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PubMed1987

Contracture induction by snake venom cardiotoxin in skeletal muscle from humans and rats.

Contracture responses to cardiotoxin (CTX) from Naja naja kaouthia venom were investigated in rat and human skeletal muscle of similar fiber type distribution to determine species differences in mechanism of action. Rat diaphragm strips and human vastus lateralis preparations were directly stimulated in a tissue bath. The calcium dependence of toxin action, synergism between CTX and phospholipase A2 (PLA2) activity and roles of Na+ + K+-ATPase activity and the sarcoplasmic reticulum Ca2+ stores in contracture induction were examined. The threshold of contracture to CTX was decreased in human and rat muscle when Sr2+ was substituted for Ca2+ in the bathing medium. In rat, but not in human muscle the threshold of contracture to CTX was decreased in a medium in which Ca2+ had been omitted. The decrease in contracture threshold may relate to toxin binding. The maximum height of contracture for preparations from humans, but not for those from rats was considerably depressed in a medium in which Ca2+ had been omitted. Exogenously added bee venom PLA2 acts synergistically with CTX in skeletal muscle in a manner similar to that in erythrocytes. Ouabain (100 microM) did not elicit contractures in any of the media tested nor affect CTX-induced contractures in Sr2+-containing medium. Dantrolene antagonized CTX-induced contractures, suggesting a role for Ca2+ derived from the sarcoplasmic reticulum in CTX action. The species difference in CTX action may reflect differences in the relative contribution of Ca2+ from the sarcolemma and sarcoplasmic reticulum to the contracture.

Animals↗
PubMed1995

Possible involvement of Ca(2+)-induced Ca2+ release mechanism in Ag(+)-induced contracture in frog skeletal muscle.

To determine if an Ag(+)-induced contracture is associated with the Ca(2+)-induced Ca2+ release mechanism in the sarcoplasmic reticulum, effects of Ca(2+)-induced Ca2+ release modulators on the Ag(+)-induced contracture were studied with single fibers of frog toe skeletal muscle. The fiber treated with 1 mM caffeine contracted significantly much more than controls without caffeine at Ag+ concentrations below 1 microM. Procaine shifted the Ag+ concentration-tension curve to the right, dose-dependently. When 10 mM procaine was applied to contracting fibers not treated with caffeine, the duration of 5 microM Ag(+)-induced contracture was shortened with a little decrease in tension amplitude, that was different from the effect of procaine on caffeine contracture. In caffeine solution, 0.5 microM Ag+ caused a long-lasting contracture with sometimes two peaks. 2 mM procaine led to disappearance of such two peaks, resulting in shortening of the contracture. K+ contracture was potentiated by 1 mM caffeine only at lower concentrations of K+, and inhibited by 10 mM procaine. These results suggest that the Ag(+)-induced contracture is composed of two components: Ca(2+)-induced Ca2+ release-dependent and -independent. 5 microM Ag(+)-induced contracture slowly relaxed with a wavy tension pattern to the resting level when 0.05 mM dithiothreitol was applied around peak of the tension. This relaxation was accelerated by procaine application. These findings may be explained by attributing a portion of Ag(+)-induced contracture to the effect of Ca2+ released through the Ca(2+)-induced Ca2+ release mechanism in the sarcoplasmic reticulum.

Animals↗
PubMed1997

[4-chloro-m-cresol-induced contractures of skeletal muscle specimen from patients at risk for malignant hyperthermia].

