[Why does the ischemic contracture occur only in children? Anatomical studies of the ischemic contracture].
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Adult↗
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Some factors affecting the time course of the recovery of contracture ability following a potassium contracture in frog striated muscle.
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Animals↗
Heat production during hypoxic contracture of rat myocardium.
Contracture due to hypoxia, to both oxygen and glucose deficiency, and to potassium chloride was induced in rat left ventricular papillary muscle preparations. Under contracture conditions, the sum of resting heat plus contracture heat was measured using Hill-type, planar vacuum-deposited thermopiles. On the basis of the measured total and initial heat output and the corresponding tension-time integral during single twitches under control conditions (Lmax, 21 degrees C, stimulus frequency 12/min), the expected heat output during contracture was calculated, assuming that the contracture tension is maintained by the same calcium-induced cross-bridge cycling as occurs in the single twitch response. With potassium chloride, the contracture tension was 1.33 +/- 0.27 g/mm2, a value which is similar to those found in hypoxic contracture and in contracture due to both oxygen and glucose deficiency. There was no significant difference between measured and calculated values for resting heat plus contracture heat (8.40 +/- 2.84 mW/g measured, 8.55 +/- 2.50 mW/g calculated); there was a linear correlation (r = 0.99) between predicted and measured values (P less than 0.05). The measured value for resting plus contracture heat in hypoxic contracture was 1.88 +/- 0.37 mW/g, whereas a value of 4.80 +/- 1.09 mW/g (P less than 0.005) was calculated on the basis of the twitch heat per tension-time integral and contracture tension (1.09 +/- 0.31 g/mm2). Contracture tension was 1.80 +/- 0.78 g/mm2 in contracture due to oxygen and glucose deficiency, whereas the value for resting plus contracture eat was 1.61 +/- 0.56 mW/g. The calculated resting plus contracture heat value for this preparation was significantly higher (7.45 +/- 3.75 mW/g; P less than 0.05). There was no significant regression between predicted and measured resting heat plus contracture heat in the hypoxic contracture preparations (slope not different from zero). In contracture due to oxygen and glucose deficiency, the linear regression had a slope of 6.06 (P less than 0.05). The results suggest that the potassium chloride contracture relies on cross-bridge cycling as in a twitch contraction, whereas hypoxic contracture and that due to oxygen and glucose deficiency may be explained by cross-bridge formations with no, or very low, heat production, i.e., contracture tensions due to hypoxia and to oxygen and glucose deficiency are maintained by rigor-like cross-bridge formation or by slowly cycling cross-bridges with a long time of cross-bridge attachment.
Animals↗
Studies on contractures induced in mouse diaphragm by caffeine and cupric and selenite ions.
Mouse diaphragm contractures induced by Cu2+, caffeine and selenite were studied comparatively. Both Cu2+- and caffeine-contractures were produced rapidly and relaxed spontaneously; the selenite-contracture occurred after a latent period of about 45 min and lasted for more than 3 hr. All contractures were myogenic, since neither d-tubocurarine nor tetrodotoxin prevented them. The susceptibility of these contractures to the depletion and replenishment of Ca2+ differed: the Cu2+-contracture increased proportionally with rising extracellular Ca2+ concentrations ranging from 2.5 to 12.5 mM and were abolished by 5 mM EGTA. Caffeine- and selenite-contractures were not affected by changes in extracellular Ca2+ concentration. The caffeine-contracture was abolished by EGTA in high concentration (30 mM) and the selenite-contracture was inhibited by 50 mM EGTA. After removal of Ca2+ with 5 mM EGTA, followed by replacement with 2.5 mM Ca2+ for 1 min, the Cu2(+)-contracture was fully restored. Caffeine- and selenite-contractures were restored only after a longer period (10-20 min) of re-exposure to Ca2+. These findings suggest that the Cu2(+)-contracture is dependent on external Ca2+ and probably caused by an increasing Ca2+ entry through sarcolemma. Caffeine- and selenite-contractures apparently result from internal Ca2+ release by sarcoplasmic reticulum. Substitution of either Sr2+ or Co2+ for Ca2+ fully supports the Cu2(+)-contracture. 45Ca2+ uptake and calcium content of the diaphragm were markedly increased by Cu2+ but not by selenite. Furthermore, the Cu2(+)-contracture was inhibited by exposing the outer membrane to trypsin, phospholipase C or saponin. The selenite-contracture was inhibited only by trypsin. The caffeine-contracture was unaffected by these treatments. These results support the notion that the Cu2(+)-contracture is induced by an increased entry of Ca2+ through the outer membrane. Cu2(+)-, caffeine- and selenite-contractures were respectively abolished, potentiated and unaffected by chronic denervation of the diaphragm. This and the other findings provide evidence that Cu2(+)-, caffeine- and selenite-contractures are induced in mouse diaphragm muscle via different sites of action.
