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Biomedical subjects

F Melis

Publications and source records attributed to F Melis.

At least 55 records · Page 3Linked to original sources
PubMed1990

The non-competitive NMDA-receptor antagonist MK-801 prevents the massive release of glutamate and aspartate from rat striatum induced by 1-methyl-4-phenylpyridinium (MPP+).

The concentrations of dopamine (DA) and of the excitatory amino acids (EAAs) glutamate (Glu) and aspartate (Asp) were measured in dialysates from the striatum of awake rats in order to study the link between the release of DA and of EAAs induced by the infusion of 1-methyl-4-phenylpyridinium ion (MPP+). DA and EAAs were detected simultaneously by HPLC-EC. The infusion of MPP+ at the concentration of 1 mM elevated DA levels in the perfusates, but did not affect EAA release. However, MPP+ at 10 mM maximally stimulated Glu and Asp release to 230- and 68-fold of baseline, respectively. In this condition, pretreatment with the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (5 mg/kg, i.p.) prevented the MPP(+)-induced EAA release. In contrast, MK-801 had no effect on DA release induced either by 1 or 10 mM MPP+. These results suggest that MPP(+)-induced DA and EAA release are independently regulated processes. In addition, the finding that MK-801 inhibits MPP(+)-induced EAA release suggests that EAAs may act on NMDA receptors to stimulate their own release through a positive-feedback mechanism.

1-Methyl-4-phenylpyridinium↗
PubMed1990

Analysis of central cardioarrhythmogenic triggers in experimental epilepsy.

The cardioarrhythmogenic potential of epileptic foci induced at mesencephalic and rhombencephalic levels was analyzed in hemispherectomized rats. Topical application of penicillin-G onto the mesencephalic quadrigeminal lamina or onto the fourth ventricle induced paroxysmal activity at the mesencephalic or bulbar neurone level. At the mesencephalic levels, the paroxysmal activity was characterized by a significant increase in the spontaneous frequency of the neurones, with the appearance of multiunit activity and rhythmical outbursts. The simultaneous recording of myocardial electrical activity and blood pressure showed that the paroxysmal activity triggered short-latency sinus bradyarrhythmias with wandering of the sinus pacemaker, the appearance of biphasic or negative P waves, some premature ventricular contractions and non-significant reduction of systolic and diastolic pressures. When the paroxysmal activity stopped, the cardiac rhythm and blood pressure returned to basal values. At the bulbar level, the paroxysmal activity appeared with longer latency and usually the rhythmical outbursts were not observed. Following bulbar paroxysmal activity only short-lasting episodes of sinus bradyarrhythmias appeared. Midcollicular transection eliminated paroxysmal activity at the bulbar level, and blood pressure and cardiac rhythm resumed basal values. After transection, an additional application of convulsant drug (penicillin-G or pentylenetetrazole) onto the fourth ventricle did not induce the reappearance of paroxysmal activity and the consequent cardiovascular alterations. The results showed the existence of a cardioarrhythmogenic trigger localized at the mesencephalic level which spreads paroxysmal activity upwards. A hypothesis to explain the appearance of fetal haemodynamic modifications and life-threatening arrhythmias has been proposed.

Animals↗
PubMed1989

Volume receptors in guinea pig labyrinth: relevance with respect to ADH and Na control.