PURPOSE: 4-chloro-m-cresol (4-CmC), commonly used as preservative, has been shown to induce contractures in skeletal muscle specimens from individuals susceptible to malignant hyperthermia (MH). It has been suggested that a defect of the calcium release channel of the skeletal muscle sarcoplasmic reticulum (ryanodine receptor) in MH susceptible (MHS) patients could be responsible for this phenomenon. 4-CmC was found to be a potent activator of ryanodine receptor-mediated Ca2+ release. The aim of this study was to determine the in vitro effects of 4-CmC on muscle specimens from MHS and normal (MHN) patients, and whether contracture testing with different concentrations of 4-CmC could result in a more precise discrimination between MHS and MHN. METHODS: In this prospective study muscle biopsies were obtained from 40 patients with clinical suspicion of MH. The patients were first classified by the in vitro contracture test (IVCT) according to the European MH protocol. After MH classification, surplus muscle specimens were subjected to the 4-CmC study. RESULTS: Cumulative administration of 4-CmC (25, 50, 75, 100, 150, and 200 mumol/l) produced contractures in a concentration-dependent manner. However, contractures developed significantly earlier and were greater in MHS (n = 17) than in MHN specimens (n = 23). After bolus administration of 50, 75, and 100 mumol/l 14-CmC MHS specimens developed distinct muscle contractures. In contrast, in MHN specimens only 100 mumol/l 4-CmC produced contractures. All contracture levels following bolus administration of 100 mumol/l 4-CmC were attained significantly earlier in MHS than in MHN. There was no overlapping in the range of times between both groups. CONCLUSION: In vitro contracture testing with 4-CmC seems to be a specific method to distinguish between MHS and MHN patients. However, the question whether 4-CmC is an MH-triggering agent is not completely solved. 4-CmC is a preservative within a large number of commercially available preparations (e.g. insulin, hormones, etc.). Regarding the results of contracture testing with 4-CmC it has been suggested that 4-CmC possibly represents a high-risk agent for MHS individuals. To reduce the risk of MH in susceptible patients due to administration of chlorocresols, we recommend avoiding preparations containing the preservative 4-CmC.

Adolescent↗
PubMed1971

High potassium and low sodium contractures in sheep cardiac muscle.

Contractures develop in sheep atrial trabeculae if Tyrode's solution is rapidly replaced by a solution containing elevated potassium, reduced sodium, or both. Two phases of the contracture can be identified on the basis of differences in physiological behavior: a rapid and transient phase that predominates during the first few seconds of the contracture, and a slowly developed phase that is responsible for the steady level of tension reached later in the contracture. The transient phase is particularly prominent if the muscle is stimulated rapidly before the contracture, and reduced or absent if the muscle is not stimulated or if calcium is not present before the contracture. Recovery of the transient phase after a contracture parallels the recovery of twitches. This transient phase appears to reflect the depolarization-induced release of activator (calcium) from an internal store, possibly the same store that is involved in the normal contraction. The slowly developed tension is dependent on the contracture solution used, and is decreased if the calcium concentration is reduced or if the sodium concentration is increased. It does not depend on conditions before the contracture and does not require time to recover. This phase of the contracture may be due to entry of calcium from the extracellular solution.

Animals↗
PubMed1986

In vitro muscle contractures induced by halothane and suxamethonium. I: The rat diaphragm.

The rat diaphragm was used as an in vitro model for studies of contractures synergistically-induced by halothane and suxamethonium. The effects of three agents reported to inhibit phospholipase A2 activity (quinacrine, spermine and indomethacin), tubocurarine and dantrolene were examined on these contractures. Contractures induced by 1% halothane (0.26 +/- 0.02 g) (mean +/- SEM) were increased (0.60 +/- 0.04 g) if suxamethonium 50 mmol litre-1 was also in the bathing medium. Suxamethonium-induced contractures (0.22 +/- 0.03 g) were also enhanced when halothane was present (0.51 +/- 0.03 g). Spermine, indomethacin and dantrolene antagonized both halothane- and suxamethonium-induced contractures. Quinacrine potentiated contractures induced by either halothane or suxamethonium. Contractures induced by suxamethonium were antagonized by tubocurarine; however, contractures induced by halothane were not antagonized by tubocurarine. These results suggest that free fatty acids may be involved in contractures induced synergistically by halothane and suxamethonium. Different mechanisms are involved in the induction of contractures by suxamethonium than by halothane.

Animals↗
PubMed1983

The control of the strength of the caffeine contracture in frog atrial trabeculae: an activity of the sodium-calcium exchange.

