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PubMed1994

Positive inotropic effect of adrenaline on potassium contractures in tonic skeletal muscle fibres of the frog.

K+ contractures were elicited in small bundles of tonic skeletal muscle fibres of the frog. Adrenaline (1 microM) increased the amplitude of K+ contractures in a [K+]o-dependent manner: maximal effects were produced between 20 and 60 mM [K+]o. In contrast, we found no effect of adrenaline on K+ contractures of twitch fibres. The potentiating effect of adrenaline depended on [Ca2+]o. Increasing [Ca2+]o from 1.8 to 10 mM doubled the positive inotropic effect of adrenaline. In a nominally Ca2+ free saline, adrenaline had no potentiating effect. The Ca2+ channel blockers nifedipine (20 microM) and Ni2+ (1.8 mM) reversibly reduced the amplitude of the tonic phase of K+ contractures and blocked the potentiation by adrenaline. The mechanical effects of adrenaline cannot be explained by changes in the membrane potential, as revealed by intracellular recordings at several [K+]o. It was concluded that the potentiating effect of adrenaline in tonic muscle fibres of the frog may be mediated through Ca2+ channels.

Animals↗
PubMed1978

Magnesium net fluxes and distribution in rabbit myocardium in irreversible contracture.

Distribution of magnesium (Mg) in heart muscle was studied by measuring fluxes of Mg and transmembrane potentials as a function of perfusate [Mg2+] after a massive increase in permeability of the sarcolemma was induced in the Langendorff prepared heart from the Nembutal-anesthetized rabbit. After onset of 0 mM [Ca2+] perfusion which produced excitation-contraction (E-C) uncoupling and mechanical arrest, action potentials recorded from subepicardial cells showed an increase in duration and decrease in amplitude, which progressed until no transmembrane potentials could be observed. Restoration of physiological salt solution perfusion after 15 min of [Ca2+]-free perfusion caused an irreversible contracture that was associated with 1) efflux of potassium (K) and myoglobin, 2) perfusate [Mg2+]-dependent flux of Mg, and 3) transmembrane potentials of 0 mV. The magnitude of net efflux of K and myoglobin during contracture was unaffected by perfusate [Mg2+]. During the first 2 min of contracture, net efflux of Mg (mumoles per gram wet muscle +/- SE) was 1.37 +/- 0.09 and 0.48 +/- 0.19 during 0 mM and 2.5 mM [Mg2+] perfusion, respectively; but a net influx of 0.56 +/- 0.23 occurred during 5 mM [Mg2+] perfusion. Total sarcoplasmic [Mg] may correspond to perfusate [Mg2+] of 3.6 mM, which was found by interpolation to prevent any net flux of Mg during contracture. 3.6 mM may, therefore, represent the upper limit of the intracellular free-ionized Mg concentration in rabbit heart.

Animals↗
PubMed1977

Myocardial contracture and accumulation of mitochondrial calcium in ischemic rabbit heart.

The relationship between myocardial contracture and cell calcium was studied in electrically paced, isolated perfused rabbit hearts. Isovolumic left ventricular dP/dt and end-diastolic pressure were utilized as indexes of contractility and ventricular stiffness. After 60 min of low flow (ischemia) without or with reperfusion at high flow for 10 min, calcium was measured in the mitochondrial fraction and used as an indicator of intracellular calcium. Low flow led to ventricular standstill and contracture, and reperfusion produced partial mechanical recovery with end-diastolic pressure remaining markedly elevated. Nifedipine (10(-7) M), an antagonist of myocardial calcium uptake, prevented contracture and permitted nearly complete mechanical recovery without elevation in diastolic pressure. Increases in mitochondrial calcium paralleled the severity of contracture and the lack of diastolic relaxation after reperfusion. Mitochondrial calcium did not increase in hearts protected by nifedipine. Results demonstrate a close relationship between mechanical changes induced by ischemia and accumulation of intracellular calcium.

