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PubMed2004

Non-surgical management of ankle contracture following acquired brain injury.

BACKGROUND AND PURPOSE: The purpose of this study was to document the outcome of non-surgical management of equinovarus ankle contracture in a cohort of patients with acquired brain injury admitted to a specialist Neurosurgical Rehabilitation Unit. METHODS: This prospective descriptive study examined all patients with a new diagnosis of moderate to severe acquired brain injury (Glasgow Coma Scale score </=12) admitted for rehabilitation over a 1 year period. Ankle dorsiflexion range and plantarflexor/invertor muscle activity were evaluated weekly during the period of hospitalization. Contracture was defined as maximal passive range of motion </= 0 degrees dorsiflexion, with the knee extended, on a minimum of two measurement occasions. Patients were retrospectively allocated to one of four treatment outcome categories according to ankle dorsiflexion range, type of intervention required and response to treatment. RESULTS: Ankle contracture was identified in 40 of the 105 patients studied. Contracture resolved with a standard physiotherapy treatment programme, including prolonged weight-bearing stretches and motor re-education, in 23 patients. Contracture persisted or worsened in 17 of 40 cases, all of whom exhibited dystonic muscle overactivity producing sustained equinovarus posturing. Ten of 17 cases required serial plaster casting (+/- injection of botulinum toxin type A) in order to achieve a functional range of ankle motion. Remediation of ankle contracture was not considered a priority in the remaining seven patients due to the severity of their overall disability. CONCLUSION: The incidence of ankle contracture identified in this population was considerably less than previously reported. Reduced dorsiflexion range was remediated with standard physiotherapy treatment in over half of the cases. Additional treatment with serial casting +/- botulinum toxin type-A injection was required to correct persistent or worsening contracture in one quarter of cases. Dystonic extensor muscle overactivity was a major contributor to persistent or progressive ankle contracture.

Adolescent↗
PubMed1964

CONTRACTURE COUPLING OF SLOW STRIATED MUSCLE IN NON-IONIC SOLUTIONS AND REPLACEMENT OF CALCIUM, SODIUM, AND POTASSIUM.

The development of contracture related to changes of ionic environment (ionic contracture coupling) has been studied in the slowly responding fibers of frog skeletal muscle. When deprived of external ions for 30 minutes by use of solutions of sucrose, mannitol, or glucose, the slow skeletal muscle fibers, but not the fast, develop pronounced and easily reversible contractures. Partial replacement of the non-ionic substance with calcium or sodium reduces the development of the contractures but replacement by potassium does not. The concentration of calcium necessary to prevent contracture induced by a non-ionic solution is greater than that needed to maintain relaxation in ionic solutions. To suppress the non-ionic-induced contractures to the same extent as does calcium requires several fold higher concentrations of sodium. Two types of ionic contracture coupling occur in slow type striated muscle fibers: (a) a calcium deprivation type which develops maximally at full physiological concentration of external sodium, shows a flow rate dependency for the calcium-depriving fluid, and is lessened when the sodium concentration is decreased by replacement with sucrose; (b) a sodium deprivation type which occurs maximally without external sodium, is lessened by increasing the sodium concentration, and has no flow rate dependency for ion deprivation. Both types of contracture are largely prevented by the presence of sufficient calcium. There thus seem to be calcium- and sodium-linked processes at work in the ionic contracture coupling of slow striated muscle.

Animals↗
PubMed2007

Genetic influences on joint contractures secondary to immobilization.

The primary research question of this study queries whether, beyond environmental conditions, genetic factors affect the development of joint contractures. We hypothesized that intrinsic genetic factors influence the severity of joint contractures developing secondary to joint immobilization. Forty rats from four inbred rat strains had one leg immobilized in knee flexion for 4 weeks. The contracture was measured mechanically as the lack of range of motion to a standardized torque. Using the contralateral leg as a control, the average severity of the contracture could be calculated and compared between strains. All immobilized legs presented knee contractures after 4 weeks of immobilization. Two strains (Dark Agouti and Fisher 344) showed a larger mean knee contracture than those of the two other rat strains (Augustus Copenhagen Irish and Brown Norway). Environmental factors, such as immobility, are usually identified as a cause of a joint contracture. These results demonstrate that, in addition to mechanical factors in the environment of a joint, intrinsic genetic factors participate in the process leading to joint contracture. This demonstration has important consequences for directing future research and may lead to interventions to help patients at risk of developing joint contractures.

Animals↗
PubMed2004

Progression and direction of contractures of knee joints following spinal cord injury in the rat.

