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Biomedical subjects

W W Hofmann

Publications and source records attributed to W W Hofmann.

At least 19 recordsLinked to original sources
PubMed1991

Comparison of stimulation and insulin effects on denervated mouse soleus muscles.

A comparison has been made between the responses of denervated mouse soleus muscles to direct electrical stimulation, as reported by earlier workers, and to incubation with supraphysiological concentrations of insulin. The parameters of interest were resting membrane potential (RMP), qualities of the active state, the amount of alpha bungarotoxin (BUTX) binding, and chemosensitivity, as measured by the strength of acetylcholine (ACh)-induced contractures. In all aspects, the changes recorded after insulin, were in the same direction as with direct stimulation, however, owing to the time limitations of in vitro testing, were smaller. It is suggested that the effects of electric shocks on denervated muscles are the result of activation of the insulin receptor, or some similar macromolecule, which appears to be sensitive to the membrane potential. The possible interrelations between acetylcholine and insulin receptors in neurotrophic control are discussed.

Animals↗
PubMed1987

Musculotrophic effects of insulin receptors before and after denervation.

Insulin binding and metabolic effects have been used to assess properties of the insulin receptor of rodent skeletal muscles before and after denervation. It has been found that the amount of insulin-displaceable insulin binding on both type I (soleus) and type II (extensor digitorum longus) muscles rises slowly for up to 3 weeks after denervation, following a brief period of reduced binding. As estimated from weight loss and unstimulated deoxyglucose uptake, the extra binding sites are not functional. Stimulation in vitro with shocks or excess potassium can temporarily cause a relative increase in sugar uptake in both types of muscle, but an excess of insulin rapidly loses its effect in the soleus muscle. The effects of stimulation are taken to mean either conformational changes in the receptor or enhancement of some postbinding step, or both. It is suggested that the slow increase of binding sites for insulin after denervation may reflect loss of a neural substance normally effective in activating receptor degradation.

Animals↗
PubMed1984

An insulin receptor defect in murine muscular dystrophy.

A study has been made of the I125 insulin binding and postbinding effects on excised soleus muscles from the 129 ReJ strain of dystrophic mice. Results are compared with those in sex- and weight-matched controls. The data suggest that, in the range of physiological hormone concentrations, the affinity of insulin receptors on dystrophic muscles is less than normal and that the insulin-dependent uptake of both 2-deoxyglucose (2-DG) and aminoisobutyric acid (AIB) is impaired. These findings are taken to indicate that many of the biochemical and electrophysiological abnormalities observed in murine dystrophy could arise from some genetic defect in the receptor proteins controlling uptake of raw materials.

Amino Acids↗
PubMed1983

The relationship of insulin receptors to hypokalemic periodic paralysis.

Single muscle fibers from a typical case of hypokalemic periodic paralysis (HOPP) have been found to be depolarized in all test media and to be cathodally blocked after exposure to insulin. The diseased fibers also bind more insulin and consume more oxygen than controls. The hypothesis proposed is that increased amount or affinity of insulin binding on the HOPP muscles causes continual depolarization in the presence of normally subthreshold concentrations of circulating insulin. presence of normally subthreshold concentrations of circulating insulin. This is because of steady effects of the hormone on passive K+ and Na+ fluxes. Additional insulin causes rapid further depolarization with paralysis. Hypokalemia follows if the insulin increment is enough to stimulate active K+ and Na+ transport.

Adolescent↗
PubMed1980

Mechanisms of muscular hypertrophy.

The effects of synergist tenotomy have been studied on rat soleus muscles after denervation and after interference with sciatic axoplasmic flow with colchicine. The results suggest that neural, as well as muscular, factors cause compensatory hypertrophy (CH) of soleus. The myogenic factor may be mild depolarization of the muscle membranes by passive stretch, as a result of which Ca++ ions enter and stimulate metabolism.

Animals↗
PubMed1979

Experimental allergic neuritis in the Lewis rat.

Purified myelin from the peripheral nervous system of guinea pig, frog (Rana catesbeiana), rat, rabbit, beef, and human in Freund's adjuvant were injected into the Lewis rat. Groups of rats receiving injections of myelin from different species were examined for signs of dysfunction and lesions in the PNS and CNS. Injection of frog PNS myelin into the Lewis rat did not produce any clinical signs or lesions typical of experimental allergic neuritis (EAN) or experimental allergic encephalomyelitis (EAE). Injection of myelin from the PNS of rat, rabbit, beef, and human elicited clinical signs and lesions characteristic of EAN, while guinea pig myelin injection caused superimposed conditions of EAE and EAN. The myelin proteins from the various species were separated by polyacrylamide gel electrophoresis, the gels were scanned and the individual proteins measured. There did not appear to be a correlation between the amount of P2 protein contained in the different myelin species and the severity of the EAN symptoms and lesions produced. Although the Lewis rat is far more susceptible to EAE caused by guinea pig CNS myelin than by any other species, EAN can be easily induced in this animal by injection of PNS myelin from a number of species.

