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1.
J Stud Alcohol ; 64(5): 662-8, 2003 Sep.
Article in English | MEDLINE | ID: mdl-14572188

ABSTRACT

OBJECTIVE: The purpose of this study was to investigate the effect of a single dose of ethanol on rat adrenal cortex and to determine whether the estrous cycle can influence this effect of ethanol. METHOD: Adult female Wistar rats showing proestrus or diestrus Day 1 (n = 12) were treated intraperitoneally with ethanol (4 g/kg body weight). Untreated (n = 15) and saline-injected (n = 14) rats were used as controls. The animals were sacrificed by decapitation 0.5 hour after ethanol administration. Stereological analysis was performed on paraffin sections of adrenal glands stained with AZAN, and the following parameters were determined: absolute volume of the zona glomerulosa, the zona fasciculata and the zona reticularis, numerical density, volume and the mean diameter of adrenocortical cells and of their nuclei, and diameter and length of capillaries. RESULTS: The diameter and volume of adrenocortical cells in the zona fasciculata and the zona reticularis were significantly increased by acute ethanol treatment at proestrus. In the same group of animals, a single dose of ethanol induced significant decrease in numerical density of adrenocortical cells and of their nuclei in all three zones. Increased length of capillaries of the zona fasciculata as well as enhanced level of serum corticosterone was found in ethanol-treated rats at both phases of the estrous cycle, proestrus and diestrus Day 1. CONCLUSIONS: The obtained results indicate that a single dose of ethanol activates adrenal cortex in female rats and that the effect is more pronounced on morphometric parameters at proestrus.


Subject(s)
Adrenal Cortex/pathology , Alcoholic Intoxication/pathology , Adrenal Cortex/blood supply , Adrenal Medulla/blood supply , Adrenal Medulla/pathology , Adrenocorticotropic Hormone/blood , Animals , Capillaries/pathology , Estrus/physiology , Female , Rats , Rats, Wistar , Reference Values
2.
Alcohol ; 26(3): 173-8, 2002 Apr.
Article in English | MEDLINE | ID: mdl-12057779

ABSTRACT

To determine whether an increased level of progesterone in adult female rats after acute ethanol treatment, described previously in our study, is the result of activation of adrenal glands, we analyzed adrenal cortex morphologically and measured serum levels of corticosterone and progesterone in ovariectomized rats. In addition, a possible involvement of the opioid system in an observed phenomenon was tested. Adult female Wistar rats were ovariectomized, and 3 weeks after surgery they were treated intraperitoneally with (a) ethanol (4 g/kg), (b) naltrexone (5 mg/kg), followed by ethanol (4 g/kg) 45 min later, and (c) naltrexone (5 mg/kg), followed by saline 45 min later. Untreated and saline-injected rats were used as controls. The animals were killed 0.5 h after ethanol administration. Morphometric analysis was carried out on paraffin sections of adrenal glands, stained with hematoxylin-eosin, and the following parameters were determined: absolute volume of the zona glomerulosa, the zona fasciculata, and the zona reticularis; numerical density, volume, and the mean diameter of adrenocortical cells and of their nuclei; and mean diameter and length of capillaries. The results showed that acute ethanol treatment significantly increased absolute volume of the zona fasciculata and length of its capillaries but did not alter other stereological parameters. Also, serum levels of corticosterone and progesterone were enhanced. Pretreatment with naltrexone had no effect on ethanol-induced changes. These findings are consistent with our previous hypothesis that an ethanol-induced increase of the progesterone level in adult female rats originates from the adrenal cortex.


Subject(s)
Adrenal Cortex/drug effects , Ethanol/pharmacology , Ovariectomy , Progesterone/blood , Adrenal Cortex/cytology , Adrenal Cortex/metabolism , Animals , Corticosterone/blood , Drug Administration Schedule , Female , Naltrexone/pharmacology , Ovariectomy/statistics & numerical data , Rats , Rats, Wistar
3.
Srp Arh Celok Lek ; 130(11-12): 371-5, 2002.
Article in Serbian | MEDLINE | ID: mdl-12751159

ABSTRACT

Postmenopause and smoking impair lipid profile, induce hypercoagulability and reduce fibrinolytic capacity [1, 2]. Postmenopause induced lipid changes can be reversed by oestrogen replacement [3]. Oestrogens also reduce fibrinogen level [4] and have beneficial effects on endothelium [5]. Although several studies showed that hormone replacement therapy may increase the risk of thromboembolic diseases, procoagulant oestrogen activity has not clearly been demonstrated. It is well known that smoking accelerates oestrogen metabolism [6, 7], which may attenuate its beneficial effects. The present study was undertaken to determine if there is difference in beneficial effects of oestrogens between smokers and non-smokers in terms of coagulation process and lipids. The examination was a longitudinal, one-year, before/after therapeutic study, which included healthy postmenopausal women (FSH levels at least 40 U/l), 30 smokers and 32 non-smokers who were under 55 years of age and postmenopausal period shorter than 5 years. Women with surgically induced menopause received unopposed oral oestrogens, while those with spontaneous menopause were treated with combined oral oestrogen/progestogen therapy. Before entering the study and in three-months intervals total LDL, HDL cholesterol, triglycerides and VLDL were determined, as well as plasma fibrinogen, prothrombin time, and activated partial thromboplastin time. Neither beneficial nor adverse effects of oestrogens on lipids and coagulation were observed during one-year follow-up in smokers, although subjects with longer smoking history had higher triglycerides levels after 12 months of therapy. On the contrary, oestrogen replacement reduced total and LDL cholesterol, and increased HDL cholesterol in non-smokers, with no change in triglycerides and VLDL level. A decrease in fibrinogen levels and coagulation activity, expressed by prothrombin time and partial thromboplastin time, were also observed in hormone replacement therapy in postmenopausal women who did not smoke. Peroral hormone replacement therapy does not induce favorable lipid changes in smokers. Higher triglycerides levels observed after one-year therapy in women with a longer smoking history indicate that transdermal replacement maybe more suitable in this group. Peroral oestrogen replacement has no anticoagulant or procoagulant activity in smokers during the early postmenopausal period.


Subject(s)
Blood Coagulation/drug effects , Estrogen Replacement Therapy , Lipids/blood , Postmenopause/blood , Smoking/blood , Female , Humans , Middle Aged
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