In frog atrial trabeculae low-Na contractures and caffeine contractures evoked in Na-poor solutions are increased by raising the external Ca concentration [( Ca]o), lowering the external Na concentration [( Na]o) or by tissue depolarization in K-rich fluids. The source of activator Ca for the low-Na and the caffeine contractures is probably different because Na-withdrawal contractures are inhibited by Mn2+ but unaffected by local anaesthetics, while the caffeine contractures are potentiated by Mn2+ and inhibited by local anaesthetics. The spontaneous relaxation of the low-Na contracture has a rate constant of 0.055 +/- 0.009 s-1, at room temperature for any [Na]o, [Ca]o or external K concentration [( K]o). The spontaneous relaxation of the caffeine contracture in Na-free fluid has a similar rate constant. However, the rate of spontaneous relaxation is increased if Na+ is present in the bathing medium and analysis of the results of experiments done in solutions with different [Na]o, [Ca]o or [K]o, suggests that two processes are involved in the reduction of the internal Ca concentration [( Ca]i) and the fall of tension. One, also responsible for the spontaneous relaxation of the low Na contracture, is dependent on metabolic energy and may be intracellular in origin. The other depends upon the activity of the sarcolemmal Na/Ca exchange, persists in the presence of metabolic inhibitors and is also activated during a low Na contracture when [Na]o is raised, or [Ca]o is lowered. The contractile response, of frog cardiac muscle to caffeine, would seem to be largely due to a release of Ca2+ from an intracellular store, but the strength of the resulting contracture depends upon a competition between the contractile proteins and the Na/Ca exchange for the released Ca2+.

Animals↗
PubMed1968

The effect of adrenaline on the tension developed in contractures and twitches of the ventricle of the frog.

1. The effect of adrenaline on contracture and twitch tension in frog's ventricle has been examined, using the superfused preparation.2. In 1 mM-Ca Ringer, contractures induced with excess KCl concentrations from 50 to 200 mM, are reduced by 1 x 10(-6) g/ml. adrenaline to an average of 0.62 of control values, in marked contrast to the well known positive inotropic effect of adrenaline on the heart twitch. This effect of adrenaline is directly dose dependent. Increasing [Ca](o) diminishes the effect of adrenaline on contracture tension, and on the twitch tension.3. Adrenaline has a significantly greater effect on the KCl contracture tension than noradrenaline or isoprenaline.4. In 1 mM-Ca Ringer, Na-free contractures are reduced to 0.72 of controls by 1 x 10(-6) g/ml. adrenaline. Adrenaline also significantly reduces tension in contractures induced by 50 c/s alternating current.5. The action of adrenaline on contracture tension is largely complete in 1-2 min at various rates of stimulation and calcium concentrations. A similar time course has been found for the effect of adrenaline on membrane potential.6. Pronethalol blocks the action of adrenaline on both twitch and contracture. The action on the contracture can also be blocked by ouabain (1 x 10(-5)M), and exposure of the tissue to K-free or Na-free Ringer solution.7. Adrenaline hyperpolarizes the membrane potential with a range of [K](o) from 0 to 200 mM. This effect is blocked by pronethalol and ouabain. After exposure to ouabain, adrenaline causes a significant decrease in the membrane potential. This may be due to an increase in the sodium permeability.8. At low values of the [Ca]/[Na](2) ratio, adrenaline takes a relatively constant number of beats for full action, but at high values of the ratio the development of full effect is largely time dependent.9. The time course of the effect on the twitch of changing from 0.5 to 2 mM-Ca Ringer has been studied at various rates of stimulation. The equilibration time has been found to depend on the heart rate.10. The effect on the contracture suggests that adrenaline decreases the calcium permeability. It is further suggested that the development of twitch tension is not due to direct Ca entry but is due to the release of Ca from a local store within or between the cells. The inotropic action of adrenaline is explained in terms of this store.

Animals↗
PubMed1988

Effect of acetylstrophanthidin on twitches, microscopic tension fluctuations and cooling contractures in rabbit ventricle.