Animals↗
PubMed1979

Effects of potassium depletion and insulin on resting and stimulated skeletal rat muscle.

The electrophysiological and metabolic responses to insulin of skeletal muscles from control and potassium-depleted rats were compared. Membrane potentials, action potentials, contraction parameters as well as oxygen uptake were measured in diaphragm strips or intact extremity muscles from the two groups, and similar measurements were made in vivo. The muscles were examined in solutions with normal potassium concentration [K]o , reduced [K]o, and in normal [K]o and in normal [K]o with ouabain, in each case before and after insulin, 400 mU/ml. In normal solution, the depleted muscle contractions were weaker and slower than control. The depleted muscles, already having low potassium conductance, are paralysed by the further reduction of potassium conductance after insulin. Hyperpolarising effects of insulin-induced Na/K pumping are offset in the depleted muscles with a high sodium conductance and low [K]o. Respiration is about normal at rest in depleted muscles, despite increased [Na]i, suggesting that the sodium is sequestered. After insulin, reduction of [K]o, or ouabain plus insulin, the depleted fibres take up more O2 than controls. In the presence of ouabain, this respiratory stimulation is believed to represent response to Ca++ influx. The K-depleted rat does not seem to be an entirely satisfactory model of the human disease hypokalaemic periodic paralysis.

Action Potentials↗
PubMed1978

Relationship of intracellular creatine concentration and uptake to muscle mass in vivo.

Attempts have been made to evaluate the role of intracellular creatine in conditions leading to increased or decreased amounts of contractile protein in rat skeletal muscles. Resting concentrations of intracellular creatine ([Cr]i) and creatine phosphate ([CrP]i) were compared in gastrocnemius and soleus muscles with those immediately after a 20-s tetanic stimulation. The hydrolysis of creatine phosphate was the same after heavily and lightly loaded contractions, suggesting that hypertrophy of isometric exercise is not mediated by creatine. With atrophy after denervation or interruption of sciatic axoplasmic flow [Cr]i also remained unchanged, though [CrP]i and the rate of Cr uptake fell after denervation. The major change in adult red and white muscle bulk with unaltered [Cr]i suggests that the Cr sensitivity found by others in developing muscle in vitro has been supplemented or replaced by other control mechanisms.

Animals↗
PubMed1977

Antimyasthenic action of corticosteroids.

Tests were made in vitro fo the action of prednisolone on nerve backfiring, muscle twitches, tetanus decay rates, miniature end-plate potential amplitude and frequency, and the block induced by curare, hemicholinium, and excess magnesium. At about 0.1 mM concentration, the steroid showed no 'veratrinic' or decurarizing action, and the probability of transmitter release was not increased in 10mM Mg++. Moreover, when acetylcholine stores were depleted in hemicholinium, there was no evidence of repair by steroid. The results are taken to mean that prednisolone and congeners do not owe their therapeutic efficacy in myasthenia to actions at the neuromuscular junction. It is therefore concluded that the clinical benefits from steroids are related to systemic, possibly immunosuppressive effects.

Action Potentials↗
PubMed1976

Oxygen consumption by human and rodent striated muscle in vitro.

Oxygen consumption has been measured in human and rodent striated muscle in vitro with a platinum-silver electrode system. The effects of excess potassium, caffeine, insulin, osmotic shock, halothane, and Na-pump blockade have been investigated and the differences from amphibian muscle responses are outlined. It has been found that normal human muscle, like that of rodents, is relatively indifferent to major surface depolarization and osmotic shock, as far as oxygen requirements are concerned. Surgical damage to muscle fibers causes them to react unpredictably to pharmacological tests. The results in normal muscles may be of use in the further study of certain muscular diseases.

Animals↗
PubMed1973

Observations on the efficiency of dystrophic muscle in vitro.

A study of muscles of the dystrophic mouse has failed to substantiate earlier claims that these muscles were especially resistant to fatigue in vitro or that fast muscles are preferentially damaged. It has been found that the fast muscle selected for previous studies is very often unable to withstand isolation in an organ bath if it is working, and both the difficulty in removing the normal gastrocnemius muscle intact and the need to trim it surgically contribute independently toward its deterioration in vitro. The smaller dystrophic gastrocnemius muscle is less liable to excision damage, is able to satisfy its resting metabolic needs in nutrient solution, and requires no damaging dissection, but is nevertheless unable to recover normally from fatigue. Using EDL and soleus muscles which are small enough to withstand isolation in vitro, no differences are found between fatigue patterns of normal and dystrophic specimens. Responses to rest, KCl, and 2 mM caffeine are also quite similar, and the only distinguishing biomechanical characteristic we have found in dystrophic mouse muscle is a weaker contraction and a longer total twitch time.

Animals↗