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Biomedical subjects

R Cuppini

Publications and source records attributed to R Cuppini.

At least 55 records · Page 3Linked to original sources
PubMed1986

Effect of ethanol on the spontaneous transmitter release by nerve endings in the process of maturation.

Ethanol stimulates the spontaneous transmitter release from motor nerve endings, as shown by the increase of miniature end plate potential (m.e.p.p.) frequency at the neuro-muscular junction. The stimulation of acetylcholine spontaneous quantal release by ethanol is greater in regenerating than in mature nerve endings. The different effects of ethanol on regenerating nerve endings may be related to changes of chemical-physical membrane properties.

Animals↗
PubMed1985

[Effect of ethanol on young nerve endings].

The ethanol changes the quantal spontaneous release of acetylcholine and it affects the reinnervation time course. The effects of ethanol on regenerated nerve endings have been tested. 20 days after crushing sciatic nerve, the m.e.p.p. frequency at the end plate of rat extensor digitorum longus muscle keep in Ringer solution without and with ethanol has been estimated by intracellular recordings. The increase of the m.e.p.p. frequency produced by ethanol is greater in immature, than in normal nerve endings.

Animals↗
PubMed1985

[Recovery of sensation and reflex activity during treatment with ethanol].

Ethanol greatly modifies synaptic function and it affects the reinnervation time course. In order to better clarify the effects of ethanol on nerve regeneration, we have observed the recovery of algesthesia and reflex activity in the rat during the treatment with ethanol. For this purpose the posterior leg of Sprague Dawley rats was denervated by crushing the sciatic nerve and the recovery of algesthesia and reflex activity was tested at the level of the metatarsus-falanx articulation of the homolateral paw. During the reinnervation period, the animals were treated daily with ethanol 3 g/Kg of body weight. The recovery of algesthesia and reflex activity comes about in a medio-lateral direction and proceeds linearly. It is completed on the 25th day after the denervation. Ethanol does not cause changes in the time course of algesthesia recovery, however it does cause a slight delay in the recovery of the reflex activity.

Animals↗
PubMed1984

[Changes in the synaptic activity in sciatic nerve-extensor digitorum longus (preparations induced by ethanol)].

The aim of this research is the study of the modification of synaptic activity caused by ethanol in the rat sciatic nerve-extensor digitorum longus (EDL) muscle preparation. For such a purpose, intracellular recordings have been carried out, keeping the muscle immersed in normal Ringer solution and in Ringer solutions containing ethanol at different concentrations up to 0,8 M. Therefore, the resting potential of muscle cells and the frequency of m.e.p.p.s were measured. Qualitative observations of m.e.p.p.s shape were also carried out. Ethanol increases the frequency of m.e.p.p.s in the rat sciatic nerve - EDL muscle preparation. The logarithm of relative frequency (frequency in Ringer solution with ethanol/frequency in normal Ringer solution) is linear with respect to the concentration of ethanol, with a slope of 1.44. Furthermore, ethanol increases the amplitude and lengthens the time course of m.e.p.p.s. The muscle cells undergo a hyperpolarization of about 2-3% at the lowest concentrations of ethanol tested.

Animals↗
PubMed1984

[Variations in the hyperpolarization potential of ethanol on muscle during reinnervation].

Ethanol causes the hyperpolarization of the excitable membranes. In the Extensor Digitorum Longus (EDL) muscle of the rat the increase of resting membrane potential is 2-5% and is independent of the concentration of alcohol between 0.2 and 0.4 M, while at higher concentrations the membrane potential falls to levels equal or inferior to the normal potential. We have studied the hyperpolarization action of ethanol on the denervated muscle by crushing the sciatic nerve. Also under these conditions in which, as is known, there is a drop in the resting potential, ethanol causes hyperpolarization, however it is in general greater and it is dependent upon the concentration between 0.2 and 0.8 M.

Animals↗
PubMed1984

[The recovery of motor innervation during treatment with ethanol].

We have studied the effects of the fluidizing action of ethanol on motor reinnervation in order to clarify if membrane fluidity changes affect synaptic plasticity and nerve regeneration. Sprague Dawley rats were denervated by crushing the sciatic nerve and subsequently, on the 16th day, the degree of reinnervation of the EDL muscle was observed by electrophysiological technique: in particular an observation was made of the resting potential and the m.e.p.p.s frequency by intracellular recordings in muscle fibers. During the nerve regeneration period, the rats were treated with 3 g of ethanol per kilogram of body weight per day. We have found that ethanol quickens the resting potential recovery but does not affect the m.e.p.p.s frequency.

Action Potentials↗
PubMed1981

[The importance of N-acetylneuraminic acid and of its interaction with Ca++ in the stability of the erythrocytic membrane].

The aim of this paper is to draw information about influence of human red cell N-acetyl-neuraminic acid and its interaction with Ca++ on membrane itself stability. Then, changes of red cell behavior in reply to osmotic stress with and without Ca++ after treatment with neuraminidase has been studied. We noted that the treatment with neuraminidase causes spontaneous hemolysis (about 9%), independently of medium osmolarity. As regards membrane resistance to osmotic stretching, N-acetyl-neuraminic acid has a destabilizing effect on most erythrocytes whereas its interaction with Ca++ don't influences significantly membrane resistance to osmotic stretching. Nevertheless, in extreme conditions of osmolarity (i.e. when hemolysis of younger red cells occurs), destabilizing effect of N-acetyl-neuraminic acid is no longer observable and, on the contrary, when it interacts with Ca++, it increases the osmotic resistance of red cells.

Calcium↗
PubMed1981

[Effects of Vipera berus venom on the activity of some coagulation factors].

The activity of some clotting factors of human blood after incubation at 37 degrees C with Vipera berus venom (400 microgram/ml of plasma) has been measured. Factor V, initially, is activated by venom, but rapidly its activity decreases, becoming lower of that of controls and it exhausts oneself almost fully after 2 hours. Changes in the prothrombin and fibrinogen activity by venom action have not been noted.

Adult↗
PubMed1981

[Coagulant and anticoagulant action of Vipera berus venom on human blood].

The effect of Vipera berus venom on coagulation of human blood has been studied. PTT and coagulation time according to Quick of normal human plasma kept with Vipera berus venom (400 microgram/ml) for variable times have been misused. The venom has an immediate coagulant and, subsequently, anticoagulant effect.

Blood Coagulation↗
PubMed1979

[Variations in human blood osmotic globular resistance by the action of Vipera berus venom in different experimental conditions. I. Hemolytic effect].

The effect of Berus Viper's venom on human blood globular resistance with changing incubation conditions has been studied. Particularly venom's concentration (from 200 to 400 microgram/ml of blood), temperature (from 20 degrees C to 37 degrees C) and time (from 1/2h to 2h) have been changed. Time and temperature are important factors in haemolytic process development, instead venom's concentration behave like a factor not significantly haemolysis modifying.

Dose-Response Relationship, Drug↗