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[Effect of low-molecular nonelectrolytes on caffeine skeletal muscle contracture in the rat].

Contractures induced in rat fast (EDL) and slow (SOL) skeletal muscles by 0.03--3 mM of caffeine in conjunction with rapid cooling of muscle from 30 to 0 degrees C (rapid cooling contructures, RCC) were studied. Uprising speed and tension of RCC were dependent on caffeine concentration and cooling gradient. The minimal necessary temperature, below which contractures still developed, was +6 degrees. The initial temperature did not play any important role. Optimal conditions for RCC (when its tension reached 80--200% of twitch) were: cooling from 30 to 0 degrees, and concentrations of caffeine being 5 mM for SOL, and 6--7 mM for EDL. Disruption of T tubules caused by the removal of glycerol and urea (400--600 mM) from muscle fibers did not influence the RCC tension. During the first hour of the removal, relaxation rate of RCC was lowered. In the presence of 400 mM of urea and 600 mM of 1.3-dimethylurea (the latter did not disrupt the T-system), RCC was depressed by 90%, and the rate of tension development was greatly lowered, while twitches remained unchanged. This effects could be reversed during non-electrolyte removal. This may suggest that Ca2+ release is inhibited selectively by urea and by dimethylurea.

Animals↗

[Nature of the dual caffeine-sodium benzoate effect on the tonic component of the potassium contracture of the myocardium in the frog].

Application of 12-24 mM caffeine-sodium bensoate (CFB) to the strip of frog ventricular or atrium myocardium in the tonic phase of K-contracture (200 mM KCl) produced a biphasic change of its isometric tension (P): first the rise and then the gradual decay to the "zero" level of P in the control Ringer's solution. A comparison of CFB effect with those of caffeine-base (CF) and sodium bensoate suggests that the first phase of CFB action (increase of P) results from the effect of CF, while the second one (fall of P) is due to the relaxing action of bensoate. Addition of 2 mM tetracaine to the K-rich solution in the tonic phase of K-contracture increases P and totally abolishes the first phase of the CFB effect, whereas the second one remains unchanged. Na-bensoate (12-24 mM) applied during the action of tetracaine induces relaxation of the strip to zero level of P. Blockade of Ca channels by 2.10(-6)-4.10(-5) g/ml D-600 or Bay-1040 does not affect the biphasic action of CFB. The dual CFB effect on the depolarized frog myocardium seems to be due to Ca ions release from the intracellular stores (action of CF) and to an inhibition of the voltage-dependent Ca influx via Na-Ca exchange mechanism (action of bensoate).

Animals↗

[Nature of the phasic component of potassium contracture in the frog myocardium].

High concentrations (4 X 10(-6) g/ml) of D-600 or BAY-1040 applied for 15 min to rhythmically stimulated strip of frog ventricular myocardium inhibited both the twitches and the K-contracture phasic component induced by 200 mM K+ (in the presence of 110 mM Na+). The phasic component, however, also disappeared after a 15-20-min resting in the Ringer solution before substitution of the latter with high K solution. Such a suppression of the phasic component due to myocardiac inactivity was prevented by an increase in Ca ion concentration up to 10 mM or by addition of ouabain (5 X 10(-6) M) to the Ringer solution during the resting period. The increase in [Ca++]0 was effective even after a 15-min preliminary resting in the Ringer solution. In these conditions the amplitude of the phasic component increased as the time of myocardium exposure to high Ca Ringer solution was prolonged from 5 to 15 min. Loading of some intracellular Ca stores seems to be a prerequisite for the phasic K-contractures generation.

Animals↗

[Selective inhibition of the tonic component of portal vein smooth muscle cell potassium contracture by verapamil].

The studies were performed on the rat portal vein smooth muscle cells, using double sucrose-gap method. 10(-9)--10(-7) M-verapamil was shown to selectively block the tonic component of potassium contracture. Since potassium depolarization of the membrane persists, it may evidence that verapramil had a specific effect on the excitation-contraction coupling by blocking the passive calcium entry into the muscle cells. At higher concentrations (10(-6)--10(-5) M) verapramil produced inhibition of the phasic component of potassium contracture by blocking the potential-dependent calcium canals of the portal vein smooth muscle cell membrane responsible for generation of the action potentials.

Action Potentials↗

Relationship between the tissue redox state potential and dak/dt changes of [K+]0 activity during k-strophantoside or acetylcholine induced contractures.

It was established that oxidosis evoked by methylene blue during k-strophantoside and acetylcholine contractures in skeletal muscle was accompanied by an increase in the changes of [K+]0 activity, while redosis evoked by ascorbate under the same conditions was accompanied by a decrease in the changes of [K+]0 activity. These changes in [K+]0 activity parallelled the alterations of contractures caused by oxidosis or redosis suggesting that changes in the [K+]0 transient play an important role in these phenomena.

