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Biomedical subjects

C Capdeville

Publications and source records attributed to C Capdeville.

30 records · Page 2Linked to original sources
PubMedDate not supplied

[Tolerability of tianeptine in 170 patients with depression treated during one year].

Tianeptine, a new antidepressant, has a tricyclic molecular structure. Its main biochemical activity consists of an increase in the reuptake of 5 HT both in men and animals, after acute and chronic administration. Tianeptine demonstrated its antidepressive clinical efficacy in several double-blind versus reference drug trials. A multicentre open trial, including depressed patients enabled us to evaluate the safety of tianeptine and to control the maintenance of the therapeutic efficacy in the course of its long-term prescription. Depressed patients included showed a major depressive episode, single (296.22) or recurrent (296.32) without melancholia or psychotic features, or a dysthymic disorder (300.40), according to DSM III criteria. A minimum MADRS score of a least 25, and the informed consent of the patients were required. The dose of tianeptine was 3 tablets per day (12.5 mg/tablet) with the possibility of increasing to 4 or decreasing to 2 tablets per day, depending on the symptomatology. Therapeutic efficacy was evaluated by item 1 and 2 of the Global Clinical Impression (CGI), the Montgomery and Asberg Depression Rating Scale (MADRS), the Hamilton Anxiety Rating Scale (HARS) and the Hopkins Symptom Check-List (HSCL). Clinical and paraclinical safety were evaluated by CGI item 3, standardized ratings of patients' complaints (CHESS 84), interruption for side effects, evaluation of blood pressure, weight, biological parameters, EKGs. This intermediate evaluation concerns the first 170 depressed patients treated over a one-year period as well as the total group of patients included (n = 447).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Model of global forebrain ischemia in the unanesthetized rat.

Global forebrain ischemia was induced in unanesthetized rats by electrocauterization of the vertebral arteries and transient occlusion of the common carotid arteries for 30 minutes. Local cerebral blood flow (l-CBF), cortical tissular pO2 (tpO2), electrocorticogram (ECoG), mean arterial pressure, pH and blood gas determinations and neurologic deficit were evaluated during and after ischemia. Cerebral ischemia induced a substantial decrease in l-CBF and tpO2 and the ECoG was flattened. One hour after ischemia, the neurologic deficit was at its maximum, l-CBF was still decreased and ECoG depressed. Twenty-four hours later, the neurologic deficit was still present but ECoG, l-CBF and tpO2 had returned to their preischemic values. Treatments with naloxone were performed during, after or during and after ischemia. When naloxone was administered during or after ischemia, postischemic neurologic deficit was not influenced by the treatment. A slight but significant improvement of the neurologic score was observed when naloxone was injected during ischemia and infused thereafter. Our results show that this experimental model of cerebral ischemia is suitable for quantification of neurologic alterations during the postischemic period. The slight improvement observed with naloxone suggests that endogenous opioids may have a minor role in the neurologic consequences of ischemia.

Animals↗
PubMedDate not supplied

Effect of indomethacin on the coupling of cerebral blood flow to brain metabolism.

The effect of indomethacin (10 mg.kg-1 i.p.) on frontal cerebral blood flow has been investigated in male Sprague Dawley rats using the hydrogen clearance technique. Indomethacin elicited a marked reduction in cerebral blood flow in awake free-moving animals. The response to indomethacin was prevented by pretreatment with pentobarbital (50 mg X kg-1, i.p.). On the other hand, indomethacin was able to antagonize the cerebral vasodilation due to apomorphine chlorhydrate (2 mg X kg-1, i.p.), dexamphetamine tartrate (3 mg X kg-1, i.p.) or immobilization stress. Taken together, the above results lead to the suggestion that indomethacin can suppress the coupling of cerebral blood flow to brain metabolism. Further investigations are needed to ascertain whether this uncoupling influence is related to brain cyclooxygenase inhibition.

Anesthesia↗
PubMedDate not supplied

[The effects of cerebral ischemia on the level of metabolites of dopamine and serotonin in the rat cerebrospinal fluid].

Hemispheric ischemia was induced in normothermic, artificially ventilated and anesthetized rats, by electrocauterization of the vertebral arteries and a transient occlusion of the common carotid arteries for 10 minutes. Cerebrospinal fluid (CSF) was continuously pumped out of the third cerebral ventricle for potassium, dopamine and serotonin metabolite determinations. Levels were stable until ischemia, which interrupted the CSF production. During early recirculation a marked increase in dopamine metabolites occurred. The metabolite of serotonin increased slightly with a delay. Potassium in CSF was transitorily increased following ischemia. Reserpine pretreatment prevented most of the changes such as the early increase in dopamine metabolites. A delayed increase of these metabolites was still observed. This model of short ischemia altered the neurological functioning and survival time of the animals especially 15 minutes after removal of bilateral carotid occlusion, as compared to the later periods of observation. This model is therefore applicable to the study of cerebral alterations secondary to ischemia in vivo. The presently observed alterations of metabolite levels could reflect an increased neuronal release of parents monoamines that could participate to the neurological deficit.

3,4-Dihydroxyphenylacetic Acid↗