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At least 19 recordsLinked to original sources

PubMed1977

The inhibitory effect of papaverine on respiration-dependent contracture of guinea pig taenia coli in high-K medium. I. The relationship between contracture and respiration.

Papaverine (Pap) inhibited a tonic tension development in guinea pig taenia coli induced by an elevation of the potassium concentration of the medium to 40 mM (40-K). The ID50 of Pap was 4.5 x 10(-6) M. Inhibition of the 40-K induced tonic tension by Pap was dependent on the calculated concentration of non-ionized form, but not the ionized form. Inhibition of the tonic tension by Pap and various metabolic inhibitors was not antagonized by raising the Ca++ concentration in the medium. Results obtained from simultaneous measurement of the 40-K induced O2 consumption and tension illustrated that the inhibition of O2 consumption rapidly induced the inhibition of the tension. Furthermore, glucose removal, amytal or Pap resulted in a progressive relationship between the inhibition of O2 consumption and the inhibition of tension. The inhibition of Pap as determined by O2 consumption was not reversed by application of 10(-4) M 2,4-dinitrophenol (DNP). These results plus graphical analysis of the mechanical response suggest that Pap may penetrate the cell membrane and inhibit mitochondrial respiration, thereby inhibiting this very respiration-dependent contracture.

Animals↗

PubMed1977

[Influence of homologous n-alcanoic acids on the function properties of isolated skeletal muscles. III. Contractures by fatty acids and relations to the effects of caffeine].

The influences of octanoic, decanoic, and hexadencanoic acid were tested on the contracture capability of isolated skeletal muscle of frogs and rats. 1. 100 mM octanoic or 10mM decanoic acid induce contractures in skeletal mucles after 20-30 min of exposure. 2. The time of exposure necessary for induction of contractures is shortened by an increase of bath temperature, electrical stimulation or KCl-depolarization of muscles. 3. Simultaneous addition of fatty acid and caffeine (10 mM) effects a depression and a delay of the caffeine contracture. The contractures evoked by 5 mM caffeine are inhibited by lower concentrations of fatty acids (1 mM octaonoic acid, 0,1 mM hexadecanoic acid). 4. After the complete development of a caffeine (or fatty acid) contracture the muscle is not able to develop an identical contracture by a second application of the same drug, even after intermediate treatment during one or two hours in Ringer solution. If the contracture is interrupted one minute after the caffeine application by changing the solution, the tension returns quickly to the resting level. A subsequent addition of caffeine (10 mM) after about 10 minutes effects an identical contracture. Thus the effect of fatty acids on caffeine contracture may be studied on the same muscle which served as its own control. 5. As mechanisms involved in the development of fatty acid contractures and in the inhibition of caffeine contractures, interactions of free fatty acids and lipids of biological membranes are disucssed. Especially, there may be changes of the calcium affinity of cellular membranes.

Animals↗

PubMed1979

Effect of SCN on potassium contracture in twitch muscle fibers of the frog.

The effect of SCN on potassium contracture, especially the time course and the mechanical inactivation of the contracture, was investigated using frog twitch muscle fibers. SCN increased the magnitude and the rate of rise of the potassium contracture tension and prolonged its time course. These effects of SCN depended on the concentration of K+ in the external medium and on the duration of pretreatment of the fibers with SCN-Ringer solution. The potentiating effect of SCN on the potassium contracture tension was pronounced at lower and moderate concentrations of K+ and this effect attained a maximum within 1 min after the pretreatment. In the contracture induced by exposure of the fibers to K-SCN-solution without the pretreatment, the time course of the contracture, especially the retardation of the spontaneous relaxation, was marked at higher concentrations of K+. This retarding effect of SCN attained a maximum at more than 10 min after the pretreatment with SCN-Ringer solution. SCN shifted the mechanical inactivation curve of potassium contracture toward lower concentrations of K+, as in the case of the activation curve, and markedly increased the rate of the inactivation induced by conditioning with 15 mM K+. In addition, SCN delayed the recovery of potassium contracture from the mechanical inactivation induced by preceding K-SCN-contracture. On the basis of these results, the sites and the mechanism of action of SCN on potassium contracture are discussed.

