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An experiment was performed in rabbits to test the effect of a textured surface of a silicone implant on the incidence and severity of capsule contracture. Contrary to the hypothesis of this experiment, texturing of the implant surface resulted in an increase in the contracture problem rather than a reduction.
Neonatal vascular compromise to limbs has been associated traditionally with perinatal injury of the brachial plexus, fracture of the clavicle or humerus, or iatrogenic causes. Congenital Volkmann's ischemic contracture is an exceptional etiology of ischemic limb in the newborn. Fewer than 10 cases had been described in the literature. The authors report a newborn presenting at birth with partial bluish discoloration of the right forearm. The clinical picture and laboratory studies lead to the diagnosis of congenital Volkmann-Lesser ischemic contracture.
Perfusion of isolated, nondiabetic rat hearts with high concentrations of regular insulin (10 mU/ml) produced earlier onset of myocardial contracture during ischemia than control perfusions without insulin. High insulin concentrations also increased total myocardial calcium content (p less than .001) and myocardial Ca-45 uptake postischemia (p less than .05). Insulin perfusion before ischemia did not enhance calcium uptake. These results support the hypothesis that insulin may increase calcium movement across myocardial cell membranes, which may lead to increased ischemic contracture. Insulin-aggravated myocardial ischemia in cardiothoracic surgery and cardiac resuscitation deserves further investigation.
Adult nude mice had 1.5 to 1.0 meshed split-thickness human skin applied to an excised area of their back. The animals were then randomized into two groups, one of which had a steroid cream applied to their graft on alternate days. The other group had no ointment applied and served as a control. The wounds were measured on a weekly basis and the rate of wound contracture was found to be identical. Topical steroids would thus appear to offer no benefit in the prevention of scar contracture.
The effects of amrinone (5.3 X 10(-4) M) on isometric contraction and K+-induced contracture force of right ventricular muscle isolated from normal cats (n = 6) and cats in right ventricular failure (RVF, n = 6), 3-14 days after partial pulmonary artery ligation, were studied. Peak isometric contractile force (Po) and maximal rate of force development (dP/dt) of RVF muscles (1.38 +/- 0.21 g/mm2; means +/- SEM, and 11 +/- 1 g/s/mm2, respectively) were significantly lower than normal muscles (2.46 +/- 0.41 g/mm2, p less than 0.025, and 24 +/- 3 g/s/mm2, p less than 0.005, respectively). Duration of contraction (DC) was significantly longer in RVF muscles (442 +/- 32 ms) than in normal muscles (361 +/- 11 ms, p less than 0.025). Times to peak twitch force (TTP) and peak K+-induced contracture force (Pc) of RVF and normal muscles were not different. Amrinone increased Po and dP/dt significantly in normal muscles (+78 +/- 24%; means +/- SEM; p less than 0.01, and +53 +/- 17%, p less than 0.025, respectively), but not RVF muscles (+11 +/- 16% and +8 +/- 19%, respectively). TTP and DC of normal muscle were unchanged by amrinone, whereas TTP was unchanged while DC was shortened (-12 +/- 3%, p less than 0.025) in RVF muscle. Amrinone relaxed Pc similarly and significantly in normal (-28 +/- 7%, p less than 0.005) and RVF (-26 +/- 4%, p less than 0.025) muscles. These results suggest that part of amrinone's salutary action in the failing heart occurs through modification of myocardial relaxation.
Spontaneous electrical and mechanical activity was abolished in isolated preparations of rat portal vein by exposure to K+-free Krebs solution. This procedure probably also increased the intracellular [Na+] owing to interference with the active transmembrane Na+-K+ transport. Contractures could be induced under these conditions by lowering extracellular [Na+] from the control level of 144 to 17 mM using sucrose, TrisCl, or LiCl as NaCl substitutes. Contractile force depended on the type of substitute: sucrose greater than TrisCl greater than LiCl. These contractures are thought to be caused by influx of extracellular Ca2+ through the Na+/Ca2+ exchanger, which otherwise transports Ca2+ in the opposite direction at normal transmembrane Na+ gradient. The contractile response to low Na+ was rapidly and completely abolished in nominally Ca2+-free medium; it was strongly inhibited by 0.4 mM MnCl2 but was not affected by high concentrations of the organic calcium antagonists, felodipine (10(-6) M), verapamil (10(-5) M), or diltiazem (10(-5) M). We conclude that the Na+/Ca2+-exchanger is an effective pathway for Ca2+ transport over vascular smooth muscle cell membrane; this pathway is not blocked by calcium antagonists.
