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Caffeine increases the force of contracture induced in cat myocardium by exposure to 140 mM KC1 in isotonic Tyrode solution. The effect of caffeine does not require prior exposure to the drug, develops rapidly, and is partially antagonized by procaine but not by verapamil. These results suggest that caffeine acts on depolarized sarcolemma to release a sarcolemmal calcium pool.
The in vitro preparation of guinea-pig ileum taken from animals which had been stressed by swimming for 5 min in water at 20 degrees C responded by a dose-dependent contracture to the narcotic antagonist naloxone. This response was antagonised by atropine (8 X 10(-8) g/ml). Ileum preparation from non-stressed guinea pigs did not respond to naloxone in concentrations up to 1 X 10(-5) g/ml. The possibility that this response is a consequence of the stress-induced release of endogenous opiate peptides is discussed.
A case of Volkmann's contracture secondary to prolonged compression of the limb is presented. The events developed in a patient who had been comatose following an overdose of alcohol and a sedative drug.
We describe a father and daughter with early-onset benign limb-girdle myopathy and contractures of elbows and hands, resembling Bethlem disease. Muscle biopsy showed a pattern of dystrophy with non specific mitochondrial changes. In both patients there was unusual facial muscle weakness. We discuss the nosologic position of Bethlem myopathy and suggest that facial involvement may be an additional feature of this disease.
1. In the frog heart, Ca2+ enters the cell by the slow inward current (Isi) and by an electrogenic, carrier-mediated, and passive Na-out/Ca-in-exchange. 2. The latter reverses to Na-in/Ca-out-exchange during depolarization and thereby controls relaxation. 3. The exchange ratio is 3 Na+ for 1 Ca2+. 4. The Na/Ca-exchange is not inhibited by organic Ca-antagonists in frog myocardium, indicating that the initiation of the heart beat may mainly depend on Isi. 5. This is not necessarily in contradiction with the Na-Ca-antagonism, since there also exists an antagonism between Na+ and Ca2+ in the slow channel. 6. However, the contractures caused by a decrease of NaO+ are mediated by the Na/Ca-exchange.
1. The slow alterations in the activity of extracellular Na+ concentrations were measured by using ion-selective electrodes. 2. In the first min there is an increase in the changes of the activity of extracellular Na+ following acetylcholine evoked contractures. 3. This increment was significantly inhibited by k-Strophantoside application, suggesting an active transport origin of this first peak. 4. In the second min a strong decrease in the activity of extracellular Na+ concentration followed. 5. Reducing agent (ascorbate) increased, while oxidant (methylene-blue) decreased both the first increment and the sequential decrement in the activity of the extracellular Na+ concentrations. 6. On the basis of these experiments a site of action of the redox regulation of excitatory processes could be the modification of Na+ fluxes.
End-plate and miniature end-plate potentials (EPP, MEPP) were recorded in the chick biventer cervicis muscle in vitro. The control frequency of discharge of MEPPs was 5.97 +/- 1.04 min-1, n = 10. Methohexitone (8.8 X 10(-5) M) did not affect the frequency of MEPP discharge, but tetraethylammonium (TEA, 2.4-9.5 mM), reduced the frequency to 32.9 +/- 8.6% of the control. In the presence of neostigmine (3.3 X 10(-6) M) methohexitone (8.8 X 10(-5) M) reduced MEPP frequency to 38.7 +/- 5.4% of the control and TEA (2.4-9.5 mM) further reduced the frequency to 8.7 +/- 2.1% of the control. After a transient facilitation of the EPP, TEA (2.4-9.5 mM) in the presence of methohexitone (8.8 X 10(-5) M) and neostigmine (3.3 X 10(-6) M) markedly reduced EPP amplitude. The contractures which TEA produced in the presence of methohexitone were not due to an increase in the spontaneous release of vesicular ACh.
