Biomedical subjects
Publications and source records attributed to F Boismare.
Treatment with cytidine diphosphocholine (20 mg/kg i.p.) in rats induces, during acute hypoxia, a reduction of vegetative responses (no modification of cerebral blood flow), a protection of conditioned avoidance response and a stabilization of dopamine and noradrenaline cerebral levels.
In dogs submitted to a normobaric hypoxia, we found an elevation of the arterial blood pressure, of the heart rate, of the cardiac output and of the regional blood flows, the total peripheral resistance remaining unchanged. Treatment with citidoline abolishes these hemodynamic responses and the authors hypothetize that this effect is correlated with the agonist dopaminergic effect of the drug.
Twenty somatic symptoms are listed, that are often met in depressive states but that are presently neglected by clinicians and by the various depression rating scales. Thanks to the data provided by animal pharmacology and clinical studies, an attempt to correlate the clinical studies with the biochemical results is proposed between those symptoms and eventual monoaminergic dysfunctions. This study leads to a clinical observation scale. In the future, the authors envisage a multifactorial analysis of the data obtained by the use of the scale. Symptomatic groupings could help establish a new classification for depressive states. They could also guide the choice of the medication according to the monoaminergic dysfunctions that are pointed out.
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A craniocervical injury has been carried out in rats (with head free to move) so that they get through a whiplash without any coma. Two days after the whiplash, comparable with a postcommotional syndrome, the acquisition of a labyrinth behavior is disturbed and, 7 days later, the retention is still disturbed. This disturbance of retention is not observed when the acquisition is performed before the whiplash. These data agree with the clinical observations, and we hypothesize a possible causal relation between the disturbance of learning behavior and the decrease of noradrenaline cerebral level induced by the whiplash. Treatment with imipramine (1 mg/kg) after the whiplash is able to remove these behavioral and biochemical disturbances.
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In the control dogs, hypoxia induced different hemodynamic modifications (i.e. an increase of arterial blood pressure, heart rate, cardiac output, regional blood flow) which seem to be related to a release of epinephrine. Pretreatment with benserazide (20 mg/kg i.v.) and L-Dopa (50 mg/kg i.p.) either lessened or completely suppressed any sign of sympathetic stimulation. These results suggest that chemoreceptors are centrally inhibited as had been previously proved for baroreceptors.
Analysis of hemodynamic parameters in untreated and treated dogs (levomepromazine 5 mg/kg i.v.) during supine and erect position showed, 1) that the regulation of cerebral blood flow remained in the anaesthetized (pentobarbital 25 mg/kg i.v.) dogs ; 2) that the sympathetic reaction induced different effects in various vascular regions ; 3) that levomepromazine induced an impairement of the mechanisms involved in the regulation of the encephalic irrigation.
The experimental reproduction of a cranio-cervical traumatism in the rat and consecutive troubles prove the organicity of the post-concussional syndrom. This syndrom seems to be due to an acceleration of the catabolism of cerebral norepinephrin, and the treatment by imipramine seems to inhibit the decrease of its rate.
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Pretreatment by benserazide (50 mg/kg i.p.) and L-Dopa (100 mg/kg i.p.) in rats induces a reduction of the diminution of motility after hypoxia and a stabilization of cerebral blood flow during and after hypoxia. An overload of cerebral dopamine and norepinephrine seems to be the original process of this phenomenon.
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The cortical evoked potential of the two cerebral hemispheres of the cat is taken as the parameter of brain function; its course is studied during strangulation which determines its disappearance, and especially during strangulation release (recovery phase). Under these experimental conditions, the injection of 9% NaCl solution in each carotid does not modify the symmetry of recovery in the two cerebral hemispheres. The unilateral injection of increasing doses of 1,6-dimethyl-8beta-(5-bromonicotinoyl-oxymethyl)-10alpha-methoxyergoline tartrate (nicergoline) (20 to 400 mug) produces more rapid recovery on the treated side. This is also the case for the unilateral injection of 40 mg of sodium malonate. Observation of this effect in the hypoventilated, hypercapnic animal, with an already dilated cerebral network suggests that the mechanism of the protection afforded is not due to vasodilatation of the cerebral network produced by either of the two products. The effect of nicergoline disappears when a previous i.v. injection of sodium malonate has inhibited anoxic depolarization of the cellular membrane and inhibited the fall in cerebral ATP caused by ischemia. It would thus appear that the anti-ischemic properties of nicergoline, acting at the level of the central nervous system, are due to an effect on the cellular membrane or to an inhibiting effect on the metabolism of the brain cell. Supplementary experiments, involving the use of more specific pharmacological reagents should allow its action to be localized at the level of the membrane and/or of cellular metabolism.