1. We have measured the effect of the aglycone acetylstrophanthidin (ACS) on twitches, cooling contractures and microscopic tension fluctuations in rabbit ventricular muscle. 2. Both developed twitches and cooling contractures are strengthened by applications of ACS in the range 1-4 microM. This positive inotropy averages 150-160% of control (zero ACS) in both twitches and cooling contractures. Cooling contracture magnitude is assumed to reflect the availability of sarcoplasmic reticulum (SR) Ca2+ for contraction (Bridge, 1986). We infer that ACS increases the availability of SR Ca2+ by enlarging SR Ca2+ stores and this may contribute to the positive inotropy. 3. However, twitches appear to increase at lower concentrations of ACS than those required to increase cooling contractures. This observation suggests that the initial ACS inotropy may be achieved without an increase in SR Ca2+. Furthermore, low doses of ACS produce positive inotropy in the presence of 10.0 mM-caffeine where cooling contractures are abolished. This also suggests that positive inotropy occurs in the absence of SR Ca2+ accumulation. 4. Rest decay of both cooling contractures and twitches is significantly slowed in 4 and 8 microM-ACS. We infer that ACS slows the rate of decline of SR Ca2+ available for contraction by slowing the rate at which Ca2+ is lost from the cell during rest. This suggests that ACS produces a net slowing of Ca2+ efflux during activity which in the absence of altered Ca2+ influx will result in net Ca2+ gain and presumably enlarged SR Ca2+ stores. 5. Increasing the concentration of ACS (6-10 microM) results in a decline in developed twitch tension, total tension and an increase in rest tension. Measurement of microscopic tension fluctuations indicates that as developed twitches decline, the root mean square (r.m.s.) of the tension fluctuations increases in a reciprocal manner. This supports the suggestion of others that the decline in developed twitch tension and the appearance of tension fluctuations are causally related. 6. Although ACS (6-10 microM) causes a decline in twitch tension, rapid cooling contractures remain elevated. We suggest that in the presence of Ca2+ oscillations the magnitude of cooling contractures reflects the sum of cytosolic Ca2+ and Ca2+ that is available for release. If microscopic tension fluctuations do represent Ca2+ moving between the SR and cytosol the sum of SR and cytosolic Ca2+ and hence cooling contracture might not decline.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Studies of the halothane-cooling contractures of skeletal muscle.

The characteristics of transient contractures elicited by rapid cooling of frog or mouse muscles perfused in vitro with solutions equilibrated with 0.5-2.0% halothane are reviewed. The data indicate that these halothane-cooling contractures are dose dependent and reproducible, and their amplitude is larger in muscles containing predominantly slow-twitch type fibers, such as the mouse soleus, than in muscles in which fast-twitch fibers predominate, such as the mouse extensor digitorum longus. The halothane-cooling contractures are potentiated in muscles exposed to succinylcholine. The effects of Ca2+-free solutions, of the local anesthetics procaine, procainamide, and lidocaine, and of the muscle relaxant dantrolene on the halothane-cooling contractures are consistent with the proposal that the halothane-cooling contractures result from synergistic effects of halothane and low temperature on Ca sequestration by the sarcoplasmic reticulum. Preliminary results from skinned rabbit muscle fibers support this proposal. The halothane concentrations required for the halothane-cooling contractures of isolated frog or mouse muscles are comparable with those observed in serum of patients during general anesthesia. Accordingly, fascicles dissected from muscle biopsies of patients under halothane anesthesia for programmed surgery develop large contractures when rapidly cooled. The amplitude of these halothane-cooling contractures declined with the time of perfusion of the muscle fascicles in vitro with halothane-free physiological solutions. It is suggested that the halothane-cooling contractures could be used as a simple experimental model for the investigation of the effects of halothane on Ca homeostasis and contractility in skeletal muscle and for study of drugs of potential use in the management of the contractures associated with the halothane-induced malignant hyperthermia syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Local↗
PubMed1989

Blockade of K+ contractures in skeletal muscle by opioid drugs: a nonstereospecific effect.