Animals↗

PubMed1979

Contractures elicited by tetraethylammonium in avian muscle treated with methohexitone.

1 The chick biventer cervicis muscle immersed in methohexitone (8.8 x 10(-5) M) responded to tetraethylammonium with contractures which were dose-related. The ED50 for tetraethylammonium was 2.1 x 10(-3) M. 2 In the absence of methohexitone, tetraethylammonium produced contractures only at much higher concentrations: these contractures were accompanied by fasciculations and neuromuscular block of the twitch fibres. 3 The contractures produced by tetraethylammonium in the presence of methohexitone were not reduced by exposure to botulinum toxin which eliminated all response of the muscle to indirect stimulation. 4 Tubocurarine (1.2 x 10(-6) M) displaced the dose-response curve for tetraethylammonium-methohexitone-induced contractures to the right. The dose-ratio was 15.63 +/- 1.98. 5 Physostigmine (1.8 x 10(-6) M) potentiated the activity of tetraethylammonium-methohexitone 3.26 or 3.84 fold, depending on the method of calculation used. 6 Physostigmine potentiated contractures elicited by indirect repetitive stimulation 4.8 to 6.0 fold more than it potentiated contractures due to tetraethylammonium-methohexitone. 7 It is concluded that in the presence of methohexitone, tetraethylammonium produces contractures of the chick muscle by releasing acetylcholine but also by a direct agonist action on the cholinoceptor.

Animals↗

PubMed1979

Protection of mitochondrial function during ischemia by potassium cardioplegia: correlation with ischemic contracture.

The effect of potassium cardioplegia on mitochondrial function was evaluated in the ischemic isolated rat heart. Mitochondrial function as well as adenosine triphosphate (ATP) levels were determined at the initiation of ischemic contracture, at the completion of ischemic contracture, and 20 minutes following contracture completion. Group I received no cardioplegia prior to ischemia, while Group II received potassium cardioplegia prior to the onset of ischemia. The respiratory control index (RCI), which is the primary measure of the intactness of mitochondrial function, was calculated with both a NAD (nicotinamide adenine dinucleotide)-linked substrate and a FAD (flavin adenine dinucleotide)-linked substrate. Potassium cardioplegia significantly delayed ischemic contracture initiation and completion. Although the RCI and ATP levels decreased significantly at successive levels of contracture, there was no difference in the RCI or ATP content between Group I and Group II at contracture initiation or completion. Unlike previous investigations that have used a time-base to examine mitochondrial function and acute cardiac ischemic injury, we correlated mitochondrial function with the measurable physiologic event ischemic contracture. The data indicated that potassium cardioplegia preserved ATP content and mitochondrial function, and that contracture initiation and completion correlate well with specific ATP levels and mitochondrial respiratory control. The relationship between mitochondrial function and ATP content indicates that the beneficial effect of potassium cardioplegia on mitochondrial function may be secondary to the preservation of high-energy phosphate levels which provide energy for mitochondrial maintenance.

Adenosine Triphosphate↗

PubMed1976

Physostigmine-induced contractures in frog skeletal muscle.

Physostigmine in 15 mM concentration at pH 8.4 produces reversible contractures of up to 0.3 Po tension output in frog's whole toe muscle or in 7-10 fiber bundles of these muscles, At pH 7.2, the 15 mM physostigmine contracture output is only about 0.10 Po. The 15 mM, pH 8.4 contractures are essentially unaffected by lack of external Ca2+, complete depolarization of the fibers, detubulation by glycerol treatment, and 0 degrees C ambient temperature. These results and other evidence indicate that physostigmine produces contracture by directly releasing activator Ca2+ from the sarcoplasmic reticulum (SR). Pretreatment of muscles with 4 mM procaine reduces physostigmine's capacity to produce contracture, evidently by means of a competitive inhibition at SR sites. The above results indicate similarities between physostagmine and caffeine contractures. But the physostigmine action differs in that it is reversible, and, especially, it lacks the ability, strongly characteristic of caffeine, to sensitize a muscle to produce a rapid cooling contracture. The internal action of physostigmine requires that it be permeant, and, since it is a weak base (pKa = 8.2), this property is provided by its uncharged base. But, once internal, where the pH = 6.8, most of the drug will be protonated and it may act on the SR in this form, in contrast with caffeine which, since its pKa is about 1.0, acts on the SR as uncharged base.

