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The management of post-prostatectomy vesical neck contracture.

Current evidence suggests that the small fibrous hyperplastic intraurethral prostate traumatized by wide extensive electroresection is the most important etiologic factor in post-prostatectomy vesical neck contracture. The preferred mode of management has not been well defined. Although transurethral resection is most often used recurrent contractures occur frequently. We report the complete objective and symptomatic relief of obstruction in 8 patients with post-prostatectomy bladder neck contracture treated with cold knife incision. This simple technique appears to obviate recurrent contracture and may well be the treatment of choice for this condition.

Follow-Up Studies↗

Adrenaline diminishes K+ contractures and Ba2+-current in chicken slow skeletal muscle fibres.

The effects of adrenaline and the beta-adrenergic agonist isoprenaline on K+-evoked tension (K+-contracture) and Ba2+ current were investigated in chicken slow (anterior latissimus dorsi (ald)) muscle using isometric-tension measurements and current recording. Addition of adrenaline (10(-7) - 10(-5) M) or isoprenaline (10(-6) - 10(-5) M) to the bath reduced the amplitude of the K+-contractures. These effects were blocked by the beta-antagonist propranolol (5 x 10(-6) M). External application of a cAMP analogue (8-bromo cyclic AMP; 1 x 10(-4) M) also decreased the amplitude of the K+-contractures. To analyze the possible relationship between the induced tension reduction and effects on sarcolemmal Ca2+ channels, a slow action potential and a slow inward membrane current were studied in intact ald chicken muscle fibres. When the ald muscle was immersed in a Na+- and Cl--free solution containing Ba2+ and depolarizing pulses were delivered from a -80 mV holding potential, the muscle fibres exhibited a small, slow Ba2+-dependent potential (observed at about -26 mV, peak amplitude, around -10 mV). The response was blocked by the addition of Co2+ (5 mM) or Cd2+ (2 mM). Using the three-microelectrode voltage-clamp technique, a slow inward membrane current underlying the Ba2+ potential could be discerned. The current had a mean threshold of -60 mV, reached maximum at about -5 mV and ranged from ca. 9 to 19 pA/cm2 (depending on the external Ba2+ concentration). It had a mean reversal potential of +45 mV. The Ba2+ inward current was diminished when adrenaline or isoprenaline was added to the bath (1 x 10(-5) M); however, this decrease did not occur when propranolol was present (5 x 10-6 M). These results suggest that the decreases in the tension of K+-contractures induced by adrenaline and isoprenaline may occur through beta-adrenergic effects on sarcolemmal Ca2+ channels in ald chicken slow muscle fibres.

Action Potentials↗

Electromyographic activity of the jaw-closing muscles during jaw opening--comparison of cases of masseter muscle contracture and TMJ closed lock.

Contracture of jaw-closing muscles is one of the causes of limitations of jaw opening. In contracture patients who have no history of trauma or infection, it is not easy to distinguish contracture from temporomandibular joint (TMJ) closed lock (TCL). The purpose of this study was to clarify whether there is any difference between electromyographic (EMG) activities of jaw muscles during jaw opening in patients with TCL and patients with masseter muscle contracture (MMC). The MMC-patient group consisted of one male and 11 females with no history of trauma or infection. The TCL-patient group consisted of one male and 11 females. Ten of the MMC patients showed certain types of EMG activities in masseter muscles (and eight in temporal muscles) during jaw opening. However, particular EMG activities were not observed in most of the TCL patients. The integral values in masseter muscles and in temporal muscles at the maximum opening position were significantly higher in the MMC-patient group than those in the TCL-patient group. These findings demonstrate that the EMG pattern of MMC patients without a history of trauma or infection is different from that of TCL patients. Therefore, EMG analysis of jaw-closing muscles during jaw opening is expected to be useful for differential diagnosis between MMC and TCL.

Adolescent↗

[Autologous tissue transplantation (TRAM/DIEP) as an option of therapy in capsular contracture].