Animals↗
PubMed1980

Barium contracture: a model for systole.

Studies of cardiac mechanics, metabolism, and coronary hemodynamics have traditionally been carried out in rhythmically beating hearts. We have developed an isolated rabbit heart preparation that is free from contractions and allows a stable graded ventricular pressure to be established. Rabbit hearts were rapidly excised and perfused at constant pressure with heated (39 degrees C) Tyrode solution bubbled with 98% O2-2% CO2. A latex balloon was inserted into the left ventricle (lv) to adjust lv volume and measure pressure. Nine hearts were depleted of calcium by reducig the calcium concentration in the Tyrode's from 5 to 0.078 mM. When barium (Ba2+) was added to the perfusate, the hearts spontaneously developed pressure that was free of an overriding beat (contracture). The intensity of the contracture increased in a sigmoid fashion as the barium concentration was increased. During contracture balloon pressure ranged between 33.8 +/- 5.0% (SE) (Ba2+ 0.5 mM) and 79.0 +/- 4.5% (Ba2+ 1.5 mM) of control systolic developed pressure Ventricular pressure-volume curves were linear (r > 0.98) and indicated increased ventricular stiffness as barium concentration increased. We believe that barium-induced contracture is a good model of systolic cardiac muscle interactions.

Animals↗
PubMed1994

Mechanism of action of 2,3-butanedione monoxime on contracture during metabolic inhibition.

The effect of 2,3-butanedione monoxime (BDM) was investigated during metabolic inhibition (MI) in papillary muscles. MI caused a rapid decrease in developed force and an increase in resting force, along with a decrease in ATP and creatine phosphate (CrP). Addition of BDM before MI decreased maximal contracture force, increased the time, and slowed the rates of ATP and CrP depletion. BDM addition at the peak of contracture did not alter the level of developed contracture. To simulate MI in skinned fiber preparations, we decreased the [MgATP] at pCa 8. [MgATP] of 3.2 microM resulted in a large increase in resting force. The force developed was less in BDM-pretreated muscles. Addition of 10 mM BDM at steady state did not affect force development ([MgATP] 3.2 microM, pCa 8.0). Cross-bridge kinetics in intact and skinned muscle fibers with and without BDM in the presence and absence of MI were studied. Intact muscles with MI revealed no frequency dependence at peak contracture and had elevated stiffness values. In skinned fibers, at [MgATP] of 3.2 microM and pCa of 8, no frequency dependence was observed, and the muscles had similarly high stiffness values. BDM pretreatment in both intact and skinned fibers inhibited rigor formation. These results suggest that BDM inhibits cross-bridge formation in the weak-binding state or actively cycling cross bridges.

Adenosine Triphosphate↗
PubMed1975

The reversible flexion contracture as a sign of peripheral nerve lesion.

Three cases were observed with the same substantial clinical features: flexion contracture of the third, fourth, and fifth finger and less extensive of the wrist. The contracture appeared after a mechanical injury not related to the involved muscles. In two cases the lesion was situated above or in the elbow region, in the third on the ulnar border of the forearm. In all cases there were some ulnar nerve signs and symptoms but the contracture involved flexor muscles which were co-innervated by the median nerve. The signs and symptoms improved or disappeared entirely after neurolysis. The question is raised, whether the contracture is due to peripheral nerves damage.

Adolescent↗
PubMed1998

Role of endothelin-A receptors in ischemic contracture and reperfusion injury.

