Biomedical subjects

P Bo

Publications and source records attributed to P Bo.

At least 37 records · Page 2Linked to original sources

PubMed1993

Neurophysiological parameters during halothane anaesthesia in experimental models of cerebral ischemia.

Types of anaesthesia in different experimental models of ischemia vary, with consequent difficulties in analysis of results obtained by the authors. The aim of this work was to evaluate EEG and SEPs parameters in a group of rabbits submitted to anaesthesia with halothane. We used White New Zealand rabbits prepared for EEG recording according to the Monnier and Gangloff's stereotaxic method. SEPs were obtained by medial nerve stimulation according to a method standardized in our laboratory. Each animal was anaesthetized with halothane plus nitrous oxide and oxygen or halothane plus oxygen for surgical MAC, which was maintained for a time corresponding to the duration of surgical intervention. We evaluated all parameters in basal conditions and after the administration of anaesthesia until EEG and SEPs returned to basal values. Evoked potentials remained altered for a longer period of time and returned to basal levels only two hours after anaestethic suspension.

Anesthesia, Inhalation↗

PubMed1993

[Electroencephalographic effects of a new triazolobenzodiazepine (Adinazolam) in the rabbit].

In this study we investigated the central effects of adinazolam, a triazolobenzodiazepine, by means of neurophysiological techniques (electroencephalogram, EEG, and quantified analysis of EEG, QEEG). The drug has been administered at the doses of 0.1-1-10 mg/kg i.v. The evaluation of the data obtained by QEEG has demonstrated that this substance acts on the central nervous system. Particularly we observed that the drug at the middle and high doses caused an increase of the "slow waves sleep" EEG pattern. This preclinical study has shown that adinazolam possesses a neuropharmacological profile similar to that of atypical antidepressive and/or anxiolytic drugs.

Animals↗

PubMed1993

[Role of the dopaminergic system in experimental models of epilepsy].

It has been shown that neuroleptics which interact selectively with either D-1 or D-2 dopamine receptors possess a marked difference in their propensity on seizures. The aim of this work was to investigate whether the D-1 antagonist SCH 23390 differs from haloperidol (D-2 antagonist) in models of experimental epilepsy induced by electrical stimulation of selected brain regions (hippocampus and amygdala), in rabbits. Haloperidol increased and SCH 23390 significantly decreased the susceptibility to seizures in both models investigated. The data suggest that the D-1 and D-2 receptor subtypes have different roles in the mechanisms underlying seizures.

Amygdala↗

PubMed1993

Chiropractic complications. Another case report.

We report the case of a 34-year-old man, treated by chiropractic manipulation for tension-type headache. The patient complained of a sharp occipital pain during the first session, followed by vomiting and loss of consciousness, and remained comatose for five days. Neurological examination detected persistence of dysarthria, ataxia, with delayed responses. Neuroradiological findings reveal an ischemic lesion in left PICA region, confirmed by angiography. Clinical and radiological findings suggested complete remission about two months later.

Adult↗

PubMed1992

Effects of remoxipride, a dopamine D-2 antagonist antipsychotic, on sleep-waking patterns and EEG activity in rats and rabbits.

The antipsychotic remoxipride, a selective dopamine D-2 receptor antagonist, was studied for its effects on sleep-waking patterns in the rat and electroencephalographic (EEG) activity in the rabbit. Haloperidol, which has lesser selectivity for D-2 receptors, was used for comparison. In the rat, remoxipride (1-10 mg/kg SC) did not affect either total sleep or non-rapid eye movement (non-REM) sleep. Only REM was slightly reduced by the high dose of 10 mg/kg. Haloperidol (0.1-1 mg/kg PO) enhanced duration of both total sleep and non-REM sleep. In the rabbit, remoxipride (3 and 10 mg/kg IV) induced no significant changes of the EEG power spectrum over 0.1-38.5 Hz or individual frequency bands. In both cortex and hippocampus the drug did not alter the arousal response to acoustic sensory stimuli. Plasma concentration of remoxipride 10 mg/kg IV in rabbits declined biexponentially and was 4 and 2 mumol/l at 30 min and 1 h, respectively. Haloperidol (0.3 and 1 mg/kg) slowed down the EEG activity, enhanced the power spectrum of the cortical and hippocampal activity, and significantly reduced the duration of arousal induced by sensory stimuli. The results indicate that, unlike haloperidol, remoxipride has weak or no sedative effects. The data also provide support to the notion that D-2 receptors are not involved in the regulation of states of sleep and sedation.

Animals↗

PubMed1992

[Early ECG changes after experimental focal cerebral ischemia. A pathogenetic hypothesis of the brain-heart syndrome].