Free microvascular abdominal tissue transfer (TRAM/DIEP) has become standard in breast reconstruction after mastectomy. A new indication for abdominal tissue transfer is severe capsular contracture after augmentation by implants. Capsular contracture following aesthetic or reconstructive augmentation mammaplasty occurs in only a small percentage of cases, but warrants adequate therapy. Between 1999 and 2003, six patients with an average age of 35 years with symptomatic capsular contracture after augmentation mammaplasty underwent autologous tissue transfer with the free TRAM/DIEP flap. The flap was harvested either with a perforator of the deep epigastric artery (DIEP) or as muscle sparing flap (TRAM) and was anastomosed to vessels of the subscapular system. Operation time was reduced by operating with two teams. Besides minor dog-ear deformities at the donor sites, no complications were noted. Postoperatively, neither, instability of the abdominal wall nor flap loss was seen. In some cases, a secondary mastopexy was necessary. Aesthetic results concerning natural feeling and breast symmetry were graded as excellent. In our experience, the free microvascular transfer of abdominal tissue (TRAM/DIEP flap) offers a treatment option for patients seeking alternatives other than repeated capsulectomies and implant changes for severe capsular contracture.

Adult↗

Effect of diisopropylfluorophosphate and soman on rat skeletal muscle contracture during tetanic stimulation.

A number of reports have documented the myopathy that accompanies exposure to irreversible acetylcholinesterase inhibitors. However, less information is available on the functional consequences of the myopathy. The purpose of this study was to examine the effects of diisopropylfluorophosphate (DFP) and soman on skeletal muscle contracture. Rats were given daily doses of DFP or soman, and the tetanic contracture of the triceps surae muscles was recorded at various exposure periods up to 20 d. DFP decreased tetanic contracture during 5-Hz stimulation. Increased stimulation up to 50 Hz did not enhance the effect. The muscles showed the greatest deficit on d 5. Continued dosing produced a slightly attenuated effect. Soman produced a frequency-dependent increase in muscle contracture. The increase was greatest on d 2 and 4, but remained elevated over the 20-d study. These results show that two drugs that presumably both raised levels of transmitter in the synaptic cleft as a result of esterase inhibition can produce either enhanced or decreased muscle contraction.

Animals↗

Caffeine- and potassium-induced contractures of frog striated muscle fibers in hypertonic solutions.

The effect of hypertonic solutions on the caffeine- and KCl-induced contractures of isolated fibers of frog skeletal muscle was tested. Hypertonic solutions, twice the normal osmotic strength, prepared by adding NaCl or sucrose, potentiate the caffeine-induced contractures. The fibers may develop tensions of 3.6 kg/cm(2) of fiber transverse section. The same hypertonic medium reduced the peak tension of KCl-induced contractures. Thus the hypertonic condition does not affect the contractile mechanism itself. These findings give further support to the view that the differential effect of hypertonic solution is on the excitation-contraction coupling mechanism. Extracellular calcium is not essentially required for the first few of a series of caffeine-induced contractures either in hypertonic or in isotonic solutions.

Animals↗

In vitro effect of ephedrine, adrenaline, noradrenaline and isoprenaline on halothane-induced contractures in skeletal muscle from patients potentially susceptible to malignant hyperthermia.

We have measured the effects of ephedrine, adrenaline, noradrenaline and isoprenaline on halothane-induced contractures in muscle biopsies from patients potentially susceptible to malignant hyperthermia (MH). At concentrations of 4-24 mmol litre-1, ephedrine induced in vitro contractures in halothane 0.44 mmol litre-1-prechallenged muscle, whilst adrenaline, noradrenaline and isoprenaline had no effect. There was a shift of the ephedrine concentration-response curve to the left and an increased maximum muscle contracture in the MH susceptible group compared with the MH negative group (P < 0.001). We conclude that ephedrine increased halothane-induced muscle contractures in vitro either by an unknown pharmacological mechanism or by an adrenergic stimulation which was different from those of the other investigated adrenoceptor agonists.

Dose-Response Relationship, Drug↗

Determinants of hypoxic contracture in isolated heart muscle preparations.

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

Animals↗

Between-center variability of results of the in vitro contracture test for malignant hyperthermia susceptibility.