BACKGROUND: Circulating endothelin (ET)-1 is elevated in ischemia/reperfusion and may exert proischemic effects. The aim of the present study was to characterize the effects of ET-1 in rat isolated hearts using subtype-selective ET receptor antagonists, agents modulating the cytosolic Ca2+ concentration, or the activity of cGMP-dependent protein kinase. METHODS AND RESULTS: Rat hearts perfused at constant pressure were made ischemic by reducing flow to 0.2 mL x min(-1) x g(-1), followed by reperfusion at normal pressure (each phase, 25 minutes). Drugs were infused during the ischemic phase only. Parameters monitored were extent and time-to-onset of contracture in ischemia, left ventricular developed pressure (LVDevP), coronary flow (CF), and diastolic relaxation during reperfusion. The ET(A) receptor-selective antagonist PD 155080 (50 nmol/L) reduced peak ischemic contracture (-49%) and delayed its time to onset (+56%) and improved recovery of reperfusion LVDevP (+12%), CF (+16%), and diastolic relaxation (+50%). Infusion of an ET(A)/ET(B)-nonselective antagonist, PD 142893 (200 nmol/L), had similar effects on all parameters, whereas infusion of BQ-788 (20 nmol/L), an ET(B) receptor-selective antagonist, was without effect. Exogenous ET-1 (100 pmol/L) hastened contracture and increased its extent (+23%) and reduced recovery of both LVDevP (-31%) and CF (-18%), effects that were counteracted by HOE 642 (10 micromol/L), a Na+/H+ exchange inhibitor, but not by nicardipine (30 micromol/L), a Ca2+ entry blocker; activation of cGMP-dependent protein kinase by the cell-permeable cGMP analog Sp-8-p-chlorophenylthioguanosine-3',5'-cyclic monophosphorothioate (10 micromol/L) improved function without preventing the effects of ET-1. CONCLUSIONS: The data indicate that ET-1 exacerbates ischemic contracture and worsens ventricular and coronary reperfusion dysfunction by activating ET(A) receptors via a mechanism likely involving activation of Na+/H- exchange in this model.

Animals↗
PubMed1987

Hypothyroidism delays ischemia-induced contracture and adenine nucleotide depletion in rat myocardium.

Isolated perfused paced hearts from rats rendered hypothyroid by chronic administration of propylthiouracil have a delayed onset of ischemia-induced myocardial contracture in contrast to hearts from control rats. In addition, the time to reach maximum contracture is delayed, and the magnitude of the contracture pressure is reduced. Preischemia myocardial adenosine triphosphate (ATP) values in the hypothyroid rat hearts are similar to those of control, but the rate of decrease in ATP is slower in the hearts of hypothyroid rats. Thus, it appears that in the hypothyroid state the development of ischemic contracture is associated with a slower fall of ATP.

Adenine Nucleotides↗
PubMed2001

Acromial hyperplasia, the sequel of deltoid contracture: A case report.

The major complications of deltoid contracture frequently encountered are abduction contracture, winging of the scapula, humeral head flattening and shoulder dislocation (Bhattacharyya 1966; Chatterjee and Gupta 1983). To our knowledge acromium hyperplasia has not been a reported complication of deltoid contracture in the English-language literature. We encountered a patient who had bilateral acromium hyperplasia that appeared to be secondary to deltoid muscle contracture due to large volumes of fluid injected intramuscularly as a child.

Journal Article↗
PubMed2005

Inhibition of sarcoplasmic Ca2+-ATPase increases caffeine- and halothane-induced contractures in muscle bundles of malignant hyperthermia susceptible and healthy individuals.