Several lines of evidence support a fundamental role for voltage-gated sodium channels in mediating ischemic Na rise. We examined the effect of the novel anti-ischemic compound KC 12291 on veratridine-stimulated and lysophosphatidylcholine (LPC)-induced sustained sodium current (I(NAL)) mediated by sodium channels in isolated myocytes obtained from guinea-pig atria, by using the whole-cell patch-clamp technique. We also analyzed the effect of KC 12291 on veratridine- and LPC-induced contractures in isolated guinea-pig atria. Veratridine as well as LPC increased I(NAL) measured at 20 ms of a 2 s pulse evoked from -100 to -30 mV (47.5 and 12 pA/pF in the presence of 40 microM veratridine and 10 microM LPC, respectively, vs. 6.7 pA/pF under control conditions). A significant reduction by KC 12291 in the quantity of charge carried by veratridine-stimulated I(NAL) in the range of test potentials between -50 mV and +10 mV was observed and similar effects were obtained on LPC-induced I(NAL). Thus, the quantity of charge carried by LPC-induced I(NAL) over a 2 s pulse to -30 mV was reduced by 48% in the presence of 10 microM KC 12291 vs. a reduction by 50% of veratridine-stimulated I(NAL) at the same test potential. Veratridine- and LPC-induced submaximal contractures in isolated atria were significantly inhibited by KC 12291 in a concentration-dependent manner, with an IC of 0.55 microM and 0.79 microM, respectively. The data indicate that veratridine- and LPC-induced increases in diastolic tension are inhibited by KC 12291 by a mechanism that involves blockade of voltage-gated sodium channels mediating sustained sodium current.
A two-stage augmentation mammaplasty was performed on 231 patients (462 implants) over a period of 3 years. Two hundred and sixteen of the cavities (47 percent) were found to have hematomas at the time of the second surgical stage. After removal of the hematomas and completion of the second stage, only 41 breast (9 percent) developed capsular contracture. Treatment of the 41 with Diapulse therapy, massage, and closed capsulotomy completely eliminated all capsular contracture. The period of observation has ranged from 3 months to 2 1/2 years.
We report five cases of children born with forearm wounds associated with motor and sensory losses to the hand and forearm. Their evolution toward muscle retraction is very similar to the classic description of Volkmann's ischemic contracture. These cases should not be confused with upper extremity gangrene of the newborn or aplasia cutis congenita. Two cases of neonatal Volkmann's ischemia have already been reported in the literature and identified as such. Another very similar case has been reported as upper extremity gangrene of the newborn, and three more cases of a forearm wound with neuromuscular involvement have been reported as aplasia cutis congenita. We believe that neonatal Volkmann's ischemic contracture of the forearm should be recognized as a separate entity. Its early diagnosis may improve treatment, especially for children with recent injury, in whom intracompartmental pressures may still be elevated. Early hand therapy and splinting are mandatory to minimize late sequelae.
In vitro pharmacological responses of fresh biopsy specimens of human skeletal muscle were used as indicators of some intrinsic muscle properties. The measured parameters that were utilized for the current study were contractures induced in vitro by caffeine or by caffeine plus halothane. The opportunity to study such specimens arose from clinical testing for diagnosing the genetic predisposition to malignant hyperthermia, a potentially fatal complication of anaesthesia. The current analysis covers data from over 1,000 subjects, most of whom were clinical suspects and relatives of these. Responsiveness of the muscle specimens varied over two orders of magnitude. The frequency distribution curves suggest that the variation does not represent a continuum but that there are three or more clusters of functional variants. Muscle specimens from males were on average more responsive to caffeine than were those from females. Correlations within father-son and brother-brother pairs indicated complete heritability of responsiveness; this might have been expected but the surprise was a lack of correlation within mother-daughter pairs. There was an intermediate correlation in father-daughter pairs. The sex difference in heritability could be due to gender-related modifying genes or due to secondary modification of the muscle response in females by sex-related, perhaps hormonal factors. Among the effects of age appeared to be poor development in early childhood of the potentiation of the caffeine contracture by halothane.
