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Biomedical subjects

G Arfel

Publications and source records attributed to G Arfel.

At least 19 recordsLinked to original sources
PubMed1978

[Unexplained electrographic temporal discharges (author's transl)].

Unilateral or bilateral electrographic temporal discharges at 5 Hz were analyzed in relation to their morphological characteristics, their topography, and their evolution in II subjects. The clinical context, in which there was no evidence of epileptic disorder, was also analyzed. These discharges were compared to other infraclinical critical phenomena reported in the literature, and related to similar manifestations described by the Gibbs "school" as "Psychomotor variant type of discharge", or by Hughes group as "Rhythmic mid Temporal discharges".

Adolescent↗
PubMed1976

[Action of ketamine of paroxysmal discharges provoked by air emboli in the baboon Papio papio].

Ketamine was administered to 18 baboons (Papio papio) to disrupt epileptic discharges elicited through intracarotid air injection. Discharge suppression was obtained in all animals but could be preceded by a phase of enhancement of the epileptic patterns, which rendered necessary the injection of a supplementary dose. The mechanisms of Ketamine action are discussed, in connection with data from the literature. Some of the latter suggest that its use in proved epileptics facilitates paroxystic patterns or even convulsions while others emphasize its antiepileptic action. Present data corroborate the ambivalent action of this drug. However, its dominant depressant effect obtained with increasing doses is somewhat favourable to its administration to epileptic patients.

Animals↗
PubMed1976

[EEG effects of sodium nitroprusside and hemodynamic references].

A study was performed on baboons (Papio papio) of various hemodynamic and EEG effects of sodium nitroprussiate (SNP), substance with powerful vasodilator action. Three different procedures of drug injection were used: (1) in isolation, either in doses close to those used in clinical practice or in high doses; (2) after neuroleptanalgesia (NLA); (3) after causing vasospasm. With isolated SNP, effects on blood pressure were unstable; in certain cases hypotension could be maintained only with toxic doses. Hypotension was facilitated when NLA had been previously induced. At low doses the cerebral blood flow (CBF) was practically unmodified, whereas at toxic doses it first increased then decreased. In animals under NLA, the CBF drop was only moderate, suggesting persistence of adequate spasm, CBF was significantly improved through SNP. The EEG did not undergo sizeable change at low SNP doses given in isolation; toxic doses always induced alterations with peculiar morphology, but developing only tardily after SNP perfusion was begun. This lag may indicate that hypotensive and toxic SNP effects are dissociated. These alterations suggest that screening of the EEG is necessary during prolonged administration of SNP, e.g., in surgical procedures. Combining NLA and SNP (at low doses) causes EEG deceleration, but no great alteration of the rhythms, as observed during other types of controlled experimental hypotension. Hence, cerebral circulation may be relatively well protected during SNP hypotension.

Animals↗
PubMed1976

[Experimental study of the cerebrovascular effects of sodium nitroprusside in the baboon Papio papio. Its action on the experimental vasospasm].

Sodium nitroprusside (SNP) has been suggested as hypotensive agent in the surgery of cerebral aneurysms. As a preliminary step to neurosurgery, a study of its cerebro-vascular and EEG action had been carried out in 42 papio-papio baboons. On the unanaesthetized analgesic-free animal, doses below 20 mumg/kg/min. induce only a moderate decrease of mean arterial blood pressure (MABP), a slight rise of intracranial pressure (ICP) and a neat fall of cerebro-vascular resistance (CVR) without EEG modifications. Doses above 50 mumg/kg/min. induce a neat fall of MABP with a rise of cerebral blood flow (CBF), of ICP and signs of poisoning with metabolic acidosis and prolonged EEG disturbances. Beyond 90 mumg/kg/min. irreversible hypotension occured accompanied by metabolic acidosis and progressive abolition of cerebral electrogenesis. The hypotensive action of SNP is potentiated by neuroleptanalgesic drugs (phenoperidine and dehydrobenzoperidol). Using this combination marked hypotension was achieved with non toxic doses of SNP (6 to 10 mumg/kg/min.). During those hypotensions cerebral auto-regulation was maintained up to a MABP of 50 mmHg. Deeper brief hypotensions up to a MABP of 25 to 45 mmHg induce a 23% fall of CBF (p less than 0, 05) but without major EEG alterations. During experimental arterial spasms induced by injection of blood in the cisterna magna or serotonin infusion, SNP has a vasodilating action. It induces a significant rise of CBF (p less than 0, 01) for doses between 8 and 19 mumg/kg/min.

Acid-Base Equilibrium↗