UNLABELLED: The in vitro contracture test (IVCT) remains the standard test for the diagnosis of malignant hyperthermia (MH) susceptibility. The aim of this study was to investigate whether results of the IVCT varied between two diagnostic centers. The study took place at the national MH centers in Denmark and Sweden. Forty-three patients investigated for MH gave informed consent to have four extra muscle specimens excised. These were sent to the other center and immediately used for a parallel IVCT, according to the protocol of the European MH Group. Results of the IVCTs performed in the two centers on muscle samples from the same patients were compared. Each patient was assigned a diagnosis according to the result obtained in the "mother-center." Identical diagnostic results were obtained for 56% of the patients. The differing diagnostic outcomes were almost exclusively seen in cases with contractures of <5 mN (0.5 g) and abnormal results in only one or two muscle strips. We suggest different criteria for the interpretation of results for clinical and scientific purposes. The clinical criteria should remain unchanged. The scientific designation of susceptibility should be used in cases with contractures of > or =5 mN and abnormal results in at least 75% of the tested muscle strips. IMPLICATIONS: The diagnostic outcomes of tests for malignant hyperthermia susceptibility were compared between two laboratories by using muscle tissue from the same patients. Identical outcomes were found for 56% of the patients. Almost all diverging outcomes were seen in cases with a few small contractures near the cutoff limit. Different diagnostic criteria for clinical and scientific purposes are suggested.

Adolescent↗

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

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

Anesthetics↗

No relationship between fiber type and halothane contracture test results in malignant hyperthermia.

Previous studies in cat, rat, and swine have implicated fiber type as influencing the halothane and caffeine contracture test used to diagnose malignant hyperthermia (MH). The authors performed fiber type analysis using myosin ATPase stains on 31 fascicles of skeletal muscle from nine patients following contracture testing. There was no significant difference in fiber type composition between fascicles from MH negative (n = 5) and MH positive (n = 4) patients. Furthermore, examining each of the 31 fascicles, the authors found no correlation (P greater than .05) of contracture magnitude with percentage of either Type I or Type II fibers using the Pearson Product-Moment correlation calculation. The authors conclude that fiber type composition does not influence contracture test results in human biopsies.

Adenosine Triphosphatases↗

Chlorocresol, an additive to commercial succinylcholine, induces contracture of human malignant hyperthermia-susceptible muscles via activation of the ryanodine receptor Ca2+ channel.

BACKGROUND: A defect in the ryanodine (Ry1) receptor Ca2+ channel has been implicated as one of the possible underlying causes of malignant hyperthermia (MH), a pharmacogenetic disorder characterized by sustained muscle contracture. The disease is triggered by common halogenated anesthetics and skeletal muscle relaxants, such as succinylcholine. This study tested whether the functional properties of the Ry1 receptor Ca2+ channel are affected by chlorocresol, a preservative added to a commercial preparation of succinylcholine (Midarine) and other parenteral compounds. METHODS: In vitro contracture testing was carried out on muscle biopsies from malignant hyperthermia-susceptible (MHS) and -negative (MHN) individual according to the protocol of the European MH group. Ca2+ flux studies on isolated rabbit sarcoplasmic reticulum fractions were measured spectrophotometrically by following the A710-790 of the Ca2+ indicator antipyrylazo III. RESULTS: Chlorocresol causes muscle contracture in MHS muscles at a concentration of 25-50 microM and potentiates the caffeine contracture response in human MHS muscles. Sub-threshold (20 microM) concentrations of chlorocresol increase both the Kd and the Vmax of caffeine-induced Ca2+ release from isolated rabbit terminal cisternae. CONCLUSIONS: These data suggest that, in muscle from MHS individuals, the enhanced Ca2+ released from the sarcoplasmic reticulum may not be due to the effect of succinylcholine alone but rather to the action of the preservative chlorocresol added to the drug.

Animals↗

Treatment of normal skeletal muscle with FK506 or rapamycin results in halothane-induced muscle contracture.

BACKGROUND: FKBP12 is a protein that is closely associated with the ryanodine receptor type 1 of skeletal muscle and modulates Ca2+ release by the channel. The immunosuppressants FK506 and rapamycin both bind to FKBP12 and in turn dissociate the protein from the ryanodine receptor. By treating healthy human skeletal muscle strips with FK506 or rapamycin and then subjecting the strips to the caffeine-halothane contracture test, this study determined that FK506 and rapamycin alter the sensitivity of the muscle strip to halothane, caffeine, or both. METHODS: Skeletal muscle strips from 10 healthy persons were incubated in Krebs medium equilibrated with a 95% oxygen and 5% carbon dioxide mixture, which contained either 12 microM FK506 (n = 8) or 12 microM rapamycin (n = 6), for 15 min at 37 degrees C. The strips were subjected to the caffeine-halothane contracture test for malignant hyperthermia according to the European Malignant Hyperthermia Group protocol. RESULTS: Treatment of normal skeletal muscle strips with FK506 and rapamycin resulted in halothane-induced contractures of 0.44+/-0.16 g and 0.6+/-0.49 g, respectively, at 2% halothane. CONCLUSIONS: The results obtained show that pre-exposure of healthy skeletal muscle strips to either FK506 or rapamycin is sufficient to give rise to halothane-induced contractures. This is most likely caused by destabilization of Ca2+ release by the ryanodine receptor as a result of the dissociation of FKBP12. This finding suggests that a mutation in FKBP12 or changes in its capacity to bind to the ryanodine receptor could alter the halothane sensitivity of the skeletal muscle ryanodine receptor and thereby predispose the person to malignant hyperthermia.