Primary CVT alterations and arrhythmias, occurring one hour after embolization were detected in several experiments about focal cerebral ischaemia in rabbits. 62 animals were fed on a standard diet and 15 on an atherogenic diet. Primary CVT alterations and arrhythmias occurred in 4 rabbits fed on a standard diet and in 6 rabbits fed on an atherogenic diet. These results gave statistic evidence of a relationship between more frequent and serious electrocardiographic alterations and an atherogenic diet. The information coming out of these experiments are discussed. Considering the data coming out of other experiments and the data of the literature it is supposed that the pathogenesis of "the cerebro-cardiac syndrome" is linked to several biohumoral alterations occurring after the stroke. If these alterations occur in animals (or in subjects) with damaged coronary arteries cardiac alterations occurring after the stroke are greater and more important than the cardiac alterations occurring in the same conditions in the animals in which coronary arteries are not jet damaged.

Animals↗

PubMed1991

Blood hypercoagulability secondary to experimental cerebral ischemia in the rabbit: influence of a hyperdyslipemia induced by an atherogenic diet.

Within the framework of a research carried out at the Neurological Institute of Pavia on experimental cerebral ischemia some biohumoral determinations were done on two groups of rabbits: one kept on a standard diet and the other on an atherogenic diet to induce dyslipemia. The aim was to find out whether induced ischemia produces an activation of the hemocoagulation processes and whether hyperdyslipemia constitutes an aggravating factor. In the animals on a standard diet there was a statistically significant increase in factor X A and a nonsignificant increase in parameter (r + k) on TEG (thromboelastogram) and of factor VIII C after embolization. In the hyperdyslipemic group the changes were definitely more marked and, in the case of factor VIII C and parameter (r + k), statistically significant, accompanied by slight variations in APTT and factor IX pointing in the same direction. We discuss the meaning of our findings.

Animals↗

PubMed1991

Urine melatonin in alcoholic patients: a marker of alcohol abuse?

Ethanol is known to alter central neurotransmission and endocrine functions. Urine melatonin was studied in 10 male chronic alcoholic patients, before and after two weeks of controlled alcohol abstinence, and in sex and age matched healthy controls. In both groups, 24-hour urines were collected in two fractions corresponding to day- (D) (08:00-20:00) and night- (N) (20:00-08:00) time. Urine melatonin was assayed by RIA after methylene chloride extraction. Twenty-four hour urine melatonin levels were calculated adding up D and N values. In patients during alcohol intake, the 24-hour urine melatonin levels were significantly higher than in controls (p = 0.004, Student's t test). A disruption of the physiological ratio between N and D values was also observed, since the higher melatonin levels occurred in the D fraction. In drinking alcoholics, melatonin D values were significantly higher than the D values found in controls (p less than 0.01, Student's t test) and in the same patients after alcohol withdrawal (p less than 0.05). The N/D ratio approximated 1 during alcohol intake and became larger than 1 after alcohol withdrawal, as in the controls. The melatonin data were correlated with the suppressive effects of dexamethasone (DXT) on cortisol secretion evaluated both during alcohol intake and during abstinence. After alcohol withdrawal, the two (out of 10) patients, who remained unresponsive to the DXT suppression test, showed high D melatonin values and a low N/D ratio. These preliminary data indicate that in chronic alcoholism the pattern of urinary "melatonin- like immunoreactivity" is altered.

Adult↗

PubMed1991

Antagonism of EEGraphic and behavioural effects of methamphetamine by selective receptor blockers (SCH 23390 and raclopride) in the rabbit.

1. The interactions between selective D1 and D2 antagonists (SCH 23390 and raclopride) and methamphetamine on EEG arousal and behaviour was studied in rabbits. Haloperidol, a "classic neuroleptic" was used as reference drug. 2. Both 23390 and raclopride, which were used at low dosage (0.03-0.09 mg/kg i.v. for the former and 1-3 mg/kg for the latter), were able to block completely the behaviour induced but do not inhibit completely the EEG arousal pattern induced by methamphetamine. 3. The blockade of both behaviour and EEG arousal took only when the two drugs were administered concomitantly at the lower dosage. 4. The antagonistic effects obtained with the concomitantly administration of the two drugs were of higher degree in confront of those obtained with the pretreatment with haloperidol 0.3 mg/kg i.v. 5. Our data indicate that both D1 and D2 antagonists are able to block, at the dosage used, motor hyperactivity and stereotyped behaviour typically induced by methamphetamine and that SCH 23390 and raclopride are potentiated also in this experimental model.