Joint contractures following central nervous system injuries remain a prevalent and significant complication, but no reports are available on evidence of contracture formation over time. The objective of this study was to determine the rate of contracture progression and the direction of loss in joint movement following spinal cord injuries (SCI). Forty-eight female Wistar rats were used. Twenty-four experimental rats underwent a spinal cord transection at the level of T8 and 24 control rats underwent a sham-operation. The animals were studied at each of 5 time points: 2, 4, 8, 12, 16, and 24 weeks after surgical intervention. The degree of contractures was assessed by measuring the femorotibial angle on both hindlimbs with the use of a goniometer. Knee joint motion was measured for flexion and extension direction. Knee flexion contractures developed in all experimental rats. The restriction in motion progressed during the first 12 weeks and plateaued thereafter. The contractures were produced almost exclusively by a loss in the extension range of motion. This study defined the time course that contracture progression was more rapid in the early stage after SCI and stabilized in the later stage of injury. Contractures following SCI occurred in flexion at the knees and resulted from a loss of extension. These findings should help guide timely treatment and provide a better understanding of contracture development.

Animals↗
PubMed1996

The prevalence of joint contractures in residents in NHS continuing care.

A group of 222 residents in NHS continuing care were studied in order to assess the prevalence of joint contractures in the very disabled elderly and to establish whether there was an association between the presence of contractures and functional ability; 121 (55%) had at least one contracted joint. There was no clear linear relationship between length of stay in continuing care and the presence of contractures. Those with upper limb contractures were nearly twice as likely to be unable to feed themselves as those without contractures (p < 0.0001). The presence of at least one lower limb contracture was significantly associated with reduced mobility (p < 0.0001). An association was also demonstrated between the presence of lower limb contractures and frequency with which the patient walked. The role of disease and immobility in the development of contractures is discussed as well as the potential for the prevention and treatment of contractures.

Activities of Daily Living↗
PubMed1994

Reversal of ventricular contracture during hypothermic cardioplegic arrest.

Ventricular contracture was produced in isolated perfused rat hearts by a novel method using repeated administration of an anoxic cold hyperkalemic cardioplegia solution. Contracture could be reversed by reperfusion with the same solution, without calcium (Group 1), oxygenated (Group 2), or oxygenated and calcium free (Group 3). Group 1 hearts underwent partial reversal of contracture; in Group 2, contracture was reversed more completely, but the effect was transient. Hearts in Group 3 had contracture reversed completely to a level lower than prearrest end diastolic pressure. Hearts in contracture were profoundly depleted of high-energy phosphates (ATP, 9% of control; creatine phosphate, 27%) and the success of contracture reversal was paralleled by the extent to which each solution repleted ATP and PCr. Ventricular contracture produced by energy depletion is rapidly reversed by restoration of oxygen to the myocardium. Reducing extracellular calcium by acalcemic perfusion is ineffective as an isolated measure but is synergistic with reoxygenation and enhances contracture reversal.

Adenosine Diphosphate↗
PubMed1987

Ultrastructural observations on the effects of different substrates on ischaemic contracture in global subtotal ischaemia in the rat heart.

Ultrastructural morphology was examined in myocardia perfused with different substrates, following the hypothesis that ultrastructural changes or differences would indicate the mechanism of early ischaemic contracture. Substrates used were glucose, acetate and no substrate (substrate-free). Isolated rat hearts were subjected to global low flow ischaemia followed by perfusion fixation at either no contracture, early contracture (5%) or full contracture (100%). Total tissue adenosine triphosphate (ATP) levels were analysed from myocardia of each group. Glucose perfused myocardia did not develop contracture for at least 30 minutes and maintained ultrastructural and ATP normality. Substrate-free and acetate perfused myocardia developed contracture after 10-12 minutes of ischaemia at which time myofibrillar morphology was altered within small sparse foci of developing mild oedema with contracture and hyperextension of myofibrils. ATP levels were normal. At full ischaemic contracture, both substrate-free and acetate perfused myocardia showed severe mitochondrial damage, oedema, myofibrillar contracture and hyperextension with accompanying distortion and swelling of the sarcoplasmic reticulum.

Animals↗
PubMed1976

Reversible Inhibition of Potassium Contractures by optical isomers of verapamil and D 600 on slow muscle fibres of the frog.