Animals↗
Contractures in burn injury: defining the problem.
This study prospectively examined the incidence and severity of large joint contractures after burn injury and determined predictors of contracture development. Data were collected prospectively from 1993 to 2002 for consecutive adult burn survivors admitted to a regional burn center. Demographic and medical data were collected on each subject. The primary outcome measures included the presence of contractures, number of contractures per patient, and severity of contractures at each of four joints (shoulder, elbow, hip, knee) at time of hospital discharge. Logistic regression analysis was performed to determine predictors of the presence and severity of contractures and a negative binomial regression was performed to determine predictors of the number of contractures. Of the 985 study patients, 381 (38.7%) developed at least one contracture at hospital discharge. Among those with at least one contracture, the mean is three contractures per person. The shoulder was the most frequently contracted joint (38%), followed by the elbow (34%) and knee (22%). Most contractures were mild (60%) or moderate (32%) in severity. Statistically significant predictors of contracture development were length of stay (P < .005) and extent of burn (P = .033) and graft (P < .005). Predictors of the severity of contracture include graft size (P < .005), amputation (P = .034), and inhalation injury (P = .036). More than one third of the patients with a major burn injury developed a contracture at hospital discharge, which highlights the importance of therapeutic positioning and intensive therapy intervention during acute hospitalization. Furthermore, this challenges the burn care community to find new and better ways of preventing contractures after burn injury.
Adult↗
Development of ischemic contracture in isolated skeletal muscles: relation to the capacity for anaerobic glycolysis.
In order to evaluate the dependence of the rate of ischemic contracture development in isolated skeletal muscles on the capacity for anaerobic glycolysis, factors affecting ischemic contracture development were examined using rat soleus and quadriceps muscles. The contracture developed faster in slow-twitch oxidative (SO) fibers than in fast-twitch glycolytic (FG) fibers. In both types of fibers, the rate of contracture development was inversely related to the medium pH. Addition of lactate increased the rate of contracture development. In FG fibers, the lactate level during contracture was directly, and the glycogen level inversely, proportional to the medium pH. An increase in muscle lactate level by 4-h swimming accelerated the contracture development, and reduced further lactate accumulation during contracture. Types of exercise training known to influence the capacity for anaerobic glycolysis (interval training and repeated fast climbing and swimming) decreased the velocity of contracture development. Isoprenaline administration in vivo accelerated contracture development in association with reduced lactate level during contracture. Swimming training counterbalanced the action of isoprenaline. Adrenalectomy accelerated contracture development in SO fibers, and decreased lactate accumulation during contracture in FG fibers. In adrenalectomized rats, the effects of exercise were more pronounced in SO fibers than in FG fibers. These results indicate that the rate of contracture development in isolated skeletal muscle is inversely related to the capacity for anaerobic glycolysis.
Adrenalectomy↗
[Severe contracture of the proximal interphalangeal joint in Dupuytren's disease: does capsuloligamentous release improve outcome?].