The effect of several opioid drugs was tested on the K+ contractures in frog's skeletal muscle. These contractures are produced by the entrance of extracellular Ca2+ ions via the voltage-dependent, slow Ca2+ channels located in the T tubules. Morphine and other opioid agonists in concentrations ranging from 10(-10) to 10(-5) M inhibited K+ contractures. The stereoisomers, dextrorphan and levorphanol, were found to have identical potency in inhibiting high K+ contractures, suggesting that this was a nonstereospecific blockade of voltage-dependent calcium channels by the opioid drugs despite the low effective drug concentrations. In agreement with this conclusion it was found that the inhibition of K+ contractures by the opioids was not antagonized by naloxone. It also was observed using a sucrose gap apparatus that these opioid drugs in concentrations used to block the high K+ contractures did not reduce the K+-induced membrane depolarization. Raising the bathing solution Ca2+ concentration from 1.08 to 5 mM produced a reversal of the opioid-induced block of K+ contractures. Finally it was shown that while opioids completely blocked K+ contractures, they did not produce any effect on caffeine contractures showing that opioids do not deplete intracellular Ca2+ stores or inhibit the release of Ca2+ from intracellular sarcoplasmic reticulum stores. It was concluded that several opioid drugs in very low concentrations block K+ contractures in frog's skeletal muscle by a nonstereospecific block of voltage-dependent slow calcium channels.

Animals↗
PubMed1987

Role of changes in [Ca2+]i in energy deprivation contracture.

Mechanisms of energy deprivation contracture were investigated in cultured chick embryo ventricular cells. In the presence of zero-extracellular-Na+, (choline chloride substitution)-nominal-zero-Ca2+ [( Ca2+] approximately 5 microM), exposure of ventricular cells to 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG)-zero-glucose solution resulted in the development of a contracture (video motion detector) in 5.9 +/- 0.5 minutes. Early after contracture development, the resupply of extracellular Na+, in the continued presence of CN + 2-DG, resulted in a rapid partial relaxation (t1/2 = 1.9 +/- 0.3 seconds), associated with an increase in 45Ca efflux, presumably due to transsarcolemmal Ca2+ extrusion due to Na+-Ca2+ exchange. Resupply of glucose and removal of CN + 2-DG, in the continued absence of Na+, resulted in an initially slower (t1/2 = 11.6 +/- 2.5 seconds), but more complete relaxation of contracture, which was not associated with increased Ca2+ efflux. Pretreatment with 20 mM caffeine delayed the onset of contracture (9.2 +/- 1.1 minutes) and resulted in a contracture that could not be relaxed by resupply of external Na+ only. Studies using the fluorescent Ca2+ probe indo 1 demonstrated that in zero-Na+-zero-Ca2+ solutions, contracture due to CN + 2-DG was associated with an initial rise in [Ca2+]i but that this did not account for all of contracture force development. In cells exposed to CN + 2-DG in the presence of normal extracellular Na+ and Ca2+ concentrations, a small rise in [Ca2+]i was associated with initial contracture development, consistently preceding the development of a larger accelerated contracture presumably due to ATP depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

Glucose flux rate regulates onset of ischemic contracture in globally underperfused rat hearts.

