 mM calcium-Krebs-Ringer solution at 25 C or in calcium-free Krebs-Ringer's solution at 37 C. Halothane did not induce contracture in normal control muscle in 2.3 mM Krebs-Ringer solution at 25 or 37 C. In the presence of halothane, addition of caffeine produced greater contracture in MH muscle than in normal controls. Halothane-caffeine-induced contractures of MH and control muscles at 25 and 37 C were similar. Elucidation that under certain experimental conditions halothane induces contracture in MH muscle, but not in normal muscle 1) may aid in development of a diagnostic test; 2) establishes further evidence for skeletal muscle as the target tissue for anesthetic-induced MH; 3) suggests that halothane may affect systems that regulate sarcoplasmic calcium concentration below contracture threshold in MH muscle. (Key words: Hyperthermia, malignant; Anesthetics, volatile, halothane; Ions, calcium; Muscle, skeletal, malignant hyperthermia.).

Animals↗
PubMed2000

Operative treatment of medial rotation contracture of the shoulder caused by obstetric brachial plexus palsy.

OBJECTIVE: To introduce an operation of subscapularis slide from its origin and anterior release from its insertion for treatment of medial rotation contracture, subluxation and dislocation of the shoulder caused by obstetric brachial plexus palsy (OBPP). METHODS: Thirty-six cases with medial rotation contracture of the shoulder were diagnosed by measurement of the inferior glenohumeral angle, passive lateral rotation of the shoulder and plain radiographs. Subscapularis slide was performed in 24 cases with simple medial rotation contracture, and anterior release in 12 cases with complex contracture-medial rotation contracture combined with subluxation, dislocation, or other deformities of the shoulder joint. Systems of Mallet scoring and Gilbert grading for the shoulder were used to evaluate the postoperative shoulder function. RESULTS: With follow up for a minimum of six months, 32 cases got apparent gains from operations, accounting for 88.8% of the total operated on. The younger the child was, the better the result. Of 4 cases with no operative effects, 3 had no flexion of the elbow preoperatively, suggesting a poor recovery of the upper trunk of the brachial plexus; the rest one had no repair of the severed subscapularis tendon. CONCLUSIONS: Subscapularis slide and anterior release of the shoulder are effective for treatment of medial rotation contracture as well as its consequence of subluxation and dislocation of the shoulder in OBPP. The operative effect is related to children's age and the recovery extent of the upper trunk of the brachial plexus.

Journal Article↗