Purpose. Evaluation of effectiveness of capsuloligamentous release in severe PIP joint contractures in Dupuytren's disease. Method. Prospective study to compare the clinical outcome of eleven patients with severe contracture of the PIP joint due to Dupuytren's disease, in whom an additional capsulotomy was performed to reduce a residual flexion contracture of the PIP joint of 20 degree and more after release and excision of all diseased fascia, with the outcome of 32 patients with severe contracture of the PIP joint due to Dupuytren's disease, in whom the PIP joint contracture could be reduced by fasciectomy alone. Preoperatively all patients had a severe flexion contracture (60 degrees or greater) of one PIP joint. All patients underwent standardized operative treatment and postoperative extension splinting program for six months. Follow-up examinations included assessment of active range of motion at two, four, ten, 16 and 24 weeks after surgery. Results. In the noncapsulotomy group, preoperative contracture averaged 70.6 degrees and intraoperative residual contracture averaged 2 degrees. In the capsulotomy group, preoperative contracture averaged 78.6 degrees. Intraoperative residual contracture averaged 61.8 degrees before and 2 degrees after capsulotomy. At the final follow-up examination, PIP joint flexion contracture averaged 15 degrees in the noncapsulotomy group compared to 16 degrees in the capsulotomy group. Conclusion. Residual flexion contracture of a PIP joint after release and excision of all diseased fascia in Dupuytren's disease can be reduced by capsuloligamentous release. The data of this study showed no significant differences in the outcome at the final follow-up examination between patients with and without capsulotomy. Therefore, we recommend capsulotomy as treatment of residual flexion contracture of the PIP joint in Dupuytren's disease.
Adult↗
A computer simulation of human walking in persons with joint contractures.
Joint contractures decrease the patient's ability to walk, but usually other parts of the body compensate the affected joint contractures. When we restore the gait performance in paraplegic patients by means of functional electrical stimulation, however, we cannot expect complications of compensation. A computer simulation was done to clarify how the contractures affect the gait pattern when no complications of compensation were expected. A seven-segment link mechanical model was used for simulation of human walking in the sagittal plane. In turn, using a personal computer stance and swing-leg joint contractures of the ankle, knee, and/or hip were simulated. When stance-leg contracture was simulated, step length became short with increasing hip flexion contracture. The trunk was tilted backward during knee flexion or ankle plantarflexion contracture simulation. When the swing-leg contracture was simulated, step length became short with increasing knee flexion contracture. We found that hip or knee flexion contracture of < or = 15 degrees, or ankle plantarflexion contracture of < 0 degrees was required to maintain positive step length and forward movement of the center of gravity. These findings suggest that 15 degrees of hip and knee flexion contracture, and 0 degrees of ankle plantarflexion contracture are critical when gait restoration is performed by functional electrical stimulation.
Ankle↗
[The pathogenic mechanism and prevention and treatment of muscle contracture after replantation of severed palm or wrist].
OBJECTIVE: To explore the pathogenic mechanism of intrinsic muscle contracture after replantation of severed palm or wrist, and put forward the prevention and treatment methods. METHODS: From 1985 to 1997, 48 cases were received replantation of severed palm or wrist, among them, 9 cases with thumb adductor contracture and 6 cases with intrinsic muscle contracture were occurred in different degree. Two cases with mild thumb adductor contracture were received conservative treatment, and 7 cases with moderate thumb adductor contracture and 6 cases with intrinsic muscle contracture were received operative treatment. The pathogenic mechanism, clinical results, and prevention methods were studied in those 15 cases. RESULTS: The postoperative function recovery was better in 4 cases, moderate in 5 cases with thumb adductor contracture, and better in 3 cases, moderate in 1 case with intrinsic muscle contracture, and moderate in 1 case, poor in 1 case with intrinsic muscle contracture of cord-like induration. Followed up 1 to 10 years, no recurrence was observed in all of 15 cases. The incidence and degree of thumb adductor contracture and intrinsic muscle contracture were closely related to the ischemia time of replanting graft. CONCLUSION: Prevention of thumb adductor contracture and intrinsic muscle contracture is most important in severed palm or wrist replantation. When the ischemia time of replanting graft is longer than 12 hours, the effective decompression in myofascial compartment is performed in time to reach satisfactory result.