This study analyzes the importance of the source and rate of ATP production (glucose flux, glycogenolysis, and oxidative phosphorylation) in the prevention of ischemic contracture in isolated rat hearts. Ischemic contracture was initiated at about 10 minutes by buffer perfusion with nonglycolytic substrates whereas the addition of 11 mM glucose prevented contracture for 2 hours. Tissue values of ATP, phosphocreatine, and lactate could be dissociated from onset of ischemic contracture. In hearts perfused with acetate or free fatty acid, with 11 mM glucose, glycolytic ATP production was 2.3-2.8 mumol/g fresh wt/min; as initial rates of glycogenolysis fell, glycolysis was maintained by a steady increase of glucose flux to values in excess of 2 mumol ATP/g fresh wt/min. Decreasing the glucose flux by lowering the perfusate glucose or by the addition of 2-deoxyglucose precipitated ischemic contracture. When oxidative phosphorylation was further reduced by hypoxia, glucose still prevented ischemic contracture; however, when oxidative phosphorylation dropped to near zero (near-anoxic) rates, glycolysis was inhibited, and glucose could only delay ischemic contracture to about 45 minutes. Combined ATP production rates could be dissociated from contracture. The metabolic parameter that correlated best with prevention or delay of ischemic contracture was the rate of glycolytic flux from glucose, which in this model of global low-flow ischemia had to accelerate to provide a rate of ATP production from glucose in excess of 2 mumol/g fresh wt/min within 30 minutes of the start of ischemia to prevent ischemic contracture.

Acetates↗
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↗
PubMed1984

Contribution of intracellular stored calcium to contractile activation in contractures of stomach circular muscle of Bufo vulgaris formosus.

Contractile responses of stomach circular muscle of Bufo to high-K, to acetylcholine (ACh) in normal Ringer or in high-K solution, and to calcium in Ca-free high-K solution showed a phasic contraction which relaxed completely in 30-45 sec. K-induced contracture was abolished in Ca-free solution containing 1 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) within 20 sec, while ACh-induced contracture was not abolished and 10-25% of control tension was kept up to 40 sec. This response increased to 40-50% when all extracellular Na was replaced with tris(hydroxymethyl)-aminomethane (Tris). K-induced contracture was inhibited completely by 1 mM La. ACh-induced contracture in the muscle depolarized by high-K solution was dependent on the depolarization time, 0-10, 60-70, and nearly 100% of control after 1, 3, and 10 min depolarization, respectively. These ACh-induced contractures were not inhibited by 1 mM EGTA or La. All contractures mentioned above were markedly inhibited by 5 mM procaine. These results suggest that activation of both contractures induced by high-K and ACh were, at least partly, dependent on the Ca at the intracellular Ca storage sites. Ca-induced contracture was dependent on depolarization time as was ACh-induced contracture, when the muscle was depolarized by Ca-free high-K solution without pre-treatment with Ca-free Ringer solution. These results suggest that activation of Ca-contracture is also dependent on intracellular stored Ca.

Acetylcholine↗
PubMed1991

[Ischemic contracture of the forearm and hand. Staging and indications for surgical treatment].

Results of long-term follow up of 66 patients with ischemic contracture of the forearm and hand, all surgically treated in the "Unfallkrankenhaus Hamburg)) between 1961 and 1982, are presented. Whereas ischemic contracture of the forearm flexors resulted mainly from fractures, ischemic contracture of the intrinsic muscles of the hand was most often seen after pressure injuries. All patients in this study presented to us with fully established ischemic contractures. Muscle and nerve damage was retrospectively evaluated according to operative notes, and the degree of damage could be classified into four groups. Most frequently, neurolysis, scar excision and muscle-sliding operations were performed; furthermore, tendon lengthening, tendon transpositions, wrist arthrodesis and nerve grafting were indicated. Results were judged according to twelve separately measured functions, each measurement giving a possible score of three to six points. Muscle-sliding operations result in an improved score regardless of ischemic contracture stage. For a stage 2 contracture, a 20 point improvement can be expected. In stage 1 contracture--presenting with extension deficiency of four or more points--, complete recovery can be expected following a muscle-sliding operation. For isolated muscle injuries, tendon lengthening is recommended. For stage 2 contracture, the transposition of superficial to deep flexor tendons results in the same score as a muscle-sliding operation; however, the transposition procedure should be reserved for special indications. In stage 3 contracture, the muscle-sliding operation is the treatment of choice, with secondary procedures such as tendon transpositions and nerve grafts often being necessary. In stage 4 ischemic contracture, muscle-sliding operations may improve extension deficiency; however, wrist arthrodesis, especially in combination with extensor tendon transpositions, may be beneficial. No experience with free muscle transplantation was made during the study period.