Animals↗

PubMed1991

Anticonvulsive efficacy of flumazenil in the electroinduced seizures in the rabbit.

The anticonvulsive efficacy of flumazenil, a specific antagonist of the ligands of the benzodiazepine receptor, was studied in the experimental seizures induced by electrical stimulation of corpus Amygdaloideum and Cornu Ammonis dorsale of the hippocampus in rabbits. In the amygdaloid seizure model flumazenil raised the threshold and/or reduced the afterdischarge duration. Results observed in the seizures induced by stimulation of hippocampus were less consistent. Possible explanations are discussed.

Acute Disease↗

PubMed1991

Neuropathological evaluation of brain damage in a rabbit model of focal cerebral ischaemia.

In the present paper we studied different methods for a qualitative and quantitative morphologic assessment of the focal brain damage in rabbits after occlusion of the middle cerebral artery with vaseline microspheres. The study of the early brain ischaemic damage (4 to 12 hours after embolisation) was performed on serial coronal cryostat sections of hemispheres frozen in liquid nitrogen and processed for NADH enzyme-histochemical method. In the ischaemic area the necrotic cells were pale or negative after enzyme-histochemical reaction, but a quantitative assessment of the ischaemic area was approximative. The Evans blue method for the identification of the region of the edema at 24 hours after embolisation showed inconstant results. A reproducible method for a quantitative assessment of the ischaemic area up to the 24th hour after embolisation was proposed by Osborne and utilised in the present experimental conditions. The volumetric assessment of the ischaemic area was obtained after delineation of brain damage areas at 8 preselected coronal levels with a computerized automatic image analyzer and by integration of areas with the distance between each level. In treated animals, the measures of the volume of cerebral infarction were accurate and reproducible, and were suitable for neurophysiologic correlations.

Animals↗

PubMed1991

Evoked potentials monitoring of a cerebral focal ischemia model.

A model of cerebral ischemia by microsphere embolization in the rabbit was monitored with somatosensory evoked potentials by median nerve stimulation (SEPs) and by flash visual evoked potential (VEPs). The degree of SEP alterations paralleled the type of lesions (focal or multifocal ischemia or diffuse oedema). Alterations present at the first hour after ischemia were generally unchanged during the follow-up, which ended at the 24th hour. The prevalence of VEP alterations was low (only 16% in focal ischemia). These results are compared to EEG modifications performed in the same animals.

Animals↗

PubMed1991

The brain-heart syndrome: remarks on early ecgraphic changes following focal cerebral ischemia in healthy and in experimentally hyperdyslipidemic rabbits.

Early cardiac effects of focal cerebral ischemia in two groups of rabbit, one of which made hyperdyslipidemic with an atherogenic diet, were detected in several experiments. In the group of 62 animals fed on a standard diet, primary CVT alterations and arrhythmias occurred in 4 rabbits (6.4%), in the group of 15 animals fed on an atherogenic diet the same cardiac alterations occurred in 6 rabbits (40%). A marked statistically significant prevalence of ECGraphic changes was observed in hyperdyslipidemic group. These results and the data coming out of other experiments and literature suggest that the pathogenesis of the "cerebro-cardiac syndrome" is linked to several biohumoral alterations occurring after the stroke. If these events affect functionally damaged endothelia, or occur in the presence of atherosclerotic plaques, cardiac alterations occurring after the stroke are greater than cardiac alterations observed in the same condition when coronary are intact or little damaged.

Acute Disease↗

PubMed1991

EEG changes and platelet aggregation in experimental cerebral focal ischemia in rabbits.

Nine white New Zealand rabbits were submitted to internal carotid embolization with microspheres which caused a histologically verified focal cerebral ischemia. Six animals were sham-operated. EEG, QEEG, ECG, blood pressure, rectal temperature and platelet aggregation were monitored in basal conditions and one hour after ischemia. Embolized animals showed an increase in power density spectrum (PDS) and delta activity (0.15-3.70 Hz) and the appearance of platelet aggregation. The QEEG changes were correlated to the degree of platelet aggregation after ischemia.

Animals↗

PubMed1990

Kappa-opioid receptor changes and neurophysiological alterations during cerebral ischemia in rabbits.