We tested the hypothesis that changes in extracellular fluid volume are reflected by pressure changes within structures of the inner ear and that through neural pathways, a control mechanism exerts an influence on antidiuretic hormone (ADH) release and Na excretion. The study was performed on 35 guinea pigs. In protocol 1, 13 animals were studied before and after decompression of the inner ear by bilateral fluid withdrawal in an experimental setting of sustained isotonic expansion that kept the osmoreceptor partially activated and the intrathoracic volume receptors suppressed. A group of six sham-operated animals served as control. In protocol 2, nine animals were studied before and after a unilateral rise in their inner ear pressure during slightly hypertonic low-rate infusions that kept the osmoreceptor and thoracic volume receptors stimulated. A group of seven sham-operated guinea pigs served as controls. Decompression of the inner ear was attended by a rise in plasma ADH from 11.9 +/- 2.4 to 29.1 +/- 6.9 pg/ml, in urine osmolality (Uosmol) from 470 +/- 48 to 712 +/- 46 mosmol/kg (P less than 0.001), and a fall in urine flow rate (V) from 184 +/- 47 to 71 +/- 11 microliters/min (P less than 0.01), whereas plasma Na (PNa) and osmolality (Posmol) did not change. During inner ear hypertension, plasma ADH fell from 25.6 +/- 3.9 to 18.4 +/- 3.1, Uosmol from 829 +/- 58 to 627 +/- 43 (P less than 0.001), and V rose from 51 +/- 11 to 130 +/- 23 (P less than 0.001), whereas glomerular filtration rate, PNa, and Posmol did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Beta-endorphin in experimental canine spinal ischemia.

Plasma and cerebrospinal fluid beta-endorphin concentrations were radioimmunologically assayed in dogs subjected to spinal cord ischemia induced by infrarenal aortic ligature and in control sham-operated dogs. Plasma beta-endorphin levels rose significantly following surgery in control dogs but were unaffected by spinal ischemia. On the other hand, a significant increase in cerebrospinal fluid beta-endorphin concentration occurred after spinal ischemia, while surgical stress had no significant effect. Thus, the origins of plasma and cerebrospinal fluid beta-endorphin may be different, with the former secreted from the hypophysis and the latter from nervous tissue. Observed changes in cerebrospinal fluid beta-endorphin concentration could be related to the ischemic lesion of nervous tissue while the changes in plasma levels may reflect general stressing factors such as the surgery in our experiments.

Animals↗
PubMed1988

Physostigmine and metoclopramide in oesophageal peristaltic spread in man.

Simultaneous recordings of electrical and mechanical activities at different levels of the oesophagus were performed in normal men before and after physostigmine and metoclopramide injections. Various parameters of the basal oesophageal peristalsis were significantly modified following drug treatment. In particular, physostigmine injections induced a shortening of electromechanical coupling time and a reduction of the propagation velocities of the electrical and mechanical oesophageal events. Metoclopramide shortened the electromechanical coupling time but increased the electrical and mechanical propagation velocities along the oesophagus.

Electrodes↗
PubMed1988

Labyrinthine projection to the hypoglossal nucleus.

Evoked potentials and responses of single hypoglossal neurons were recorded in response to electrical stimulation of the labyrinth. In addition, the spontaneous electrical activity of hypoglossal neurons was significantly modified in response to ipsi- and contralateral static tilt of the whole animal and thermic stimulation of the labyrinth. The experiment showed that the labyrinth modulates the electrical activity of hypoglossal neurons with phasic inputs in response to ampullar stimulation and with tonic inputs in response to macular stimulation. The vestibular phasic influence of hypoglossal neurons represents the most adequate functional pattern to obtain a quick, short lasting response of the tongue muscles instantly modifiable with every abrupt head displacement. On the contrary, the vestibular tonic influence of hypoglossal neurons represents the most adequate functional pattern to obtain not only adjustment but also maintenance of the muscular lingual response to static displacement of the head.

Animals↗
PubMed1988

Improvement of vestibular plasticity in the guinea pig with a calcium entry blocker.

The influence of flunarizine on vestibular compensation was investigated in hemilabyrinthectomized guinea pigs. The results showed that the vestibular deficits from hemilabyrinthectomy disappeared more rapidly in the treated animals than in the controls. To elucidate the mechanism by which the drug could affect the compensatory process, further studies on the spontaneous and evoked activity of vestibular nuclei were performed in normal, labyrinthectomized and labyrinthectomized-cerebellectomized animals. These electrophysiological data implied that flunarizine improved the vestibular compensation by inhibiting the receptor and nuclear activities of the intact labyrinth. The drug excited the cerebellar cortex, which modulated the activity of the vestibular nuclei of both sides, restoring the balance disrupted by hemilabyrinthectomy.