Adult↗
Studies on the contracture of the mouse diaphragm induced by sodium selenite.
In this study, we found that sodium selenite was potent in inducing contracture of the mouse diaphragm. The possible mechanism of action of selenite was investigated. Contracture was induced by a direct action of selenite on the muscle membrane rather than that selenite enhanced transmitter release from the motor nerve terminals, since denervation, d-tubocurarine and tetrodotoxin did not inhibit the selenite-induced contracture. Although selenite decreased both the membrane potential and the amplitude of the muscle action potential, neither high K+ nor glycerol treatment, which closed the transverse tubule, reduced the selenite-induced contracture, suggesting that depolarization of the muscle membrane was not essential for the induction of the contracture. EGTA (1-50 mM) inhibited the selenite-induced contracture in a concentration-dependent manner. In contrast, varying the external Ca2+ concentrations from 10(-3) to 10 mM or raising Mg2+ concentration to 10 mM did not affect the contracture. Similarly, the contracture induced by caffeine was not affected by lowering the external Ca2+ concentration to 10(-3) mM but was completely inhibited by 30 mM EGTA. Selenite pretreatment markedly potentiated the caffeine contracture and prolonged treatment with caffeine inhibited the selenite contracture. All of these findings suggest that the selenite contracture was not dependent on external Ca2+ but was induced by the release of Ca2+ from internal membranes such as the sarcoplasmic reticulum. Pretreatment with trypsin, glutathione or cyanide blocked the selenite-evoked contracture. Therefore, we postulate that the selenite-induced contracture was induced by the initial binding of selenite to the sulfhydryl groups of the muscle membrane, which then triggered the release of Ca2+ from internal membranes such as the sarcoplasmic reticulum.
Animals↗
Modulation of ischaemic contracture in mouse hearts: a 'supraphysiological' response to adenosine.
While inhibition of ischaemic contracture was one of the first documented cardioprotective actions of exogenously applied adenosine, it is not known whether this is a normal function of endogenous adenosine generated during ischaemic stress. Additionally, the relevance of delayed contracture to postischaemic outcome is unclear. We tested the ability of endogenous versus exogenous adenosine to modify contracture (and postischaemic outcomes) in C57/Bl6 mouse hearts. During ischaemia, untreated hearts developed peak contracture (PC) of 85 +/- 5 mmHg at 8.9 +/- 0.8 min, with time to reach 20 mmHg (time to onset of contracture; TOC) of 4.4 +/- 0.3 min. Adenosine (50 microm) delayed TOC to 6.7 +/- 0.6 min, as did pretreatment with 10 microm 2-chloroadenosine (7.2 +/- 0.5 min) or 50 nm of A(1) adenosine receptor (AR) agonist N(6)-cyclohexyladenosine (CHA) (6.7 +/- 0.3 min), but not A(2A)AR or A(3)AR agonists (20 nm 2-[4-(2-carboxyethyl) phenethylamino]-5' N-methylcarboxamidoadenosine (CGS21680) or 150 nm 2-chloro-N(6)-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA), respectively). Adenosinergic contracture inhibition was eliminated by A(1)AR gene knockout (KO), mimicked by A(1)AR overexpression, and was associated with preservation of myocardial [ATP]. This adenosine-mediated inhibition of contracture was, however, only evident after prolonged (10 or 15 min) and not brief (3 min) pretreatment. Ischaemic contracture was also insensitive to endogenously generated adenosine, since A(1)AR KO, and non-selective and A(1)AR-selective antagonists (50 microm 8-sulphophenyltheophylline and 150 nm 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX), respectively), all failed to alter intrinsic contracture development. Finally, delayed contracture with A(1)AR agonism/overexpression or ischaemic 2,3-butanedione monoxime (BDM; 5 microm to target Ca(2+) cross-bridge formation) was linked to enhanced postischaemic outcomes. In summary, adenosinergic inhibition of contracture is solely A(1)AR mediated; the response is 'supraphysiological', evident only with significant periods of pre-ischaemic AR agonism (or increased A(1)AR density); and ischaemic contracture appears insensitive to locally generated adenosine, potentially owing to the rapidity of contracture development versus the finite time necessary for expression of AR-mediated cardioprotection.