Adolescent↗
PubMed1995

Preserving plantar flexion strength after surgical treatment for contracture of the triceps surae: a computer simulation study.

Contractures of the triceps surae commonly are treated by surgical lengthening of the gastrocnemius aponeurosis or the Achilles tendon. Although these procedures generally relieve contractures, patients sometimes are left with dramatically decreased plantar flexion strength (i.e., decreased capacity to generate plantar flexion moment). The purpose of this study was to examine the trade-off between restoring range of motion and maintaining plantar flexion strength after surgical treatment for contracture of the triceps surae. A computer model representing the normal moment-generating characteristics of the triceps surae was altered to represent two conditions: isolated contracture of the gastrocnemius and contracture of both the gastrocnemius and the soleus. The effects of lengthening the gastrocnemius aponeurosis and the Achilles tendon were simulated for each condition. The simulations showed that nearly normal moment-generating characteristics could be restored when isolated gastrocnemius contracture was treated with lengthening of the gastrocnemius aponeurosis. However, when isolated gastrocnemius contracture was treated with lengthening of the Achilles tendon, the moment-generating capacity of the plantar flexors decreased greatly. This suggests that lengthening of the Achilles tendon should be avoided in persons with isolated gastrocnemius contracture. Our simulations also suggest that neither lengthening of the gastrocnemius aponeurosis nor lengthening of the Achilles tendon by itself is an effective treatment for combined contracture of the gastrocnemius and soleus. Lengthening the gastrocnemius aponeurosis did not decrease the excessive passive moment developed by the contracted soleus. Lengthening the Achilles tendon restored the normal passive range of motion but substantially decreased the active force-generating capacity of the muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Achilles Tendon↗
PubMed1985

Classification and management of burned thumb contractures in children.

Based on the position of the thumb metacarpal, 102 burned thumb contractures in children were classified into four categories: adduction, opposition, extension and flexion. The contractures were further classified as mild, moderate or severe, based on the amount of motion lost. All thumbs were surgically released. Coverage was obtained with local flaps or Z-plasties, skin grafts or a combination of local flaps and skin grafts. Factors influencing the results were as follows: Classification category: Extension contractures generally did poorly, whereas flexion contractures did well. Severity of contracture: The more severe the contracture, the worse the final results. Complexity of contracture: Contractures with a subluxated or dislocated joint did not do as well as those with undisturbed bony alignment. Type of surgical release: There was a trend towards better results when skin grafts (as opposed to local flaps) were used, especially in the treatment of moderate and severe contractures.

Adolescent↗
PubMed1994

Natural history of uncorrected flexion contractures following total knee arthroplasty.

Over a 2-year period, 29 patients were identified that had preoperative flexion contractures less than 30 degrees and were not fully corrected to neutral following total knee arthroplasty. They were followed after surgery at 3, 6, and 12 months, and yearly thereafter with complete clinical and roentgenographic examinations to determine the natural history of the flexion contracture and its effect on the clinical outcome. The mean age of the 10 women and 19 men was 66 years (range, 47-80 years). The mean preoperative flexion contracture was 11 degrees (range, 5 degrees-30 degrees). The mean follow-up period was 33 months (range, 24-60 months). The mean values of the flexion contractures at each follow-up period were; immediately after surgery, 10.5 degrees; at 3 months, 5 degrees; at 6 months, 2 degrees; at 12 months, 1 degree; and at 24 months, 1 degree (P < .0001). Resolution of the flexion contracture did not vary between patients under and over the age of 65 years. There was no statistically significant difference in the residual flexion contracture when knees with preoperative contractures from 0 degrees to 14 degrees and 15 degrees to 30 degrees were compared. The clinical outcome was not affected by the residual flexion contracture after 6 months of follow-up evaluations. Significant improvements can occur after surgery with rehabilitation, and it appears that complete intraoperative correction is not necessary. There appears to be no difference in the natural history of flexion contractures with regard to age or severity up to 30 degrees.

Aged↗