Adolescent↗

Insulin worsens ischemia-induced myocardial contracture in the isolated rat heart.

We used a modification of Langendorff's isolated perfused nonworking rat-heart model to study the effects of diabetes, insulin-treated diabetes, and hyperinsulinemia on left ventricular pressure, force of ventricular contraction, and myocardial contracture, before, during, and after 20 min of complete normothermic global ischemia. Untreated diabetic rat hearts behaved the same as normal hearts, but insulin-treated diabetic hearts had more ischemic and postischemic contracture (p less than .01), and less return of left ventricular function. Chronic insulin treatment potentiated ischemic contracture in diabetic and nondiabetic rat hearts. These results support the hypotheses that insulin can increase Ca++ actin-myosin ATPase activity, and increase the affinity of myofibrillar receptors for calcium, which may lead to increased ischemic contracture. Insulin as a risk factor in myocardial ischemia, cardiothoracic surgery and cardiac resuscitation, and other pathogenetic factors of "stone heart" development, deserve further investigation.

Animals↗

Effects of trimetazidine on ischemic contracture in isolated perfused rat hearts.

Trimetazidine (1-[2,3,4-trimethoxibenzyl)]-piperazine, TMZ) is a drug with a proposed metabolically based antiischemic action. Because ischemic contracture is a serious complication of ischemia and is considered metabolic in origin, we studied the effect of trimetazidine (TMZ) on development of ischemic contracture in experimental low-flow ischemia. TMZ was either added to the perfusion fluid or given as pretreatment to the donor rats. Langendorff-perfused isolated rat hearts were submitted to 30-min subtotal global ischemia (residual flow = 0.2 ml/min, n = 6 per group) (normal flow = 12.4 +/- 0.8 ml/min, heart fresh weight = 0.9 +/- 0.3 g). Ischemic contracture was measured by a water-filled intraventricular balloon. Thereafter, the hearts were reperfused for 20 min and recovery of intraventricular pressure was monitored. Furthermore, because the mechanisms of action of TMZ may involve cellular energy metabolism, we assessed throughout glycolytic flux by collecting the coronary effluent every 5 min during control perfusion, ischemia, and reperfusion periods. Animals from the pretreated groups received TMZ [3 mg/kg orally (p.o.) twice daily] for 5 days. Animals from the control group received placebo for the same time period. Concentrations of 10(-6) and 10(-4) M were used when the drug was added to the perfusate. In our experimental conditions, TMZ pretreatment alone had no measurable cardioprotective effect, but addition to the perfusate of TMZ 10(-6) M, approximately a therapeutic concentration in humans, reduced ischemic contracture in both pretreated and control groups and improved postischemic recovery of developed pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Propranolol diminishes cardiac hypertrophy but does not abolish acceleration of the ischemic contracture in hyperthyroid hearts.

This study was undertaken to define the contributions of left ventricular hypertrophy (LVH) and increased adrenergic activity to the acceleration of ischemic contracture (IC) that occurs in chronic hyperthyroid rat heart. Acute and chronic hyperthyroidism (THYR) were induced by thyroxine administration for 2 and 14 days, respectively, and normal animals (NORM) served as controls. Isolated hearts were perfused in a Langendorff mode. NORM alpha acute, n = 6; THYR alpha acute, n = 8; and THYR alpha, n = 13; and NORM alpha, n = 13 were subjected to 20-min zero-flow global ischemia (I) and 45-min reperfusion (R). Additional THYR and NORM hearts treated with propranolol (prop) were subjected to 30-min I; THYR beta prop, n = 6 and NORM beta prop, n = 8, and THYR beta, n = 6, NORM beta, n = 8 served as controls. Acceleration of IC was measured by the time to peak contracture (Tmax). Left ventricular hypertrophy (LVH) was assessed by the ratio of left ventricular weight in milligrams (LVW) to animal body weight (BW) in grams. Cardiac hypertrophy developed in chronic but not acute hyperthyroidism. Propranolol reduced the extent of LVH. Contracture occurred earlier in chronic than in acute hyperthyroid and normal hearts. Propranolol did not alter contracture. In conclusion, IC is accelerated by thyroxine administration, and this is probably not due to LVH or increased beta-adrenergic activity. Propranolol diminishes LVH in hyperthyroidism.