2-Chloroadenosine↗
A local anesthetic, tetracaine, similarly inhibits Ag+ and K+ contractures in frog skeletal muscle.
To evaluate usefulness of Ag+ contracture as a tool for elucidating the mechanism underlying the excitation-contraction coupling, the effects of tetracaine on Ag+ contracture were compared with those on K+ and caffeine contractures in frog skeletal muscle. Tetracaine less than 100 microM shortened the duration of 120 mM K+ contracture, without affecting tension amplitude. At higher concentrations of tetracaine, K+ contracture was inhibited dose-dependently and the duration shortened. Treatment of the fibers with 20-500 microM tetracaine for 3 min did not block the contracture induced by 25 mM caffeine. Effects of tetracaine on Ag+ contracture were similar to those on K+ contracture. In the presence of 200 microM tetracaine, 41% inhibition was observed in 120 mM K+ contracture, while 43% in 100 microM Ag+ contracture. Also, 200 microM tetracaine completely inhibited the contractures induced by 40 mM K+ or 5 microM Ag+. These findings suggest that the Ag+ may induce contractures via its action on the T/SR junction, not a direct action on the SR. Therefore, understanding the mechanism involved in the development of Ag+ contracture would be helpful to elucidate the mechanism of excitation-contraction coupling.
Action Potentials↗
Severe contractures of the proximal interphalangeal joint in Dupuytren's disease: combined fasciectomy with capsuloligamentous release versus fasciectomy alone.
Severe proximal interphalangeal joint contracture in Dupuytren's disease presents a frustrating problem for hand surgeon. Some surgeons argue for fasciectomy alone, avoiding violation of the proximal interphalangeal joint, which may prolong morbidity and result in permanent limitation of flexion; this loss of flexion can be more disabling than a mild flexion contracture. Others favor capsulotomy in addition to fasciectomy, especially for severe contractures, to obtain additional release, arguing that one cannot completely correct secondary contracture by fasciectomy alone. We performed a retrospective review of severe flexion contractures (60 degrees or greater) involving 42 proximal interphalangeal joints in 28 patients with Dupuytren's disease. Twenty-seven joints in 18 patients underwent fasciectomy alone, and 15 joints in 10 demographically similar patients underwent capsulotomy in addition to fasciectomy. In the noncapsulotomy group, preoperative contracture averaged 78.4 degrees. Postoperative contracture averaged 36.6 degrees, with a 53 percent improvement. In the capsulotomy group, preoperative joint contracture averaged 82.5 degrees. Postoperative contracture averaged 36.8 degrees, with a 55 percent improvement. Intraoperative residual contracture for 21 of the 27 joints in the noncapsulotomy group averaged 7 degrees compared with 8 degrees for 9 of the 15 joints in the capsulotomy group. Preoperative proximal interphalangeal joint flexion averaged 100.6 degrees in the noncapsulotomy group and 98.6 degrees in the capsulotomy group. Postoperative flexion averaged 92.2 degrees in the noncapsulotomy group, which was 91.7 percent of preoperative flexion, and 82.7 degrees, which was 83.9 percent of preoperative flexion, in the capsulotomy group. No statistically significant difference was seen in the percentage of contracture correction in the capsulotomy group compared with the noncapsulotomy group at follow-up. The degree of correction initially obtained at surgery using either method was not maintained during the short follow-up period. There was a significant decrease in postoperative proximal interphalangeal joint flexion compared with preoperative flexion following either surgical approach; however, there was no significant difference between the two groups with respect to the percentage of flexion lost. Complications developed in both groups but tended to occur more commonly in the capsulotomy group. This study failed to show any advantage to capsuloligamentous release in addition to fasciectomy in treating severe proximal interphalangeal joint contracture due to Dupuytren's disease.
Acute Disease↗
Orbital socket contracture: a complication of inflammatory orbital disease in patients with Wegener's granulomatosis.