Acetylcholine↗

The effect of X-537A (lasalocid) on potassium contracture in rat ventricular muscle.

The effects of the carboxylic ionophore X-537A on contracture induced by high external K+ were determined in stimulated and unstimulated rat papillary muscles. X-537A (5 X 10(-6) M - 10(-5) M) increased peak K+-contracture force in stimulated but not unstimulated muscle. X-537A may alter myocardial force development by influencing transport of Ca2+ across the sarcolemma or Ca2+ release from sarcoplasmic reticulum.

Animals↗

[Lipid peroxidation activation and the focal contracture injuries in the myocardium under emotional-pain stress].

Emotional-pain stress reproduced in the form of so called anxiety-neurosis provokes long-term activation of lipid peroxidation associated with an increased content of its products in the myocardium and the development of focal lesions of the contracture type in myocytes. These heart lesions are likely to be related to the impairment of active calcium release from myofibrils due to lipid hydroperoxides-induced injury to cell membranes responsible for the cation transport. While progressing the morphologic changes in the heart reach maximum, i. e. lead to complete contracture and necrosis of myocardial cells.

Animals↗

[Prevention of stress injury to the heart and its hypoxic contracture by using the natural antioxidant alpha-tocopherol].

Experiments on the isolated hearts of rats, subjected to emotional and painful stress have shown it to potentiate the ischaemic and hypoxic damage of the heart, evaluated by the loss of CPK enzyme by the myocardium and the degree of hypoxic contracture. Preliminary administration to animals of alpha-tocopherol prevents contractility disorders of the heart provoked by stress and the potentiating effect of stress on the ischaemic damage and the development of hypoxic contracture. alpha-Tocopherol also limits the damaging action of hypoxia on the heart and that of reoxygenation. The data obtained suggest the possibility of alpha-tocopherol use in the treatment of myocardial infarction.

Animals↗

Redistribution of myocardial calcium during ischemia. Relationship to onset of contracture.

Cytosolic calcium accumulation has been proposed as a mediator for the pathologic changes that occur during myocardial ischemia. Whether the rise in cytosolic calcium is a result of influx or redistribution from internal stores has not been elucidated. Isolated retroperfused rabbit hearts were subjected to ischemia at 37 degrees C. The distribution of calcium between cytosol and internal membrane stores and the relationship between cytosolic calcium and the onset of left ventricular contracture were investigated. One group of hearts was loaded with the fluorescent calcium probe Fura 2-AM to measure cytosolic calcium and a second group with chlortetracycline to indicate changes in membrane-bound calcium. After the onset of ischemia there is a rise in cytosolic calcium, at least in part attributable to redistribution of calcium from intraorganellar sites to cytosol. The release of membrane-bound calcium and rise in cytosolic calcium preceded the onset of irreversible ischemic injury, that is, contracture.

Animals↗

Total joint replacement in multiplex congenita contractures: a case report.

A 34-year-old man with multiplex congenita contractures underwent replacement of 2 hips and 1 knee. Even though a good range of movement was achieved at surgery and intensive physiotherapy, his joints returned to their preoperative status within 2 years. This outcome suggests that total joint replacement has little to offer the patient with multiplex congenita contractures who has immobile joints.

Adult↗

Crushing injury of the hand; prevention of ischemic contracture.

Crushing injury of the hand usually causes "explosive" damage. Subsequent swelling of the palmar structures further impairs venous outflow, and hemorrhage into structural spaces increases the pressure. The arterial system and the large dorsal veins, however, are seldom obstructed and provide adequate circulation unless hampered by improper bandaging. A bandage that compresses the dorsal veins causes back-pressure, which increases the swelling further and brings about ischemia. Swelling and pain cause the patient to restrict exercise of the injured hand, which permits contractures to develop. The author has averted this sequence in more than 100 cases by preserving integrity of veins during debridement, arresting hemorrhage, bandaging the hand with compression dressings in functional flexion, and reducing swelling with hyaluronidase. In these cases, on removal of bandages in 24 hours, swelling was reduced and continued to diminish. All patients exercised the hand at this time without discomfort and only a few required aspirin for pain.

Bandages↗

Percutaneous accessory collateral ligament release in the treatment of proximal interphalangeal joint flexion contracture.

A percutaneous release or capsulo-ligamentous proximal interphalangeal joint contracture is described, the indications are outlined and the advantage over open releases are discussed. The results of a small pilot study are reported which we feel are comparable to the results of open techniques. The procedure in itself, however, merely allows operative correction to be achieved. Its maintenance depends upon a stringent post-operative rehabilitation regime.