Adrenergic beta-Antagonists↗

Functional results after treatment of Volkmann's ischemic contracture: a long-term followup study.

The main objective of this retrospective study was to evaluate the long-term functional outcome in patients treated for Volkmann's ischemic contracture. In this study, functional outcome (measured as mobility, grip strength, and sensibility) and arm length difference after treatment of Volkmann's ischemic contracture were analyzed and discussed. Twenty-five patients treated between 1969 and 2001 were evaluated. The method of treatment was related to the severity of the infarction, ranging from conservative to free vascularized muscle transplantation. Although the study population was small, we could observe a wide range of functional outcome. Substantial improvement of function was obtained in patients who had free vascularized muscle transplantation. Unfortunately in one patient with an occlusion of the distal brachial artery and an insufficient flow through the collateral circulation of the radial artery, the gracilis muscle was lost. Tendon lengthening had unsatisfactory results because of recurrence of the contracture. Excision of fibrotic muscle tissue, neurolysis and tenolysis sometimes combined with a tendon transfer gave good hand function results in patients with sufficient remaining muscle tissue. In most of the patients in whom the contracture developed during childhood, a difference in forearm length was observed.

Compartment Syndromes↗

Matrix metalloproteinases, tissue inhibitors of metalloproteinases, aminoterminal propeptide of procollagen type III, and hyaluronan in sera and tissue of patients with capsular contracture after augmentation with Trilucent breast implants.

In various fibrotic diseases, matrix metalloproteinases (MMPs) and their natural inhibitors, the tissue inhibitors of metalloproteinases (TIMPs), play an important role. In our study, serum concentrations of MMP-1, MMP-2, MMP-9, TIMP-1, and TIMP-2 were determined by enzyme-linked immunosorbent assay in 17 female patients with Baker grade II (n =9), III (n =7), and IV (n =1) capsular contracture after bilateral cosmetic mamma augmentation with Trilucent implants (AEI, Inc., Caversham, United Kingdom). Samples of capsular tissue for standard histology and immunohistochemistry were obtained from all patients. Sera from 20 female patients who had plastic surgery for reduction mammaplasty were used as the control group. The aminoterminal propeptide of procollagen type III (PIIINP) and hyaluronan were analyzed as markers for fibrogenesis in both groups, too. Statistical analysis was performed using the Mann-Whitney test and Spearman rank correlation. Patients with capsular contracture presented significantly higher concentrations of TIMP-1 and TIMP-2 in their sera than did the control group (p < 0.05), which correlated with Baker grade (r = 0.7 versus r = 0.65; p < 0.05). The concentration of MMP-2 was significantly higher in the sera of patients with capsule fibrosis, whereas there were no significant differences in MMP-1, MMP-9, and PIIINP serum concentrations. Patients with capsule fibrosis had a significantly lower MMP-to-TIMP ratio (1.1 +/- 0.4, p <0.05) than the control group (1.5 +/- 0.4), which correlated with the Baker classification (r =0.7; p <0.05). The hyaluronan serum concentration of patients with capsular contracture was significantly higher (p < 0.05) and correlated with the Baker grade (r = 0.73; p < 0.05), whereas PIIINP showed no difference. In the histologic evaluation, there was a chronic inflammatory reaction in the capsules around the breast implants and refracting material within the substance. Immunohistochemically, TIMP-1 and TIMP-2 showed an intensive accumulation, and MMP-2 showed a local reaction. PIIINP could be detected, too, whereas there was no staining for MMP-1 and MMP-9. The elevated systemic MMP-2 concentration and the local positive staining in the tissue might be due to the chronic inflammatory reaction. Nevertheless, the balance between MMPs and their natural inhibitors is disturbed in patients with capsule contracture. The elevated systemic concentration of TIMPs might be a pathway in the pathogenesis of severe fibrosis after breast augmentation with alloplastic material. Hyaluronan might be a useful marker for early prediction of capsule fibrosis, whereas PIIINP is not useful as a predictor.

Adult↗