BACKGROUND: Malignant hyperthermia (MH) is triggered by halogenated anaesthetics and depolarising muscle relaxants, leading to an uncontrolled hypermetabolic state of skeletal muscle. An uncontrolled sarcoplasmic Ca2+ release is mediated via the ryanodine receptor. A compensatory mechanism of increased sarcoplasmic Ca2+-ATPase activity was described in pigs and in transfected cell lines. We hypothesized that inhibition of Ca2+ reuptake via the sarcoplasmic Ca2+-ATPase (SERCA) enhances halothane- and caffeine-induced muscle contractures in MH susceptible more than in non-susceptible skeletal muscle. METHODS: With informed consent, surplus muscle bundles of 7 MHS (susceptible), 7 MHE (equivocal) and 16 MHN (non-susceptible) classified patients were mounted to an isometric force transducer, electrically stimulated, preloaded and equilibrated. Following 15 min incubation with cyclopiazonic acid (CPA) 25 microM, the European MH standard in-vitro-contracture test protocol with caffeine (0.5; 1; 1.5; 2; 3; 4 mM) and halothane (0.11; 0.22; 0.44; 0.66 mM) was performed. Data as median and quartiles; Friedman- and Wilcoxon-test for differences with and without CPA; p < 0.05. RESULTS: Initial length, weight, maximum twitch height, predrug resting tension and predrug twitch height of muscle bundles did not differ between groups. CPA increased halothane- and caffeine-induced contractures significantly. This increase was more pronounced in MHS and MHE than in MHN muscle bundles. CONCLUSION: Inhibition of the SERCA activity by CPA enhances halothane- and caffeine-induced contractures especially in MHS and MHE skeletal muscle and may help for the diagnostic assignment of MH susceptibility. The status of SERCA activity may play a significant but so far unknown role in the genesis of malignant hyperthermia.

Journal Article↗
PubMed2005

The influence of contractures and variation in measurement stretching velocity on the reliability of the Modified Ashworth Scale in patients with severe brain injury.

OBJECTIVE: To determine the influence of contractures and different stretching velocities on the reliability of the Modified Ashworth Scale (MAS) in patients with severe brain injury and impaired consciousness. DESIGN: Cross-section observational study. SETTING: A rehabilitation centre for adult persons with neurological disorders. SUBJECTS: Fifty patients with impaired consciousness due to severe cerebral damage of various aetiologies. MEASUREMENT PROTOCOL: Three experienced and trained medical professionals rated each patient in a randomized order once daily for two consecutive days. Shoulder, elbow, wrist, knee and ankle spasticity were assessed by the use of the MAS with different stretching velocities. The presence of contractures was assessed by a goniometer. MAIN OUTCOME MEASURES: Retest and inter-rater reliability (k(w) = weighted kappa) of the MAS. RESULTS: The retest reliability of the MAS was good (shoulder joints (k(w) 0.74), elbow joints (k(w) 0.74), wrist joints (k(w) 0.72), knee joints (k(w) 0.72), ankle joints (k(w) 0.77)) and the inter-rater reliability was moderate (shoulder joints (k(w) 0.49), elbow joints (k(w) 0.52), wrist joints (k(w) 0.51), knee joints (k(w) 0.54) ankle joints (k(w) 0.49)). The presence of contractures significantly influenced the reliability of MAS in shoulder and wrist joints. No influence of stretching velocity on the reliability of the MAS was found. CONCLUSION: In patients with impaired consciousness due to severe brain injury the MAS has good retest, but only limited inter-rater, reliability. The presence of contractures may influence reliability of the MAS, but stretching velocity does not.

Brain Injuries↗
PubMed1991

A blinded comparison of noninvasive, in vivo phosphorus nuclear magnetic resonance spectroscopy and the in vitro halothane/caffeine contracture test in the evaluation of malignant hyperthermia susceptibility.