Skin defects are often present following surgery for Dupuytren's contracture. The first dorsal metacarpal artery island flap (FDMA) has been used by others for soft tissue reconstruction about the radial and dorsal aspect of the hand, thumb and fingers. We have used it successfully to fill the skin defects often seen following palmar fasciectomy for Dupuytren's contracture. The thin nature of the flap makes it suitable for this application. The FDMA arises from the radial artery just before the radial artery enters the first dorsal interosseous muscle and divides into three branches: 1 to the thumb, 1 to the index finger (radiodorsal branch) and a muscular branch. It is the radiodorsal branch that supplies the skin over the index finger. The island flap based on this artery includes the dorsal terminal branches of the radial nerve and venae comitantes. The flap is formed to include the fascia of the first dorsal interosseous muscle to avoid injury to a possible deep artery and to yield sufficient fat to promote venous drainage. The flap is passed subcutaneously through the first web space and sutured in place to cover the skin defect in the palm. A full thickness skin graft is used to cover the defect over the proximal phalanx of the index finger.
Congenital Volkmann ischaemic contracture or neonatal compartment syndrome has rarely been discussed in the literature of dermatology. The condition often involves the upper extremity with cutaneous lesions, contractures and neuropathy. Because the lesions can be mistaken for other entities including necrotizing fasciitis, neonatal gangrene, congenital varicella, aplasia cutis congenita, amniotic band syndrome, subcutaneous fat necrosis and epidermolysis bullosa, dermatologists play a significant role in the diagnosis and, consequently, the treatment of the patient. We describe a premature newborn who had a unilateral, well-demarcated necrotic plaque with a central pallor at birth. The plaque extended circumferentially over the left forearm from the wrist to the elbow. Left wrist oedema, bullae over the fingers and flaccid paralysis at the wrist were also noted.
Muscle fiber typing and in vitro contracture tests were performed in 59 patients investigated for susceptibility to malignant hyperthermia (MH). Eighteen patients were found to be susceptible to MH. There was no difference in age or fiber type distribution between MH susceptible and non-susceptible patients. No correlation was found between age and fiber type distribution. Separate analyses for each diagnostic group revealed no relationship between age or fiber type distribution and response to halothane or caffeine. When all caffeine results were pooled, however, there was a significant effect of age on the caffeine specific concentration (the concentration eliciting a contracture of 1 g), but not on the caffeine threshold concentration (the minimal concentration eliciting an increase in tension). It is concluded that age and fiber type distribution have no influence on MH diagnosis, if the protocol of the European MH Group for evaluation of susceptibility to MH is followed.
1. Following a 5 min in vitro exposure to morphine (1.3 x 10(-7) M), U-50,488H (2.5 x 10(-8) M) and deltorphin (1.6 x 10(-8)-6.5 x 10(-9) M), the rabbit isolated jejunum exhibited a precipitated contracture after the addition of naloxone (2.75 x 10(-7) M). 2. The precipitated responses to U-50,488H and deltorphin but not to morphine were reproducible in the same tissue. 3. The precipitated contractures were blocked completely by tetrodotoxin (3 x 10(-7) M), partially by atropine (1.5 x 10(-7) M) and not affected by hexamethonium (1.4 x 10(-5) M). 4. Naloxone administration (2.75 x 10(-7) M) before the agonist prevented the development of the adaptive response to morphine and U-50,488H but not to deltorphin. 5. The selective antagonists norbinaltorphimine (2.7 x 10(-8)-2.7 x 10(-9) M) and naltrindole (1.1 x 10(-7) M) prevented the adaptive response development only to the respective agonists. 6. The opioid agonists partially inhibited the spontaneous activity of the tissue. This study has shown that independent activation of mu-, kappa- and delta-opioid receptors can induce dependence in this isolated tissue. Rabbit jejunum is a suitable tissue for studying the acute effects of opioids on the adaptative processes determined by their administration.
