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Biomedical subjects

W W Hofmann

Publications and source records attributed to W W Hofmann.

8 recordsLinked to original sources
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↗
PubMedDate not supplied

Prednisone-neostigmine interactions at cholinergic junctions.

The effect of corticosteroid (prednisone) and/or chronic anticholinesterase (neostigmine) treatment on alpha-bungarotoxin binding was examined in the diaphragms of male rats. In endplate regions of the diaphragm, prednisone treatment had no effect on the density of toxin binding sites, either when given alone or when administered in conjunction with neostigmine while neostigmine was observed to reduce specific binding to less than half after one week.

Animals↗