Adult↗

A genetic variant of Emery-Dreifuss disease. Muscular dystrophy with humeropelvic distribution, early joint contracture, and permanent atrial paralysis.

A 38-year-old woman, a product of consanguineous parents, had been observed to have limited neck flexion and elbow joints contracture since early childhood. In addition, she experienced humeropelvic muscular weakness and atrophy, so that she was unable to walk by age 27. At 34 years of age, she required a permanent pacemaker to treat complete atrioventricular block with ventricular bradycardia. A myocardial biopsy confirmed cardiomyopathy. The clinical features of the present case are similar to those of the Emery-Dreifuss syndrome; however, this case may be inherited through an autosomal recessive trait.

Adult↗

Quadriceps contracture as a result of multiple intramuscular injection.

Quadriceps contracture in children can result from multiple intramuscular injections. We describe here seven patients with this complication. These patients were unable to completely flex the involved knee. At surgery, extensive fibrosis of the quadriceps muscle was found. Lengthening of the scar and contracted muscle and tendon restored a good deal of flexion. If long-term antibiotic treatment is anticipated, the intravenous route should be employed if possible.

Child↗

Condition of microcephaly, growth retardation, joint contractures, atopic dermatitis, and mental retardation in two Japanese sisters: a new autosomal recessive MCA/MR syndrome?

We report on two sisters in a family with a hitherto undescribed MCA/MR condition characterized by growth retardation, severe microcephaly, a peculiar facies, congenital contractures of the interphalangeal and patellar joints, atopic dermatitis, and growth and developmental delay. The disorder in the family we describe is similar to but clearly distinguished from tricho-rhino-phalangeal syndromes or Bavinck syndrome. We propose that the condition in the sisters represents a new autosomal recessive MCA/MR syndrome.

Abnormalities, Multiple↗

Progressive erosive arthropathy with contractures, multicentric osteolysis-like changes, characteristic craniofacial appearance, and dermatological abnormalities: a new syndrome?

We report a 27-year-old man with an apparently new syndromic form of progressive erosive arthropathy and contractures of small and large joints associated with mild epiphyseal changes, normal vertebrae, and generalized osteopenia. The patient had a characteristic craniofacial appearance, dermatological abnormalities, and normal intelligence. The head was large with frontal bossing. The face was elongated with malar hypoplasia, thin upper lip, prominent lower jaw, high arched palate, dental malocclusion, and prominent ears with absent ear lobules. Dermatological abnormalities included malar erythema and facial telangiectasia together with multiple nevi and lentigenes all over the body. Pseudorheumatoid arthropathy, spondyloarthropathy, and Borrone dermatocardioskeletal syndrome were considered in the differential diagnosis and were excluded. Also, no similar cases have been found in POSSUM or the London Dysmorphology databases.

Abnormalities, Multiple↗

A new X-linked syndrome with muscle atrophy, congenital contractures, and oculomotor apraxia.

Six men from three generations of one family had manifestations of a possible new syndrome. All had congenital contractures of the feet at birth, a slowly progressive predominantly distal muscle atrophy, dyspraxia of the eye, face, and tongue muscles, and mild mental retardation. The pedigree is compatible with X-linked recessive inheritance with no detectable manifestations in the obligate carriers. Linkage analysis excludes close linkage with the Xg locus and a polymorphic DNA sequence from the long arm of the X chromosome (DXS17).

Adolescent↗

Congenital contractures, edema, hyperkeratosis, and intrauterine growth retardation: a fatal syndrome in Hutterite and Mennonite kindreds.

We present clinical findings in infants from three kindreds (two Hutterite and one Mennonite) with an apparently unique, fatal disorder. The major manifestations consist of severe intrauterine growth retardation, congenital contractures, and tense skin which is easily eroded. The skin is tightly drawn over the face, giving an abnormal appearance consisting of a narrow, pinched nose, small mouth, limited jaw mobility, and ectropion (in one). One infant had first-degree hypospadias. Apart from this, there were no organ malformations and the infants did not have hydrops. Histologically, the skin showed hyperkeratosis. It is postulated that this is a tissue dysplasia and that all of the clinical effects are secondary. The disorder appears to be an autosomal recessive trait. The two Hutterite families are from different endogamous subdivisions. They are related as fourth cousins once-removed and fifth cousins in multiple ways through the six nearest common ancestors of all four parents. There are 25 founders (11 couples and three individuals) who are common ancestors. We computed the probability of joint descent of the four alleles in each pair of parents and in a sample of Alberta Hutterite couples, assuming that each of the common founders in turn was the original carrier. For an allele from one particular founder couple, there is a relatively greater probability of identity by descent for each pair of parents than on the average for other couples of the same endogamous subdivision.

Abnormalities, Multiple↗