Animals↗

PubMed1977

Prenylamine-induced contracture of frog skeletal muscle.

1. Experiments were performed to determine the influence of prenylamine on excitation-contraction coupling in frog sartorius muscle. 2. Prenylamine (0.2-1.0 mM) produced a biphasic contracture in skeletal muscle characterized by an initial phasic and subsequent tonic contracture. 3. Neither dantrolene nor procaine blocked the prenylamine-induced contracture. Pretreatment with 100 mM K+ blocked the phasic but not the tonic component of the prenylamine contracture. 4. Prenylamine produced a sustained increase in 45Ca efflux at all concentrations that produce contracture. These concentrations of prenylamine also depressed the action potential, muscle twitch and resting potential. 5. Low concentrations of prenylamine (0.05 mM) which produced neither contracture, 45Ca efflux nor 45Ca influx, depressed the action potential, muscle twitch and K+ contracture. 6. The results suggest that prenylamine not only alters calcium mobility but also membrane permeability to other ions.

Action Potentials↗

PubMed1977

Time- and Na-dependent effects of Ca depletion on potassium contracture in frog twitch muscle fiber.

The effect of the extracellular Ca depletion on potassium contracture was investigated in single fibers isolated from frog semitendinosus muscle mainly in relation to its time and Na dependency. The shortening of plateau duration and the increase in the rate of relaxation of the potassium contracture appeared within 3--5 sec and 15 sec, respectively, after the fiber was immersed in Ca-free Na Ringer solution containing 1 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) (EGTA-Na Ringer solution) or Ca-free choline Ringer solution containing 1 mM (EGTA (EGTA-choline Ringer solution). These effects were independent of the presence or absence of extracellular Na. In EGTA-Na Ringer solution, the potassium contracture tension was inhibited only by about 20% after 20--90 min and was abolished after 120 min. The inhibition of the peak tension was accelerated by the depletion of extracellular Na; in EGTA-choline Ringer solution, the tension was gradually inhibited by about 20% during the first 7 min and abolished after 10--12 min. When the peak tension of potassium contracture was abolished in EGTA-choline Ringer solution, the depolarization by Ca depletion was about 10 mV and the caffeine contracture was sufficiently produced. The results suggest that the inhibition of the potassium contracture tension in EGTA-choline Ringer solution is due to the dissociation of excitation-contraction coupling. On the basis of these results, an aspect of the inactivation of the potassium contracture was proposed.

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↗

PubMed1976

Possible role of cyclic AMP in the relaxation process of mammalian heart: effects of dibutyryl cyclic AMP and theophylline on potassium contractures in cat papillary muscles.

The effect of dibutyryl cyclic AMP (DB-c-AMP; 3 X 10(-4)-3 X 10(-3) M) on electrically induced twitch and high potassium (142.4 mM KCl)-induced contracture tension was studied in papillary muscles from normal and reserpinized cats ([Ca]0 1.8 mM; 25 degrees C; pH 7.4). In both groups of preparations, the increase in twitch tension evoked by DB-c-AMP was accompanied by an abbreviation of the time to peak force and of relaxation time. In the same preparations, the high potassium contracture was markedly depressed by DB-c-AMP in a concentration-dependent manner. Similar results were obtained with the N6-monobutyryl derivative of cyclic AMP. The relaxing effects of the cyclic nucleotides on KCl contractures did not appear to be due to possible non-cyclic breakdown products: adenosine, 5'-AMP and sodium butyrate did not attenuate contracture tension at concentrations up to 3 X 10(-3) M. The same applies to ATP and non-cyclic N6-2'-0-3'-0-tributyryl-adenosine-monophosphate. Theophylline (10(-2) M) was found to prolong the relaxation time of the twitch and to enhance the high KCl contracture. It is concluded that cyclic AMP may be capable of modulating the relaxation process of mammalian heart and that not only the positive inotropic but also the relaxant effects of catecholamines on myocardium described before may be mediated by the cyclic AMP system. The relaxant effects of cyclic AMP derivatives on intact myocardial preparations are attributed to a stimulation by cyclic AMP of the calcium transport of the sarcoplasmic reticulum (SR) and are interpreted to be a corollary to the effects of cyclic AMP previously obtained on isolated SR preparations.