Endogenous opioids have been shown to produce beneficial effects in experimental stroke. To evaluate both neurophysiological and biochemical parameters, we induced massive cerebral ischemia in 11 rabbits according to the method standardized in our laboratory, using microspheres injected through the internal carotid artery. Binding studies were performed in the 11 embolized, in nine control, and in five sham-operated rabbits using the appropriate concentration of [3H]dynorphin A (1-8). Neurophysiological parameters were evaluated under baseline conditions and 1 hour after embolization, surgical preparation, or sham operation in 17 rabbits. Comparison of visual readings of the electroencephalograms and analyses of the quantified electroencephalograms under baseline conditions and after embolization indicated a marked and statistically significant (p less than 0.01) increase in bilateral delta activity; histologic examination confirmed bilateral brain edema. Binding studies on kappa-opioid receptors indicate that 1 hour after embolization there were significantly more (28%) kappa-opioid receptors (Bmax) in six embolized rabbits than in five sham-operated animals. No significant changes were observed in the affinity parameters, particularly in the dissociation constant (Kd). Our results indicate a role for endogenous dynorphin peptides in the pathogenesis of stroke.

Animals↗

PubMed1989

[Spontaneous platelet aggregation after experimental focal ischemia in the rabbit. "Sensitivity", "specificity" and value of the test used].

Within the framework of an investigation at present under way at the Neurological Clinic of Pavia on experimental focal ischaemia, the peculiarities of platelet aggregation observed, have led to a more accurate assessment of both the phenomenon itself and the validity of the method used. In a group of 30 rabbits (17 of them submitted to embolization by means of microspheres introduced into the carotid and 13 used as controls), biohumoral electrical and histological parameters were examined. The spontaneous platelet aggregation test proved significantly related to the extent of changes taking place, as measured by PDS levels and QEEG "delta" activity (respectively, P less than 0.005 and P less than 0.05). Platelet aggregation, in relation to the occurrence or absence of focal ischaemia, revealed a "sensitivity" of 80% and a "specificity" of 92.3%. When not only the onset of but also the increase in aggregation is taken into account, the "sensitivity" figure appears to go up to 93.3%. Endothelial damage and "cascade" platelet aggregation appeared to be a prerequisite for the occurrence of the changes found. In these changes, the pathogenetic role of the regional vasospasm as opposed to mere mechanical obstruction seems to be confirmed. On the basis of these findings, it is concluded that the identification of spontaneous platelet aggregation using K. Breddin's method and its quantification based on Born's turbidimetric principle, may be usefully employed to assess the risk factor constituted by an abnormal tendency to platelet hyperaggregation.

Animals↗

PubMed1988

Synchronization of the EEG and sedation induced by neuroleptics depend upon blockade of both D1 and D2 dopamine receptors.

Blockade of dopamine (DA) receptors by neuroleptics tends to produce sedation, as shown by increased sleeping time, reduction of the arousal response to sensory stimuli and slowing of the electrical (EEG) activity of the brain. The EEG and behavioural effects of the selective compounds, SCH 23390 and raclopride, which block either D1 or D2 receptor subtypes, respectively were evaluated. Groups of rabbits were prepared for the measurement of EEG activity (neocortex and hippocampus). The EEG was analyzed visually and by spectral power analysis. Gross behaviour was also observed. The D1 antagonist, SCH 23390, by itself (0.03-0.3 mg/kg i.v.) produced small changes in the EEG and no evidence of sedation. Periods of slow waves occurred sporadically. Computerized EEG analysis showed moderate increases of total power density. The D2 receptor blocker, raclopride, alone (1-3 mg/kg i.v.) produced changes of the activity of the EEG, mostly, short periods of slow waves and slight increases of total power. No sedation was noted. Although both selective antagonists were studied at larger doses than those minimally effective, they produced slight EEG and behavioural changes which were not comparable with the marked actions produced by classical neuroleptics, such as haloperidol. However, when raclopride (1 mg/kg) was given after treatment with SCH 23390 (0.03 mg/kg) there was a marked synchronized activity in the EEG, associated with a state of sedation and diminished responsiveness to sensory stimuli. The data indicate that EEG synchronization and sedation, classically associated with treatment with neuroleptics, do not depend upon the selective blockade of either D1 or D2 receptors but, instead, require concurrent blockade of both subtypes of receptor.

Animals↗

PubMed1988

Experimental study on central effects of carboxyethyl-gamma-aminobutyric acid (CEGABA).

The central effects of carboxyethyl-gamma-aminobutyric acid (CEGABA) have been studied both in rabbits and in the guinea pig myoclonus model. This drug caused EEG synchronization and behavioural sedation both after intravenous (i.v.) and intracerebroventricular (i.c.v.) administration in a dose-dependent manner, in rabbits. CEGABA showed a protective action against myoclonus induced by means of L-5-HTP in young guinea pigs. These data substantiate the hypothesis that CEGABA is a drug active on the central nervous system and probably exerts its action by strengthening cortical inhibition and/or directly acting on lower brainstem.

5-Hydroxytryptophan↗