Malignant hyperthermia (MH) is a potentially fatal, anesthetic-induced syndrome. Currently, the only accurate means of diagnosing susceptibility to this syndrome is the testing of biopsied skeletal muscle for its contracture response to halothane and caffeine. A less invasive means of diagnosis is needed. The authors previously reported that MH-susceptible patients studied by in vivo phosphorus nuclear magnetic resonance (31P NMR) spectroscopy demonstrated a higher resting inorganic phosphate (Pi) to phosphocreatine (PCr) ratio in their skeletal muscle, as well as a slower postexercise recovery of PCr/Pi, when compared to normal controls. In the present blinded study, the authors compared in vivo 31P NMR determination of resting Pi/PCr and recovery rate of PCr/Pi in forearm muscles to in vitro halothane/caffeine contracture test results in 42 patients. Forty-three control subjects were studied to establish normal NMR values of resting Pi/PCr and recovery rate of PCr/Pi. Their findings were compared with those of 27 patients shown to be MH-susceptible and 15 patients MH-negative by contracture testing. The MH-susceptible group had a significantly (P less than 0.005) higher resting Pi/PCr value (0.202 +/- 0.044) than either the MH-negative (0.152 +/- 0.043) or the control (0.141 +/- 0.026) group. The MH-susceptible group also had a significantly (P less than 0.02) slower postexercise recovery rate of PCr/Pi (1.50 +/- 0.872 PCr.Pi-1.min-1) than either the MH-negative (2.11 +/- 1.07 PCr.Pi-1.min-1) or control (2.25 +/- 0.828 PCr.Pi-1.min-1) group. Twenty-six of the 27 MH-susceptible patients demonstrated abnormal NMR test results (a resting Pi/PCr greater than or equal to 0.18 or recovery rate less than 1.0 PCr.Pi-1.min-1), and 13 of the 15 MH-negative patients had normal NMR results. Although neither NMR parameter alone was diagnostically reliable, an NMR test utilizing both parameters was quite accurate. The NMR test and contracture test demonstrated an overall agreement of 93% with a copositivity of 96% and conegativity of 87%. The sensitivity and specificity of the NMR test is estimated to be 98.8% +/- 11.8% and 95.3% +/- 20.3%, respectively. The role of 31P NMR in the diagnosis of MH susceptibility and possible mechanisms underlying the observations are discussed.

Adolescent↗
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↗
PubMed1980

Effects of alpha blockers on blood pressure and on the Ca-contracture of cat aortic strips.

To further clarify the hypotensive mechanism of adrenergic alpha blockers, effects of several alpha blockers on systemic blood pressure and on Ca-contracture of isolated, cat aortic strips were studied. For this purpose, the effects of known adrenergic alpha blockers, phentolamine, phenoxybenzamine, and a newly synthesized adrenergic alpha blocker (2-(N-(n-Butyloyl)homopiperazine-N'-yl)-4-amino-6,7-dimethoxy quinazoline; E-643) were compared with those of nitroglycerin and verapamil. Systemic blood pressure was decreased by administration (2 x 10(-8) moles/kg i.v.) of all drugs except phenoxybenzamine. The order of maximal fall of diastolic blood pressure after the injection was; nitroglycerin greater than E-643 greater than phentolamine greater than verapamil greater than phenoxybenzamine. Although "adrenaline reversal" was observed after 2 x 10(-7) moles/kg of phenoxybenzamine, i.e. a 10-fold increase in the dose of phenoxybenzamine, there was no decrease in systemic blood pressure with this dose. All these drugs in a concentration of 2 x 10(-6) M inhibited the Ca-contracture (phasic and tonic) of the depolarized aortic strips. The order of inhibition of phasic and tonic contracture was: nitroglycerin greater than E-643, verapamil greater than phentolamine greater than phenoxybenzamine. The pA2 values for phentolamine and E-643 in antagonizing contractions produced by noradrenaline of cat aortic strips were 7.8 and 8.2, respectively. Hypotensive effects of these drugs (except phenoxybenzamine), parallel the inhibitory effects on the Ca-contracture of the aortic strips. These results suggest that alpha blockers such as phentolamine and E-643 exert a systemic hypotensive effect not through their alpha blocking action but by an inhibitory action on the contractile Ca-mechanism.

Adrenergic alpha-Antagonists↗
PubMed1979

Volkmann's contracture in children: aetiology and prevention.