Animals↗
PubMed1986

The vestibular cortical projection during spinal decompensation.

The removal of spinal afferents in rabbits submitted to unilateral lesion of the labyrinth and fully compensated greatly modified the field potentials as well as the single unit responses recorded from the cortical vestibular area during stimulation of the intact eighth nerve. In particular, an increase of contralateral and a decrease of ipsilateral potentials were observed. These asymmetrical responses indicate that the influence of the spinal cord in compensating the effects of unilateral lesion of the labyrinth is directed to balance not only the electrical activity of the brain-stem structures, but also that of the cerebral cortex. It appears, therefore, that spinal signals intervene not only in the compensation of vestibulospinal and vestibulo-oculomotor functions but also of cortical functions, such as that related to vestibular sensation.

Animals↗
PubMed1984

Correlations between cerebellar activity and chronic nontoxic administration of phenytoin in rats.

The effect of long-term nontoxic treatment with phenytoin on the cerebellar Purkinje cell activity as determined by simultaneous monitoring of plasma and cerebellar levels of the drug has been studied in rats for the first time. The electrophysiological observations allowed the analysis of the spontaneous firing rate of the Purkinje cells and of the cerebellar field potentials generated by electrical stimulation of the ipsilateral radial nerve. The responses of single Purkinje cells to radial nerve stimulation were studied by constructing poststimulus time histograms and cumulative frequency distributions. The chronic treatment with phenytoin, which did not induce motor impairment or cerebellar symptoms, modified the firing rate of the Purkinje cells and the two modalities of Purkinje cell activation. In fact, phenytoin decreased significantly the spontaneous activity of the Purkinje cells and modified the strength of the mossy and climbing afferents.

Animals↗
PubMed1983

Protective effects of Ca++-antagonist agents on the cerebral electrical activity during anoxia in the rat.

Transient anoxia obtained in curarized rats by momentary stopping of the artificial respiration (80 sec duration) induced a failure of the cerebral electrical activity. This effect was characterized by cessation of the spontaneous unitary discharge of cortical neurons and reduction of amplitude of somatosensory evoked potentials. Pretreatment with flunarizine (10 mg/kg/os) or suloctidil (50 mg/kg/os) induced a distinct improvement of the resistance to anoxia and of the recovery of the cerebral electrical activity.

Animals↗
PubMedDate not supplied

Effects of phenytoin administration on vestibular function in the rat.

Acute or chronic treatment of epileptic patients with phenytoin is often associated with the appearance of disturbances such as postural impairment and ocular nystagmus, probably due to high toxic plasma levels of the drug. We describe the changes in spontaneous electrical activity of vestibular units in cerebellectomized rats following an acute nontoxic dose of phenytoin, in static conditions and after macular stimulation. Administration of phenytoin induced an inhibition of Deiters cells and a drug level-dependent biphasic effect (excitation followed by inhibition) on medial and superior vestibular cells. The experiments pointed to a direct action of phenytoin on the vestibular nuclear complex, indicating that postural and motor disturbances are not only cerebellar but also vestibular in origin.

Animals↗
PubMedDate not supplied

Postrotatory nystagmus during phenytoin treatment.

This article reports an investigation into the vestibuloocular reflex (VOR) recorded in rats during acute nontoxic treatment with phenytoin (PHT). In animals adapted to the dark, latency and duration of postrotatory nystagmus (VAN), cumulative trend of slow phases (CTSP), slow-phase velocity, temporal trend of the frequency and amplitude of the nystagmic beats, and mean frequency-amplitude ratio were analyzed. Observations were correlated with plasma and brain levels of the drug. Results showed that an acute nontoxic dose of PHT impairs some parameters of the VAN. At low concentrations (8.24 +/- 2.56) (microgram/ml in plasma and 6.02 +/- 3.24 micrograms/g in brain), only CTSP and slow-phase velocity were remarkably modified in each animal. At higher concentrations but still subthreshold for evoking the appearance of evident signs of drug toxicity (17 +/- 6.13 micrograms/ml in plasma and 11.4 +/- 5.28 micrograms/g in brain), all parameters were modified in each animal. In the same animal, VOR impairment was always linearly correlated to the plasma and brain drug levels. A considerable individual biovariability in the drug response appeared, and an individual subtoxic threshold for each animal was evident. Thus, when results of all experiments were averaged, the statistical significance of the differences of the greater part of the VOR parameters disappeared. However, VOR analysis performed before and after drug administration, i.e., with each subject as its own control, proved to be an excellent diagnostic pointer to the approach of the particular subject's toxic threshold before the appearance of spontaneous nystagmus or postural impairments.