We present a 17-year-old boy with Becker muscular dystrophy (BMD) who developed hyperthermia and heart failure after general anesthesia. He presented clinical features of malignant hyperthermia (MH), and had masseter spasm and elevated body temperature (38.7 degrees C) with very high serum CK activity (107,000 IUl-1). Dystrophin tests confirmed a clinical diagnosis of BMD in the patient, i.e. faint and patchy immunostaining pattern of skeletal muscle, truncated dystrophin protein and a deletion of exons 3 and 4 of the dystrophin gene. To inquire into the mechanism of MH associated in the patient, we tested caffeine contracture reaction by the skinned fiber method. We found an increased sensitivity to caffeine only in type 1 muscle fibers. The rate of Ca(2+)-induced Ca2+ release (CICR) was normal, suggesting that the mechanism of "MH" observed in our patient with BMD is not the same as that of classical MH. A possible mechanism might be related to derangements of the sarcoplasmic reticulum membrane in BMD, which sensitize the membrane to caffeine or other agents.
We present a case of a gradually developing ischaemic contracture of the forearm muscles of an infant who developed without any trauma or acute gangrene at birth. Release of the middle and ring finger digitorum profundus muscles and pronator quadratus at 2 years of age corrected the deformity. Histopathology showed no evidence of fibromatosis or any other tumor. Although a dynamic splint was used to maintain the range of motion, the range of the middle finger motion deteriorated gradually 2 years after surgery. Though the pathogenesis of this problem was unclear, we assume that it was caused by fibrosis of muscles as a result of bleeding before or during delivery.
Two children with isolated ischaemic contractures of the mobile wad (extensor carpi radialis longus, extensor carpi radialis brevis and brachioradialis), which developed after treatment of a supracondylar fracture, are presented. Z-lengthening of the extensor carpi radialis longus and brevis tendons improved wrist flexion.
OBJECTIVES: To report our experience using a two-stage, rather than a synchronous, approach in the management of bladder neck contracture (BNC). Anastomotic BNC associated with urinary incontinence is a major complication after radical prostatectomy. Patients may present with a decreased force of stream, urinary retention, or stress, urge, or overflow urinary incontinence. METHODS: The pertinent data of 15 patients (age range 52 to 78 years, mean 62) with postradical prostatectomy BNC associated with stress urinary incontinence (mean pad use 3 per day) were retrospectively reviewed. Video-urodynamic evaluation in 10 of 15 patients revealed a Valsalva leak point pressure of less than 80 cm H2O in all 10 patients. Bladder outlet obstruction was noted in 4 of 10 patients. Of the 15 patients, 2 declined an artificial urinary sphincter (AUS), the other 13 proceeded with our two-stage management. Step one consisted of deep transurethral incision of the BNC (TUIBNC) with Collin's knife electrocautery. Step two consisted of implantation of an AUS (AMS-800) 6 to 8 weeks after TUIBNC once bladder neck patency had been demonstrated cystoscopically. RESULTS: During a mean follow-up of 15 months, 3 patients developed early recurrence of BNC: 2 at the 5-week cystoscopy, 1 at 8 weeks discovered at the scheduled AUS placement. All 3 patients underwent repeat TUIBNC and remained clinically patent at a mean follow-up of 9 months. The remaining 10 patients were clinically patent after a single TUIBNC, with good subjective flow and postvoid residual volume of less than 30 mL at a mean follow-up of 11 months. Of the 13 patients who underwent AUS placement, 12 were socially continent (wearing 0 to 1 thin pad daily). The thirteenth patient remained incontinent after AUS placement. One of the 12 continent patients developed an infection at the device 8 months postoperatively and required explantation. CONCLUSIONS: We recommend a two-stage approach (TUIBNC followed by AUS insertion) rather than synchronous management for postprostatectomy BNC associated with stress urinary incontinence. Such an approach allows identification of BNC recurrence and its safe management before AUS implantation.
Ischemic contracture of the left ventricle ("stone heart") was studied utilizing a previously described stone heart model. Our studies suggest that beta-adrenergic blockade is not quantitatively as important as hypothermia in protecting ischemic myocardium. On the basis of reduced fibrillatory activity and a slight protective effect shown by electron microscopy, it would appear that combining propranolol with hypothermia may be superior to either used singly.
