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Biomedical subjects

M A Tran

Publications and source records attributed to M A Tran.

At least 109 records · Page 6Linked to original sources
PubMedDate not supplied

Fluoxetine-induced pressor response in freely moving rats: a role for vasopressin and sympathetic tone.

The present study was performed in order to assess, in freely moving rats, the cardiovascular effects of central administration of fluoxetine, a serotonin reuptake inhibitor. Two kinds of experiments were performed: 1) acute central administration of fluoxetine. and 2) chronic intraperitoneal administration of fluoxetine plus selegiline, a monoamine oxidase B inhibitor. Intracerebroventricular (i.c.v.) administration of fluoxetine (5-50 microg) induced an increase in blood pressure. This fluoxetine-induced pressor response reached its maximal 1 hour after injection without any significant change in heart rate. At the dose of 10 microg i.c.v., fluoxetine significantly increased mean blood pressure by 16 +/- 4 mmHg. This pressor response was reduced by an intravenous (i.v.) pretreatment with the alpha1-adrenoceptor antagonist, prazosin (500 microg kg(-1)) (+ 7 +/- 4 mmHg, P <0.05) or with the V1A-vasopressin receptor antagonist (20 microg kg(-1)) (+5 +/- 3 mmHg, P < 0.05). The pressor response was completely abolished by a concomitant pretreatment with prazosin plus the V1A-vasopressin receptor antagonist. Pretreatment with the beta-adrenoceptor antagonist, propranolol (1 mg kg(-1) i.v.), or the 5-HT2 receptor antagonist, ketanserine (5 mg kg(-1) i.v.), did not modify the fluoxetine-induced pressor response. In freely moving rats receiving fluoxetine (10 microg i.c.v.), vasopressin plasma levels were significantly higher (39 +/- 5 pg mL(-1) than in rats receiving 10 microL i.c.v. saline (14 +/- 4 pg mL(-1)). A 30 day intraperitoneal (i.p.) administration of fluoxetine in association with selegiline induced an increase in noradrenaline plasma levels and locomotor activity without any significant change in blood pressure and heart rate. These data suggest that, the pressor response elicited by central acute administration of fluoxetine is mediated by both an increase in sympathetic tone and vasopressin release. This observation could suggest the putative interest of alpha1-adrenoceptor and or V1A-vasopressin receptor antagonists in the treatment of "Serotonin Syndrome".

Analysis of Variance↗
PubMedDate not supplied

Adrenergic neurohumoral influences on FFA release from bone marrow adipose tissue.

It is well known that both the sympathetic nervous system and several hormones control adipose tissue lipolysis. However, the relative importance of these different lipolytic agents may vary according to the animal species and according to the adipose territories in a same species. The action of noradrenaline administration on tibial intraosseous lipolysis was compared with the effects of splanchnic nerve and lumbar sympathetic chain stimulation in chloralose-anaesthetized dogs. The osseous nutrient artery was infused through the homolateral femoral artery in order to check constant blood flow. The levels of free fatty acids (FFA) were compared in femoral artery blood and in the osseous nutrient vein. Noradrenaline was injected in the infusion line. Lumbar sympathetic chain and splanchnic nerve were stimulated at frequencies of 3-10 Hz and 5-10 Hz respectively. Noradrenaline (at 411 p mol/min i.e. a dose three times higher than that required for adrenaline) induced FFA mobilization from tibial adipose bone marrow. Splanchnic nerve stimulation elicited an increase in the FFA levels in the nutrient vein whereas lumbar sympathetic chain stimulation had no remained without any effect. It is concluded that circulating adrenaline seems more important than noradrenaline released by sympathetic nerve endings in the control of activity of tibial bone marrow adipocytes.

Adipose Tissue↗
PubMedDate not supplied

Effect of clomipramine treatment on dog platelet alpha 2-adrenergic receptivity.

The effects of clomipramine treatment (5 mg/kg s.c. a day during 21 days) on dog platelet alpha 2-adrenoreceptivity were investigated. The radioligand binding studies on platelet membrane preparations showed that the antidepressant treatment promotes a decrease in the number of [3H]-yohimbine binding sites. The measurement of the inhibition of PGE1-induced cyclic AMP accumulation in the whole platelet indicated that the biological event immediately associated with alpha 2-adrenergic stimulation was not modified. The aggregatory response to ADP or ADP plus adrenaline was totally abolished in clomipramine-treated platelets. The diastolic pressor responses to noradrenaline or adrenaline injections (after propranolol and prazosin administration) in chloralose anaesthetized dogs were not affected by clomipramine treatment. This work shows that variations in the binding capacities of alpha 2-adrenergic sites are not always linked to modifications of related physiological events.

Adenosine Diphosphate↗