Potassium-induced contractures were measured isometrically in slow fibres of gastrocnemius muscle from the frog Leptodactylus ocellatus. Optical isomers of verapamil and of D 600 decreased the tension of K-contractures with the following characteristics: 1. 90 min exposures of the muscles to the (-)isomers of the drugs were more effective in decreasing tension of 40 mM KCl-contractures when successive challenges to 40 mM KCl were made each 10-15 min than without challenges during the incubation time. 2. In contrast to the depressing effect of (-)isomers of verapamil and D 600, the decrease of K-contractures by 1 mM EGTA in "Ca-free" solutions was independent on the history of 40 mM KCl-contractures. 3. The threshold concentration of K to cause contractures was the lower the lower the Ca-concentration. This relationship was little affected by (-)verapamil at concentrations of the drug which depressed by 50% the tension of 40 mM KCl-contractures in 1.8 mM CaCl2. 4. Verapamil and its methoxy-derivative D 600 were equipotent in depressing 40 mM KCl-contractures. Their optical (-)isomers were 4 to 5 times more potent than their corresponding (+)isomers. 5. K-tension curves in the presence of 6.1 muM (-)verapamil in 1.8 mM CaCl2 were similar to curves in 0.18 mM CaCl2 without the drug. 6. K-tension curves in 10 mM CaCl2 were shifted by (-)verapamil in nearly parallel manner towards higher K-concentrations. 7. The stereoselective decrease of K-contractures by verapamil and D 600 may be due to blockade of inward Ca-flux and to retardation of the reavailability of Ca2+ for release during partial depolarizations with K.

Animals↗
PubMedDate not supplied

The ryanodine contracture test may help diagnose susceptibility to malignant hyperthermia.

PURPOSE: The ryanodine contracture test (RCT) using the plant alkaloid ryanodine as the triggering agent has been proposed to reduce equivocal results of the in vitro caffeine-halothane-contracture test (IVCT), which is the accepted and standardized procedure to diagnose malignant hyperthermia (MH). However, the response of skeletal muscle of non-MH affected patients (controls) to ryanodine has not yet been characterized. METHODS: Skeletal muscle biopsies were studied in 33 controls and in six patients with a history of fulminant MH. Following the IVCT, the RCT was performed in all specimens using ryanodine 1 micro M. Onset time of contracture and time to reach a contracture level of 10 mN above lowest resting tension and above predrug tension were calculated. RESULTS: With the standard IVCT, all controls were labelled MH non-susceptible; all clinically diagnosed MH patients were labelled MH susceptible. With ryanodine, control muscle differed from MH susceptible muscle regarding onset time of contracture (26 vs 3.8 min, P < 0.05) and time to reach a contracture of 10 mN (49 vs 12.5 min, P < 0.05; all median). Tissue viability and patient's age significantly influenced contracture times. CONCLUSIONS: Despite the highly specific binding of ryanodine at the myocytic sarcoplasmic reticulum, the wide range of contracture times of the controls points toward heterogeneity of ryanodine receptors within physiologic limits. This may also be caused in part by tissue viability and the patients' age. The ryanodine contracture test performed in addition to the IVCT may add clarity into diagnosing a patient as MH-susceptible or not.

Adult↗
PubMed1995

Coronary flow and glucose delivery as determinants of contracture in the ischemic myocardium.

Ischemic contracture may be avoided by the provision of glucose under low flow conditions (Owen et al., 1990). However, accumulation of harmful metabolic end products may inhibit glycolytic flux and lessen the benefit of glucose. We assessed whether during increasingly severe flow restriction, provision of glucose might be harmful rather than beneficial, using the Langendorff perfused rat heart. Ischemic contracture (resting tension expressed as percent of preischemic developed pressure) was measured via a left ventricular balloon. Reductions in flow to 0, 0.015, 0.03, 0.06, 0.1, 0.2 or 0.4 ml/min/g wet wt over 60 min were tested. At zero flow, peak contracture was 61.4 +/- 3.5% (+/- S.E.) but fell to 15.6 +/- 6.3% with 0.4 ml/min/g wet wt (P < 0.05) in the presence of 11 mmol/l glucose. Time-to-onset of contracture was significantly delayed by the higher coronary flows. At coronary flows down to zero, the effect of glucose was inconstant or absent, but not harmful. With the residual flow at 0.2 ml/min/g wet wt, a dose response to glucose in ischemia was elicited, using concentrations of 0, 2.5, 5.5, 11 or 22 mmol/l. Maximum protection against ischemic contracture was found with 11 mmol/l glucose. However, once contracture occurred, functional recovery was severely impaired in all cases. Reducing glycogen prior to low flow ischemia (0.2 ml/min/g wet wt) with 11 mmol/l glucose increased peak contracture, and reduced the time-to-onset of contracture. Increased preischemic glycogen had little effect on contracture. Glycolytic flux fell in proportion to the coronary flow. However, there was an increased glucose extraction at lower flows of 0.1 and 0.2 ml/min/g wet wt, suggesting that it is the rate of delivery (i.e. coronary flow) which is the rate limiting step rather than enzyme inhibition by accumulated metabolites. If flow were further reduced, metabolite accumulation would become more important, such that with no flow, this would be the determinant of glycolytic flux rate. In our model, the two requirements for optimal protection from ischemia were (i) provision of glucose (11 mmol/l was optimal) and (ii) an adequate coronary flow to deliver the glucose and remove end product inhibition (greater than 0.06 ml/min/g wet wt).