AIM: To describe the clinical characteristics of orbital socket contracture in patients with Wegener's granulomatosis (WG). METHODS: A retrospective cohort study The medical records of 256 patients with WG examined at the National Institutes of Health from 1967 to 2004 were reviewed to identify patients with orbital socket contracture. Details of the orbital disease including Hertel exophthalmometry readings, radiological findings, and results of eye examinations were recorded. Orbital socket contracture was defined as orbital inflammation with proptosis followed by the development of enophthalmos and radiographic evidence of residual fibrotic changes in the orbit. To examine for risk factors in the development of a contracted orbit, patients with orbital socket contracture were compared to patients without contracture with respect to multiple variables including history of orbital surgery, orbital disease severity, and major organ system involvement. The main outcome measures were the clinical characteristics of orbital socket contracture associated with inflammatory orbital disease in patients with WG. RESULTS: Inflammatory orbital disease occurred in 34 of 256 (13%) patients and detailed clinical data on 18 patients were available and examined. Orbital socket contracture occurred during the clinical course in six patients; the features included restrictive ophthalmopathy (five), chronic orbital pain (three), and ischaemic optic nerve disease (two) resulting in blindness (no light perception) in one patient. The orbital socket contracture occurred within 3 months of treatment with immunosuppressive medications for inflammatory orbital disease in five patients and was not responsive to immunosuppressive medications. The median degree of enophthalmos in the contracted orbit compared with the fellow eye was 2.8 mm (range 1.5-3.5 mm) by Hertel exophthalmometry. There were no risk factors that predicted development of orbital socket contracture. CONCLUSIONS: In six patients with WG and active inflammatory orbital disease, orbital socket contracture occurred during the treatment course with systemic immunosuppressive medications. The orbital socket contracture, presumably caused by orbital fibrosis, led to enophthalmos, restrictive ophthalmopathy, chronic orbital pain, and optic nerve disease and was not responsive to immunosuppressive therapy. Orbital socket contracture has not been previously reported as a complication of inflammatory orbital disease associated with WG and was an important cause of visual morbidity in our cohort of patients.
Adolescent↗
Ryanodine contracture threshold times for diagnosis of malignant hyperthermia susceptibility: an experimental approach from a single laboratory.
STUDY OBJECTIVES: To define threshold times for ryanodine contracture testing (RCT) using skeletal muscle specimens from malignant hyperthermia-susceptible (MHS) and control individuals. DESIGN: Prospective study. SETTING: Malignant hyperthermia (MH) laboratory at a university hospital. PATIENTS: 8 patients with previous fulminant MH and 53 control patients undergoing in vitro contracture test (IVCT) for diagnosis of MH susceptibility. INTERVENTIONS: Biopsies of the quadriceps femoris muscle were performed with a 3-in-1 nerve block, with spinal anesthesia, or with trigger-free general anesthesia. MEASUREMENTS AND MAIN RESULTS: Patients were classified as MHS, MH normal (MHN), or MH equivocal (MHE) by the IVCT according to the protocol of the European MH Group (EMHG). Ryanodine 1 microM was added as a bolus to the organ bath to extra vital muscle specimens. Contracture levels were defined as: 1 = start of contracture (OT; min); 2 = time (min) to reach a contracture of 2 mN, and 3 = time (min) to reach a contracture of 10 mN. The effects of ryanodine on contracture responses were measured. Ryanodine induced contractures in all specimens. MHS specimens reached all defined contracture levels significantly sooner than did the controls. Ryanodine contracture test enables a clear discrimination of MHS specimens from controls at contracture levels of OT and 2 mN, whereas at 10 mN a small overlap was observed. CONCLUSIONS: Using this test, which is an experimental approach from a single laboratory, an assignment to MHS or MHN is possible. To define contracture levels for RCT more precisely and to agree on commonly used thresholds, multicenter studies with larger numbers of patients are required.
Adolescent↗
Multicentre evaluation of in vitro contracture testing with bolus administration of 4-chloro-m-cresol for diagnosis of malignant hyperthermia susceptibility.