Animals↗

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↗

PubMed1978

Coenzyme dependent suppression of 2,2-PDS induced contractures in Spirostomum.

Spirostomum ambiguum was stimulated to contract by addition of the thiol inhibitor, 2,2-dithiobispyridine (PDS), which depletes intracellular reducing equivalents which are generated by coenzyme dependents reactions. PDS induced contractures were not suppressed after 2--4 h of pre-incubation in a medium enriched with ascorbic acid, thiamine, or riboflavin, singly. Two h of incubation with nicotinamide did not suppress contractures; however, 50% suppression occurred after 3 h incubation. Incubation of the cells in a medium enriched with all four coenzymes for up to 4 h, resulted in the suppression of PDS induced contractures to a level as low as 30% of control values. Suppression of contractures by the mixed coenzymes was concentration dependent. Cells that were stimulated with PDS and contracting, exhibited a 50% suppression of contractures within 3 min after transfer to a complementary medium enriched with mixed coenzymes. These results suggest that coenzymes interact synergistically with cellular metabolic processes to inhibit pharmacodynamic responses to PDS.

2,2'-Dipyridyl↗

PubMed1978

[Contracture of the myocardial fibers of the frog ventricle after high frequency stimulation while the calcium channels were blocked by manganese ions].

The contractile force of the myocardial strip of the frog ventricle stimulated by impulses of 0.5 Hz was diminished to 3--5% of the initial value when perfused with Ringer's solution containing 2.5 mM manganese. Under this condition the action potential duration was significantly decreased. An increase in frequency of stimulation up to 5 Hz leads to the development of contracture. The amplitude of contracture was about 30% of the initial contractile force in normal perfusion solution. The amplitude of contracture was more than doubled under the effect of ouabain (2 X X 10(-6) g/ml). Similar experiments with lanthanum failed to discover contracture produced by the increase of the stimulation frequency. In these experiments ouabain was also ineffective. It is supposed that contracture observed in the presence of manganese was caused by nonelectrogenic calcium transport into the muscle fibers.

Animals↗

PubMed1979

Mechanical and structural correlates of contracture induced by metabolic blockade in cardiac muscle from the rat.

We performed morphological studies of myocardial contracture to define its nature and relationship to mechanical changes occurring during metabolic blockade. Isolated rat papillary and trabecular muscles were stretched to the apices of their length-tension curves and stimulated to contract isometrically 12 times a minute at a temperature of 28 degrees C. Incomplete and total metabolic blockade were induced by 1 hour of hypoxia (95% N2, 5% CO2) or by hypoxia plus glycolytic blockade with iodoacetic acid, 10-4M, respectively. In oxygenated control preparations, mechanical performance was stable for the 60-minute experimental period. In preparations exposed to hypoxia, developed tension fell to 7 +/- 2% of prehypoxia values at 60 minutes. Contracture tension increased progressively to 2.5 +/- 0.4 g/mm2. With total metabolic blockade, developed tension declined to zero by 10 minutes, contracture tension rose to an average peak value of 5.3 +/- 0.4 g/mm2 by 15 minutes, and subsequently slowly declined. All preparations were fixed at Lmax in the muscle bath. Light and electron microscopic studies revealed focal irregularities of A, I, and Z bands with sarcomere malalignment, hypercontraction, and fiber disruption, which increased in severity with increasing metabolic blockade. Linear densities appeared in mitochondria following total metabolic blockade, but mitochondria appeared normal otherwise. Thus, myocardial contracture after metabolic blockade is a focal process beginning within the sarcomere; morphological alterations in the contractile apparatus correlate with mechanical changes and are more severe than those in the mitochondria.

Animals↗

PubMed1976

[Angiopasm and lesion of the ulnar nerve in Dupuytren's contracture (author's transl)].

