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    STUDIA BIOLOGIA - Ediţia nr.2 din 2003  
         
  Articol:   ATENUAREA MODIFICĂRILOR GRAVIMETRICE INDUSE DE TRATAMENTUL CU FLUOCINOLON-ACETONID N PRIN ADMINISTRAREA DE PROPRANOLOL.

Autori:  ERIKA KIS, CONSTANTIN CRĂCIUN.
 
       
         
  Rezumat:  Attenuation of the Fluocinolone-acetonid N-Induced Gravimetric Disorders by Propranolol. Our results, in compliance with those from the literature, show that the epicutaneously absorbed dermocorticoids in rats cause a glucocorticoid excess, specific to the state of steroid-diabetes, manifested by hyperglycemia, hepatic and thymic glucose overproduction, elevated serum lipids. All these metabolic disorders are based on endocrine modifications due to the alteration of the functioning of hypothalamo-pituitary-adrenal (HPA) axis. Some of these endocrino-metabolic disorders and HPA structural alterations, according to our recent observations, are reducible by in vivo β-adrenoreceptor blockage with Propranolol. Experimental data point to the fact that the action of dermocorticoids is facilitated by the presence of β-adrenoreceptors in epidermis, in keratocytes and Langerhans cells of its basic layer. β-Adrenoreceptors stimulate the epicutaneous absorption of glucocorticoids as well as their accumulation in organism, which explains the appearance of systemic secondary side-effects. The alterations inferred by the epicutaneous absorption of dermocorticoids are more obvious in the young organism, due to the fact that the epidermis is thinner, thus facilitating the absorption of glucocorticoids. The epicutaneous treatment with Fluocinolone-acetonid N determines, under conditions of our experiments, thymolysis, adrenal and spleen atrophy, associated with a reduced growth rate of the individuals. When daily dermocorticosteroid treatment for three days was associated with Propranolol administration (50 μg s.c./100 g b.w/day) in rats, the above-mentioned alteration in gravimetric parameters were significantly attenuated, as compared to the corresponding dermocorticosteroid-treated group. It is concluded that β-adrenoreceptor stimulation significantly participates in glucocorticoid excess-induced metabolic and gravimetric alterations.  
         
     
         
         
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