BACKGROUND AND OBJECTIVE: The in vitro contracture test with halothane and caffeine is the gold standard for the diagnosis of susceptibility to malignant hyperthermia (MH). However, the sensitivity of the in vitro contracture test is between 97 and 99% and its specificity is 78-94% with the consequence that false-negative as well as false-positive test results are possible. 4-Chloro-m-cresol is potentially a more specific test drug for the in vitro contracture test than halothane or caffeine. This multicentre study was designed to investigate whether an in vitro contracture test with bolus administration of 4-chloro-m-cresol can improve the accuracy of the diagnosis of susceptibility to MH. METHODS: Three hundred and fifty-two patients from 11 European MH laboratories participated in the study. The patients were first classified as MH susceptible, MH normal or MH equivocal by the in vitro contracture test according to the European MH protocol. Muscle specimens surplus to diagnostic requirements were used in this study (MH susceptible = 103 viable samples; MH equivocal = 51; MH normal = 204). 4-Chloro-m-cresol was added to achieve a concentration of 75 micromol L(-1) in the tissue bath. The in vitro effects on contracture development and muscle twitch were observed for 60 min. RESULTS: After bolus administration of 4-chloro-m-cresol, 75 micromol L(-1), 99 of 103 MH-susceptible specimens developed marked muscle contractures. In contrast, only two of 204 MH-normal specimens showed an insignificant contracture development following 4-chloro-m-cresol. From these results, a sensitivity rate of 96.1% and a specificity rate of 99.0% can be calculated for the in vitro contracture test with bolus administration of 4-chloro-m-cresol 75 micromol L(-1). Forty-three patients were diagnosed as MH equivocal, but only specimens from 16 patients developed contractures in response to 4-chloro-m-cresol, indicating susceptibility to MH. CONCLUSIONS: The in vitro contracture test with halothane and caffeine is well standardized in the European and North American test protocols. However, this conventional test method is associated with the risk of false test results. Therefore, an improvement in the diagnosis of MH is needed. Regarding the results from this multicentre study, the use of 4-chloro-m-cresol could increase the reliability of in vitro contracture testing.
Biopsy↗
The time course of potassium contractures of single muscle fibres.
1. At 3 degrees C the long duration of potassium contractures and the delay in the repriming process allow one to carry out solution changes while the responses are still in progress, making it possible to study the processes that determine the contracture time course.2. The contractures can be cut short by suddenly lowering the external potassium concentration to normal values. Re-exposure to the high potassium medium causes the fibres to redevelop tension, in a way that depends on the time at which the original response was interrupted.3. The period of interruption can be prolonged beyond the duration of the original contracture without affecting the second response. This redevelopment of tension is not associated with repriming since this process is much delayed. For thirty-five interrupted contractures the mean of the sum of the time integrals of tension in the two responses amounts to 98% of the mean of the time integral of tension in the uninterrupted contractures.4. Addition of tetracaine or removal of calcium also causes the fibre to relax from a potassium contracture, although at a slower rate than that obtained by lowering the external potassium concentration. In these cases, however, no tension is redeveloped when the standard contracture medium is reapplied. When calcium in the contracture medium is replaced by nickel, the contracture time course is not diminished.5. The results obtained with potassium contractures clearly show that the contractile activator is released continuously during a contracture. The prolonged time course of contractile responses in the cold can be explained at least in part by a prolonged release of calcium. There are no reasons to believe that at low temperature there is more activator available for release, and therefore it can be concluded that in the cold release of calcium proceeds at a slower rate.6. Release of calcium is under control of the membrane potential, and its time course can be determined either by a fixed store of available calcium that is depleted or by a membrane mechanism which is activated upon depolarization and later inactivates with time. The evidence obtained in the present work does not allow one to decide in favour of one of these two possibilities. However, the fact that contractures are prolonged in the cold, and the finding that repriming is delayed, can be utilized in further studies to clarify the mechanism that controls the release of calcium.
Anesthesia, Local↗
[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↗