Animals↗
PubMed1984

Effects of calcium flux inhibitors on contracture and calcium content during inhibition of high energy phosphate production in cultured heart cells.

The effects of inhibition of oxidative phosphorylation by 1 mM cyanide (CN) and of glycolysis by 20 mM 2-deoxyglucose (2DG) on contraction and relaxation of cultured monolayers of chick embryo heart cells were determined. Exposure to these agents first induced a gradual decline in contractility and a transient impairment of relaxation. Spontaneous beating then ceased, associated with increased relaxation, followed by a marked and prolonged contracture. This contracture was completely reversible after washout of metabolic inhibitors. The effects of calcium flux inhibitors on the time course of development of contracture were studied. Verapamil, which inhibits Ca influx via the slow Ca channel, delayed the onset of contracture when used in pretreatment, but had no effect if added to cultures after exposure to CN + 2DG. Lanthanum, which inhibits Ca influx both via the slow Ca channel and via Na-Ca exchange, delayed onset of contracture if added after exposure to CN and 2DG, but accelerated contracture if added prior to treatment with CN + 2DG. Cellular exchangeable calcium content, measured after exposure to CN and 2DG for the same time period that produced contracture, was reduced compared to the control level while unidirectional Ca influx rate was not measurably altered. Exchangeable Ca content was unaffected by pretreatment with verapamil and La, but was reduced if cells were exposed to La after metabolic inhibition. These findings suggest that after metabolic inhibition intracellular storage capacity for Ca+ is reduced in cultured heart cells. Ca influx via the slow Ca channel after metabolic inhibition does not appear to contribute to development of contracture in this model system. However, Ca entry via Na-Ca exchange may accelerate cellular contracture developing after metabolic inhibition of ATP production.

Adenosine Triphosphate↗
PubMed1998

[Diagnosis of susceptibility to malignant hyperthermia with an in vitro contracture test with the phosphodiesterase iii inhibitor enoximone].

PURPOSE: Inhibition of phosphodiesterase III (PDE-III) by enoximone elevates cyclic AMP (cAMP) content and intracellular calcium in human cardiac muscle. An involvement of cAMP in the pathogenesis of malignant hyperthermia (MH) has been suggested, because a higher basal content of cAMP was found in skeletal muscles from MH susceptible (MHS) than in normal (MHN) individuals and swine. In this study the in vitro effects of enoximone on skeletal muscles and the possibility to distinguish MHS from MHN patients were investigated. METHODS: Muscle biopsies from 37 patients with clinical suspicion for MH were obtained. The patients were first classified as MHS, MHE (equivocal result) or MHN by the caffeine halothane contracture tests according to the procedure of the European MH Group (EMHG). MHE-patients and patients with neuromuscular diseases were excluded from the study. Enoximone was added cumulatively every five minutes to surplus muscle specimens to obtain organ bath concentrations of 0.2, 0.4, 0.6, 0.8, 1.2 and 1.6 mmol/l. The in vitro effects of enoximone on muscle contractures and twitch were measured. RESULTS: Twelve patients were classified as MHS and 21 as MHN by the EMHG criteria. Enoximone induced contractures in skeletal muscles from all patients. MHS muscles developed contractures at significantly lower bath concentrations of enoximone than MHN muscles. Contractures of MHS compared to MHN muscles were significantly larger at bath concentrations of 0.4, 0.6, 0.8 and 1.2 mmol/l enoximone. No overlap in maximum contractures was seen between MHS and MHN muscles at bath concentrations of 0.6 and 0.8 mmol/l enoximone. Muscle twitch increased in both groups after administration of enoximone. CONCLUSION: The PDE-III-inhibitor enoximone induces contracture development in skeletal muscles. These contractures were attained at lower concentrations and were larger in MHS compared to MHN muscles. In vitro diagnosis of MH by a contracture test with enoximone appears to be possible. Furthermore, regarding these results a trigger potency for MH by enoximone could not be proved, but the use of enoximone in MHS patients might be dangerous.

