[Metabolic influences on the onset of fibrillation and on membrane potentials of denervated muscles]. / Influenze metaboliche sull'insorgenza della fibrillazione e sul potenziale di membrana nei muscoli denervati.

Fibrillation activity and membrane depolarization which follow denervation, were studied in skeletal muscles of control and pretreated adult rats. The investigation was carried out on both fast (Tibialis Anterior) and slow (Soleus) muscles. The pretreatment consisted in prolonged (4 days) starvation, or Streptozotocin-induced diabetes, preceding denervation. Denervation was performed by cutting the sciatic nerve. In fast as well as in slow muscle, both pretreatment significantly delayed the onset of fibrillation. Starvation enhanced depolarization only in fast muscle, while diabetes was effective also in slow muscle. The results support the view that membrane depolarization (but not fibrillation activity) in denervated muscle is related to an altered carbohydrate metabolism.

An experimental model of myasthenia myopathy.

Normal and thymectomised rabbits been have immunized by means of a thymic extract emulsified with Freund's Complete Adjuvant. The experiment was conducted over a three month period, in order to reproduce an experimental model of chronic myasthenia. During this period immunological, electromyographic and histologic studies were undertaken. Typical findings of partial neuromuscular block were invariably obtained from all the non thymectomized animals, while such signs were constantly absent both in non-treated control rabbits and in the immunized thymectomized ones. This neuromuscular block was intermittent. The compromised neuromuscular conduction was associated to an histological pattern of autoimmune myopathy. Evidence was put on antibodies directed against the thymus, muscular and nervous tissue. The results indicate the important role of the thymus gland both in altering conduction at the neuromuscular junction level and causing histopathologic muscle lesions.

Computer simulation of calcium-induced myotonia.

In an extensive research project on myotonia, the ionic mechanisms which are at the basis of the phenomenon of calcium-induced myotonia have been taken into consideration. A mathematical model of a muscle fibre was constructed to demonstrate the possibility that anomalous values of the membrane permeability to Calcium ions have an active part in the genesis of myotonia.

Carnitine and acetylcarnitine in skeletal and cardiac muscle.

The acetylcarnitine/carnitine ratio has been found significantly increased in tibial muscles of swimming rats in comparison with normal rats. Analogous increase occurred in electrically stimulated tibial muscle in comparison with the unstimulated controlateral muscle of the same animal. Swimming also induced a statistically significant increase of the acetylcarnitine/carnitine ratio in heart, while norepinephrine administration resulted in a decrease of carnitine not accompanied by a corresponding increase in acetylcarnitine in a severe carnitine depletion of cardiac muscle. These results are discussed in terms of carnitine function in the acetyl metabolism, assuming the acetylcarnitine as a possible acetyl reservoir in the working muscle.

Differential effects of disuse preceding denervation on the onset and development of fibrillation in fast and slow muscles.

Section of the sciatic nerve, performed after a week of muscular disuse, is followed by fibrillation earlier in the soleus (S) than in the anterior tibialis (AT) muscle of the rat. The subsequent development of fibrillation, which is different in the control denervated S as compared with the control denervated AT, tends to become similar in the disused-denervated muscles.