The influence of intramural noradrenaline on potassium induced contractures was studied in isolated preparations of the uterus and the portal vein of the rat. Uterine strips of oophorectomized rats responded with contraction followed by transient relaxation when immersed in a medium containing 127 mM potassium chloride. Reserpinization or blockade of beta-adrenoceptors with propranolol greatly diminished the transient relaxation. In the isolated portal vein, both noradrenaline depletion with reserpine and alpha-adrenoceptor blockade (phentolamine) reduced the active tension produced in response to the isotonic potassium solution. These results suggest that intramural noradrenaline plays a significant role in the development of contractures evoked by potassium in the uterus and the portal vein of the rat. In the uterus, the released noradrenaline counteracts the development of active tension, whereas in the portal vein, noradrenaline has a contractile effect which is added to that of potassium. Estrogen treatment reduced (portal vein) or abolished (rat uterus) the contractile effects of intramural noradrenaline. The adrenolytic effect of estrogen is possibly due to reduction in the release of noradrenaline from the sympathetic nerve-endings.
Guinea-pigs treated with a single dose of morphine, 15 mg kg-1 s.c., exhibited an increase in locomotor activity 2 h later on injection of naloxone, 4 mg kg-1 i.p. At the same time, contracture of ileal preparations isolated from morphine-treated guinea-pigs occurred on addition of naloxone 1 microM. Contracture of the ileum was inhibited by the tachykinin antagonist, spantide, and was therefore presumably mediated by a substance P-like agent. This study has established a useful model for the parallel investigation of central and enteric nervous system mechanisms of opiate dependence.
1. Frog toe muscles and isolated fibres from frog semitendinosus muscles were allowed to develop maximum K-contractures, and after reaching peak tension were transferred to media containing intermediate [K](0) (20-40 mM-K). Under these circumstances, relaxation displayed an early rapid phase, and a subsequent slower phase whose magnitude and rate varied with [K](0). The removal of activator (calcium ion) from the sarcoplasm appears to have a potential-dependent component.2. The relation between relaxation and [K](0) suggests that, with progressive depolarization, membrane sites from which calcium is initially released become converted into sites which are again capable of binding calcium and removing it from the sarcoplasm.3. The rate of relaxation of frog toe muscle after maximum K-contractures can be either accelerated or retarded by abrupt alterations in [Ca](0) or by sudden replacement of the major extracellular anion. These effects are attributed to shifts in the relation between calcium rebinding and membrane potential.
1. The tension generated by isolated frog atrial trabecules, during exposure to solutions containing a high potassium concentration, is not maintained but spontaneously relaxes. The final part of this relaxation can be fitted by a single exponential function.2. The recovery of the tension generating mechanisms following the spontaneous relaxation of a potassium contracture depends on the preceding membrane potential and the time since the last contracture.3. The rate of the exponential phase of the spontaneous relaxation is independent of the [K](o) and hence the membrane potential, the [Ca](o); and when the [Ca](o)/[Na](o) (2) ratio is maintained it is also independent of the [Na](o). This relaxation is not influenced by atropine or pronethalol.4. When sodium is totally excluded from the bathing medium the rate of relaxation of a later potassium contracture is much increased. It is argued that this change is due to a fall in the intracellular sodium concentration.5. The consequences of these results are discussed, and the hypothesis that is favoured would require that contraction is induced by a transient release of calcium into the sarcoplasm, probably triggered by a potential dependent, and probably also transient, influx of calcium through the cell membrane. Relaxation is supposed to occur when this activator-calcium is then removed by an intracellular relaxing system that resembles the sarcoplasmic reticulum of other muscles. What this intracellular structure might be, is also discussed.