Adolescent↗
PubMed1990

The effects of simulated knee-flexion contractures on standing balance.

The effects of simulated unilateral and bilateral knee-flexion contractures on standing balance were studied by testing 15 normal subjects on a Kistler force platform. Postural sway (mediolateral and anteroposterior travel) and the mean position of the center of pressure (as a percentage of the distance between the midlines of the feet and from heels to toes) were determined from 20 s of data. Unilateral and bilateral knee-flexion contractures of 15 degrees and 30 degrees were simulated for each subject by means of an adjustable line from the subject's waist to the sole of each foot. Paired t tests were used to compare balance parameters while standing with the simulated contractures with those during relaxed standing. Mediolateral travel increased by a mean difference of 3.6 cm with a 30 degree unilateral contracture (P less than 0.01) and by 5.0 cm with 30 degrees bilateral contractures (P less than 0.01). Anteroposterior travel increased by 4.7 cm (P less than 0.05) and 8.8 cm (P = 0.08) with 15 degrees and 30 degrees bilateral contractures, respectively. With a unilateral contracture of 30 degrees, the center of pressure shifted 15.6% (P less than 0.0005) toward the unflexed side, changes that were not eliminated by correction of the induced leg-length discrepancy. The center of pressure moved anteriorly by 8.3% with 30 degrees bilateral contractures (P less than 0.001). The results provide insight into how knee-flexion contractures alter standing balance, and underline the importance of preventing and treating this common disorder.

Adult↗
PubMedDate not supplied

Multimodal versus progressive treatment techniques to correct burn scar contractures.

The treatment of burn scar contractures is a major emphasis in the rehabilitation of patients with burn injuries. Many treatment techniques have been used successfully but without a critical investigation of the best practice of care. In this study, we compared the outcomes for pediatric and adult patients treated with a multimodal therapy approach to treatment techniques that are considered to be progressive to determine if differences existed in the techniques. The medical records of 52 patients with documented burn scar contractures were reviewed for patient and rehabilitation treatment parameters. Included were population demographic information and type of treatment intervention used to correct the scar contracture. In particular, the postburn day when the contracture appeared, the percentage of range of motion deficit, the day when definitive treatment that eventually corrected the contracture was begun, and the days required to correct the contracture were noted. With equal range-of-motion deficits identified, the burn scar contractures of patients in the progressive treatment group were corrected in less than half the time of the burn scar contractures of the patients in the multimodal treatment group. This result occurred despite scar contractures that appeared significantly earlier and later initiation of definitive treatment.

Adolescent↗
PubMed1966

Contractures in a superfused frog's ventricle.

1. A new perfused preparation of frog's ventricle is described, whose main advantage is that there are short diffusion distances between the cells and the washing fluid.2. This preparation responds within a few seconds to alterations in sodium, potassium or calcium concentration, or alteration in the osmotic pressure of the bathing fluid. The speed of these alterations is consistent with the diffusional distances involved measured histologically.3. On depolarizing the preparation with Ringer + excess potassium, tension development starts at about -25 mV and is still increasing at -8 mV (the lowest voltage studied). As in earlier experimetns in frog ventricle (Niedergerke, 1956b) and in skeletal muscle (Hodgkin & Horowicz, 1960) the relation between potential and tension is very steep.4. Sodium free contractures (Lüttgau & Niedergerke, 1958) are very rapid in onset with this preparation. To maintain the tension developed, a rapid rate of washing is necessary for 1-2 min. After this, slow washing is sufficient. It is proposed that this is due to the leaching out of cellular sodium.5. In fresh preparations the twitch and maximum K contracture are of similar size when stimulated at 30/min in 1-2 mM-Ca. With the onset of hypodynamia the twitch tension falls, but the K contracture remains unaltered. In hypodynamic ventricles the sensitivity of the twitch to the ratio [Ca]/[Na](2) declines, whereas that of the K contractures remains unaltered. Hypodynamia therefore does not affect the contractile elements themselves.6. During the staircase phenomenon the K contracture and twitch size alter in a similar manner, as previously described by Niedergerke. The sodium free contracture, however, remains unaltered. This tends to favour the hypothesis that the staircase phenomenon is due to effects at the cell membrane rather than in the cell interior.7. Maximum K contractures occur at a [Ca]/[Na](2) ratio of about 0.7 x 10(-4) mM(-1), a figure similar to that obtained in earlier experiments (Lüttgau & Niedergerke, 1958).8. The length-tension curves of K contractures are similar to those previously described for heart muscle, using single twitches to generate tension.9. Application of K free solutions produced no rapid contractures in this preparation.