30 patients with Dupuytren's contracture were investigated by venous occlusion plethysmography of the index and ring fingers of both hands. The results are evaluated in respect to the clinical and electroneurophysiological findings. Special attention was given to the blood flow disturbances which have plethysmographically appeared to be a significant feature of Dupuytren's contracture and also to ulnar nerve lesions in individual cases. The finger venous occlusion plethysmography technique of Goetz (1934) has been further developed and a suitable apparatus constructed for the purpose of these investigations. Temporary vasopasm occurs in 77% of the patients suffering from Dupuytren's contracture when the fingers are cooled to 15 degrees C and a significant diminution of blood flow, as in the Raynaud syndrome, is evident. These neurovascular changes always appeared on the fingers of both hands and were similarly found in the region of the median nerve and of the ulnar nerve. They did not depend on the localization or the stage of the disease. 68% of the patients had symptoms suggestive of an ulnar nerve lesion, which corresponds with the findings of Mumenthaler (1961). In a comparison of the patients with normal plethysmographical findings and the patients with vasospasm, there is no correlation with the accompanying ulnar lesion. It is, thus, suggested that temporary vasopasm is not a consequence of the ulnar nerve lesion, but is related to an independent constitutional factor. In view of the high incidence of the ulnar lesion in patients with Dupuytren's contracture, a special neurological investigation is recommended and appropriate therapy, in addition to the fasiectomy, must be undertaken.

Adult↗

PubMed1979

Determinants of hypoxic contracture in isolated heart muscle preparations.

Further studies on hypoxic contracture are described, using resting and contracting isolated muscle preparations from several species. The effect of temperature, pH, substrate, calcium concentration, osmolality and inotropic interventions was explored. The 'protective' effect of acidosis was not contingent on its negative inotropic influence. No evidence was adduced that hypoxic contracture can be modulated other than by altering energy supply or demand. The study does not discriminate between rigor and rised cytosolic calcium as mechanisms causing hypoxic contracture, but demonstrates that hypoxic contracture is not directly dependent on the availability of intracellular calcium.

Animals↗

PubMed1978

An in-vitro model of malignant hyperthermia: differential effects of inhalation anesthetics on caffeine-induced muscle contractures.

Clinical concentrations of anesthetics augment caffeine-induced contracture of frog sartorius muscle; however, anesthetics differ in this characteristic. The potentiation was quantitated using six paired sartorius muscles for each specified concentration of anesthetic and controls. At a concentration of 1 MAC, the greatest potentiation occurred with 2 mM caffeine for all anesthetics studied. Under these conditions the order of magnitude of augmentations was: chloroform (15 times); halothane (11 times); methoxyflurane (10 times); cyclopropane (5 times); enflurane (4 times); isoflurane (3 times); diethyl ether (2 times); Baxter 3224 (2 times); fluroxene (1.4 times); nitrous oxide (1.3 times). Halothane at .5 MAC augments the 2 mM caffeine-induced contracture almost seven times, and at 2 MAC almost 13 times, whereas 2 MAC isoflurane potentiates the caffeine-induced contracture only four times and 4 MAC diethyl ether only two and a half times. It is postulated that those anesthetics that most potentiate caffeine-induced contracture may be the most potent triggering agents of malignant hyperthermia.

Anesthetics↗

PubMed1979

[Simulation of K-contracture curve in smooth muscle (author's transl)].

40 mM K-induced isometric contracture of guinea pig taenia coli in the presence of 30 microM dantrolene showed a rapidly rising peak followed by a plateau and then a low sustained tonic contraction. The plateau was delayed by low Ca so that two phasic contractions, fast and slow, were separated from each other. In K-contracture after 15 sec contact with normal Ca following low Ca condition, the fast phasic contraction but not the slow one regained its tension depressed by preceding low Ca, while the slow phasic contraction recovered from its delay. In the presence of 0.2 microM verapamil, K-contracture consisted of the fast phasic contraction without plateau and of the low tonic contraction. The results suggest that K-contracture in the normal state consists of three components, the fast and slow phasic contractions and the tonic contraction, and that dantrolene inhibits a tonic contraction, whereas verapamil inhibits the slow phasic and the tonic contraction. Thus, the contraction curve of each component was tentatively expressed by exponential function, and for simulation of the observed curves a computer was utilized to synthesize the curves using the components of varying parameters. The simulation was successful when based on the above suggestion.

Animals↗