A review was conducted of the records of fifty-five children who were admitted to the Hospital for Sick Children in Toronto between 1955 and 1975 with a diagnosis of Volkmann's contracture in fifty-eight limbs. Ten patients had been transferred to this hospital with established ischaemia after Bryant's traction for a fractured femur; all had a very poor outcome. Thirteen other cases of Volkmann's contracture affecting the superficial posterior compartment had been treated with a fixed Thomas' splint and a Bradford frame after fractures of the femoral shaft. Supracondylar fractures of the elbow resulting in Volkmann's contracture frequently had both an arterial injury and a compartment syndrome. Most of the fifty-five children reviewed here had not had early appropriate treatment. For the past twenty-one years the frequency of Volkmann's contracture has not declined in spite of many published reports on the compartment syndrome, and the hazards of supracondylar fractures and of Bryant's traction.

Adolescent↗
PubMed1990

Mechanisms of the depolarization and contracture due to Na removal in the circular muscle of the guinea-pig stomach.

Verapamil (10(-6) M) significantly reduced a development of the membrane depolarization and the contracture which were induced by Na removal. The fully developed depolarization, after exposure to Na-free solution, was reduced greatly by verapamil, excess Ca (15 mM) or sodium nitroprusside (10(-6) M), but some depolarization still remained. This remaining depolarization was completely blocked by readmission of 10 mM Na to Na-free solution containing verapamil, excess Ca or sodium nitroprusside. However, Mn (1.5 mM) did not block the depolarization due to Na removal and if Mn was present in Na-free solution, readmission of 15 mM Na to Na-free solution was not able to block the depolarization. On the other hand, the contracture due to Na removal was inhibited by addition of Mn (1.5 mM) or sodium nitroprusside (10(-6) M), but partially by addition of verapamil (10(-6) M) or excess Ca, to Na-free solution. These remaining contractures were also abolished by readmission of 10 mM Na to Na-free solution containing verapamil or excess Ca. Thus, these results suggest that the depolarization and the contracture due to Na removal are induced by increase in cytoplasmic Ca concentrations through (1): verapamil-sensitive Ca channel, (2): Na-Ca exchange system and (3): some mechanism which is inhibited by sodium nitroprusside.

Animals↗
PubMed2004

Recovery of action potentials and twitches after K-contractures in frog skeletal muscle.

To give information about intracellular Ca2+ translocation during and after K-contractures in vertebrate skeletal muscle fibers, we examined recovery of action potentials and twitches after interruption and spontaneous relaxation of K-contractures at low temperature (3 degrees C) that greatly reduced the rate of Ca2+ reuptake by the sarcoplasmic reticulum. On membrane repolarization interrupting K-contractures, the amplitude of both action potentials and twitches recovered quickly, while the falling phase of action potential was markedly slowed at first to prolong its refractory period, so that repetitive stimulation (20 Hz) did not produce a complete tetanus. Meanwhile, on membrane repolarization after spontaneous relaxation of K-contractures, the action potentials were markedly reduced in amplitude and prolonged in duration at first, also resulting in prolonged refractory period. These results are discussed in connection with Ca2+ absorption to the surface and transverse tubule membranes, producing changes in action potential kinetics.

Action Potentials↗
PubMed1978

Inhibitory action of hypertonic urea solution on the potassium contracture of the heart ventricular muscle.

Effects of hypertonic urea solution on potassium contracture were investigated in a bullfrot ventricular strip. In a medium of three times hypertonic urea, the contracture induced by 100 mM potassium solution was markedly inhibited whereas the twitch contraction was augmented in the hypertonic urea solution. The extent, as well as the time course, of the membrane depolarization produced by high potassium solution was essentially identical in both isotonic and hypertonic conditions. Endogeneous catecholamine does not seem to participate in this inhibition since the treatment with propranolol did not modify the results. Thus, the possibility of the well-known catecholamine-induced inhibition of potassium contracture can be excluded. The myocardial contractility was never suppressed, or even augmented, at this stage of urea perfusion although a prolonged hypertonic urea perfusion gradually suppressed the contractility. It was suggested that hypertonic urea exerts its negative inotropic action on the potassium contracture independently of its positive inotropism on the twitch contraction by accelerating the uptake of the activator calcium ion to some undefined intracellular sites.

Action Potentials↗