Journal Article↗
PubMed1976

The effect of temperature on potassium chloride contracture in cat myocardium.

1. Contracture was induced in cat myocardium by exposure to 140 mM-KC1 In isotonic Tyrode solution. Force of contracture expressed as mg/mm2 (muscle cross-sectional area) falls with increasing cross-sectional area. 2. The effect of temperature on isometric force developed during contracture was evaluated both in normal (untreated) atrial and ventricular muscle and following treatment with sympatholytic drugs. 3. The force of contracture was not significantly affected by sympatholytic drugs at 36 degrees C. 4. In normal atrial and ventricular muscle, force of contracture decreased when the muscle was cooled from 36 to either 29 or 20 degrees C. 5. In atrial muscle, the effect of temperature was not changed by sympatholytic drugs. In contrast, exposure to sympatholytic drugs increased contracture force developed by ventricular muscle at 20 degrees C. Also, contracture force was significantly greater at 20 than at 36 degrees C in ventricular muscle from reserpine-pretreated cats. 6. It is suggested that ventricular muscle becomes more sensitive to the relaxing effects of endogenous catecholamines at temperature is lowered. 7. The differences shown between atrial and ventricular muscle with respect to the effect of temperature and sympatholytic drugs on contracture force may result from the differing amounts of sarcoplasmic reticulum found in these types of cardiac muscle and also from different mechanisms of "excitation-contracture" coupling in atrial and ventricular muscle.

Animals↗
PubMed1990

Potentiation of the halothane-cooling contractures of mammalian muscles by denervation.

Denervation potentiated the cooling-induced contractures and the halothane-cooling contractures of isolated extensor digitorum longus and soleus muscles of the mouse. These effects were more striking in extensor digitorum longus than in soleus muscles. Significant increases in the peak amplitudes of the halothane-cooling contractures of both muscles and of the cooling contractures of soleus muscle were observed within 2 and 7 days of denervation. The potentiation of the contractures persisted for 90 days, the period of this study. Denervation (greater than 2 days) endowed extensor digitorum longus with the ability to generate cooling contractures in the absence of halothane. The rate of tension development of cooling-induced contractures in the absence or presence of halothane was significantly greater in denervated (2-90 days) than in innervated muscles. Denervation also reduced the effectiveness of procaine in inhibiting the halothane-cooling contractures. It is proposed that the potentiation of cooling-induced contractures in denervated muscles results primarily from an increase in the rate of efflux and in the quantity of Ca2+ released from the sarcoplasmic reticulum, upon cooling and (or) when challenged with halothane.

Animals↗
PubMed2002

Effect of zinc ions on caffeine-induced contracture in vascular smooth muscle and skeletal muscle of rat.

The effect of zinc ions on caffeine-induced contracture in vascular smooth muscle and skeletal muscle of rat was studied. In aortic strips, caffeine contracture was depressed by Zn2+ in a dose-dependent manner. Moreover, the extent of the depression of caffeine contracture in the Zn2+ loaded smooth muscle increased with repetitive caffeine exposures. For instance, in the preparations perfused with a medium containing 100 microM [Zn2+] for 15 or 30 min, the first caffeine contractures were similarly depressed to about 60% of the control. However, the subsequent caffeine exposure at 15 min interval could not evoke any contracture. In this study this feature is referred to as activation dependence of the Zn2+ effect. In small bundles of soleus muscle 2ñ100 microM [Zn2+] similarly caused a depression of caffeine contracture, and the activation dependence also was evident. However, an evident potentiation of caffeine contracture was seen in the preparations loaded with lower [Zn2+] such as 0.5 microM, indicating that the effect of Zn2+ on caffeine contracture of skeletal muscle was somewhat different from that seen in smooth muscle. By observing how the depression effect depends on the intervals between caffeine exposures as well as on caffeine concentrations, it is indicated that the activation dependence of the Zn2+ effect, at least in skeletal muscle, may not be explained by depletion of intracellular Ca2+ stores alone. The possible mechanism for that caffeine contracture of smooth muscle and skeletal muscle was differentially affected by Zn2+ ions is discussed.

Animals↗