Ceramides are known to play a major regulatory role in apoptosis by inducing cytochrome c release from mitochondria. We have previously reported that ceramide, but not dihydroceramide, forms large and stable channels in phospholipid membranes and outer membranes of isolated mitochondria. C(2)-ceramide channel formation is characterized by conductance increments ranging from <1 to >200 nS. These conductance increments often represent the enlargement and contracture of channels rather than the opening and closure of independent channels. Enlargement is supported by the observation that many small conductance increments can lead to a large decrement. Also the initial conductances favor cations, but this selectivity drops dramatically with increasing total conductance. La(+3) causes rapid ceramide channel disassembly in a manner indicative of large conducting structures. These channels have a propensity to contract by a defined size (often multiples of 4 nS) indicating the formation of cylindrical channels with preferred diameters rather than a continuum of sizes. The results are consistent with ceramides forming barrel-stave channels whose size can change by loss or insertion of multiple ceramide columns.
Frog sartorius muscle treated with 5.0 mM or greater caffeine exhibits stiffness similar to that obtained from muscle in iodoacetate rigor. The data provide quantitative evidence that suggests that caffeine at irreversible contracture-producing concentrations somehow induces a rigor or rigorlike state in skeletal muscle.
To determine whether catecholamines produce alterations in myocardial myosin-actin cycling kinetics, we investigated the effects of isoproterenol upon mechanical characteristics of constantly activated heart muscle thought to reflect crossbridge behavior. In isolated rabbit right ventricular papillary muscles in barium contracture at 24 degrees C, we found that 10 microM isoproterenol caused: (a) a 23% reduction of the 10 to 90% rise time of slow tension recovery in force transients induced by rapid, small amplitude stretches; and (b) a 23% increase in the frequency of sinusoidal length perturbation at which stiffness amplitude exhibited a minimum. Based upon previous mechanistic interpretations of force transients, and on an analysis developed here to relate crossbridge events to the frequency-dependence of stiffness, we argue that our observations provide evidence that isoproterenol induces an acceleration of crossbridge cycling rate. This raises the intriguing prospect that beta-adrenergic stimulation regulates contraction, not only by well-known alterations in calcium metabolism, but also by intrinsic modulation of the force-generating machinery itself.
We describe a procedure to expand contractures of the tunica albuginea by multiple full thickness relaxing incisions followed by inlay of tailored temporalis fascia free grafts. This technique is performed without resection of the tunica albuginea, although in the case of calcified plaques the calcifications themselves are removed, preserving the overlying tunica. Between September 1988 and February 1990, 12 patients have undergone this procedure, all of whom have greater than 3 months of followup and have experienced spontaneous erections within the first week postoperatively. Of the patients 11 resumed intercourse within 8 weeks of surgery and 1 required 12 weeks. No patient had sensory loss postoperatively and there has been no donor site morbidity. Correction of curvature was accomplished in all patients and there have been no recurrences within a maximal followup of 22 months. Within the limitations of such a small study we believe that there is evidence supporting this approach in potent patients with severe acquired penile curvature.
Freeman-Sheldon syndrome is a rare congenital anomaly that is characterized by facial, hand, and foot deformities. We describe a female infant who had severe adduction contractures of the thumbs. A two-stage reconstruction was done. The first web space soft tissues were stretched with a transversely oriented external skeletal distractor, then a conventional first web space deepening and release was performed.
To diagnose malignant hyperthermia susceptibility (MHS), caffeine and halothane contracture tests were performed on six patients. One of them, who presented a peroperative crisis, was recognized as MHS; the five others were negative (MHN). By means of 31P-NMR spectroscopy, the muscular energetic metabolism of these patients was studied during and after moderate exercise in normal and moderate ischaemic conditions. Metabolic abnormalities appeared in the MHS patient. It must be concluded therefore that malignant hyperthermia is a latent myopathy. 31P-NMR spectroscopy appeared to be a useful non-invasive tool for screening for this affliction.
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