Animals↗
PubMedDate not supplied

Neurogenic myocardial arrhythmias in experimental focal epilepsy.

The potential for cardiac arrhythmia was studied in an experimental focal epilepsy induced in hemispherectomized rats by topical application of buffered penicillin G onto the thalamus. The epileptic burst triggered cardiac and hemodynamic responses, as simultaneously monitored by arterial pressure, and hypothalamic and heart activity. During interictal epileptic activity, the single burst triggered a short-latency cardiac arrhythmia, characterized by sinus bradyarrhythmia and junctional rhythm, and lengthening of intervals between sphygmic waves with significant reduction of diastolic pressure. When the epileptic burst stopped, the cardiac activity resumed normal rhythm, and diastolic pressure returned to basal value. During ictal epileptic activity, the sinus and junctional bradyarrhythmic episodes lasted longer, and supraventricular extrasystoles, sinus arrest, and bigeminal ventricular extrasystoles were observed. Both systolic and diastolic pressures decreased from 120/85 to 100/65 mm Hg. The end of the ictal episode always marked resumption of normal cardiac rhythm and systemic pressure. Considering the absence of metabolic complications (blood-gas analytic parameters and acid-base balance being controlled) and the short latency of the cardiac and hemodynamic responses, it is suggested that during paroxysmal hypothalamic activity the observed cardiac arrhythmias and the hemodynamic modifications were neurogenic in origin. A role for cardiovascular alterations in sudden unexplained epileptic death is postulated.

Animals↗
PubMedDate not supplied

Effects of ketamine anesthesia on phenytoin biodisposition.

After oral administration (10% suspension in arabic gum, at 500 mg/kg), total phenytoin (PHT) concentrations were measured in the blood and brain of rats anesthetized with ketamine (60 mg/kg, intraperitoneally i.p.) and in a control group that received only PHT. The concentration of PHT in blood and brain was significantly higher in the ketamine than in the control group. At 1, 1.5, 2, and 3 h, increased brain PHT reflected increased blood concentrations. At all times, the plasma protein binding of PHT was similar in both groups. After intravenous (i.v.) administration, instead, at 10 mg/kg, total PHT concentrations were similar in rats anesthetized with ketamine (60 mg/kg, i.p.) and in a control group that received only PHT under mild ether anesthesia. Thus, the main factor involved with the altered PHT biodisposition caused by ketamine anesthesia appears to be increased absorption of the drug.

Administration, Oral↗
PubMedDate not supplied

Motor responses of the esophagus and lower esophageal sphincter (LES) to vestibular stimulation in man.

Pressure recordings in the esophageal body, LES and stomach were performed in 10 healthy subjects before and after caloric stimulation of the labyrinth. While esophageal and stomach responses varied or were absent, all subjects showed variations at the LES level. Duration of LES relaxation was increased and both time and amplitude of LES augmentation were significantly reduced. The physiological mechanism of labyrinthine-digestive connections and the possibility of clinical applications are discussed.

Acoustic Stimulation↗
PubMedDate not supplied

[Nonodontogenic facial pain of dental significance].

The authors review the main facial pain syndromes, which put often important diagnostic problems to the chephalic district specialists. The syndromes are discussed with modern nosographic criteria. Epidemiologic data and pain peculiarities, both essentials for a correct diagnosis, are stressed for each of the reported syndromes.

Facial Neuralgia↗