The effect of surgical menopause on the intima-media thickness of the carotid and coronary arteries.

OBJECTIVE: To evaluate the effect of prior bilateral oophorectomy on the intima-media thickness (IMT) of coronary and carotid arteries. METHODS: A total of 25 Wistar albino rats, aged 8-10 weeks, were assigned to three groups: ovariectomized (n = 10), control (n = 10) and sham (n = 5). The rats in the sham group only underwent midline laparotomy, while the other rats' ovaries were removed by the same type of laparotomy. All rats were sacrificed to evaluate microscopically the impact of a prolonged 26-week surgical menopause (menopausal period) on the IMT of the carotid and coronary arterial structure. RESULTS: The mean IMTs of both the carotid and coronary arteries in the ovariectomized group were significantly thicker than those of the control and sham groups (carotid arteries: 268.69 ± 53.67, 195.61 ± 47.60 and 193.86 ± 75.01 µm, p = 0.014; coronary arteries: 182.40 ± 30.22, 136.00 ± 35.82 and 165.24 ± 40.68 µm, p = 0.022, respectively). CONCLUSION: According to the results of this study, surgical menopause results in a noteworthy increase in the IMT of the carotid and coronary arteries when compared with the controls. This interventional effect may have a significant role in accelerating the process of atherosclerosis.

Assessment of follicular and serum VEGF and IGF-1 in ICSI patients: hMG vs rFSH.

PURPOSE: To investigate the effect of recombinant follicular stimulating hormone (r-FSH) and human menopausal gonadotropin (hMG) on follicular microenvironment via assessment of follicular and serum vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1) levels in intracytoplasmic sperm injection (ICSI) cycles. MATERIALS AND METHODS: Designed as a prospective cohort study. Twenty-five patients underwent controlled ovarian hyperstimulation (COH) with r-FSH and 20 patients underwent with hMG. RESULTS: Both groups were comparable regarding the women's mean age and body mass index (BMI). The amount of VEGF (pg/ml) in serum and follicular fluid in the group I and II were comparable (275 ± 135.3 vs 330.7 ± 190.0; p > 0.05 and 2,081.1 ± 1095.1 vs 1,971.1 ± 975.6; p > 0.05, respectively). The amount of IGF-1 (ng/ml) in serum and follicular fluid in the group I and II were also comparable (225.3 ± 69.3 vs 204.1 ± 56.3, p > 0.05 and 176.1 ± 67.2 vs 185.8 ± 48.7, p > 0.05, respectively). Pregnancy rates were also comparable between groups. CONCLUSIONS: The hMG and r-FSH in COH produced comparable follicular microenvironment regarding follicular VEGF and IGF-l.

Umbilical CORD S100B levels in active and passive smoker women.

OBJECTIVES: In utero fetal exposure to tobacco smoke has been found to be associated with adverse pregnancy outcome and increased maternal and fetal risks. The aim of this study was to compare umbilical cord blood S100B levels of infants of active smoker, passive smoker and non-smoker mothers. SUBJECTS AND METHODS: A total of 82 women, 26 habitual smokers, 27 passive smokers and 29 controls, who were admitted for repeat elective cesarean delivery with uncomplicated term gestations were included in the study. The age, gravidity, parity and gestational week at delivery were recorded on admission for the delivery. Ultrasonographic evaluation was routinely done on admission and birth weights of the newborns were measured immediately upon delivery. Umbilical cord blood was collected following delivery of the infants and serum S100B levels were analyzed at the end of the study period. The groups were compared according to S100B levels. RESULTS: No significant difference was found between the three groups regarding age, gravidity, gestational week at delivery or birth weight of the infants (p > 0.05). Biparietal diameter of the fetuses of active smoker mothers were significantly smaller than passive smokers and controls (90.3 ± 1.8 vs 94.2 ± 2.8 and 93.8 ± 2.5, respectively). Mean S100B level in the umbilical cord blood of active smokers was lower than passive smokers and controls (768.9 ± 446.9 vs 1050.1 ± 383.2 and 1035.3 ± 405.2) (p = 0.024). CONCLUSIONS: Fetuses of active smoker mothers had lower cord blood S100B levels, suggesting a possible injury of glial cells.

Chronic ethanol consumption impairs adrenoceptor- and purinoceptor-mediated relaxations of isolated rat detrusor smooth muscle.

OBJECTIVE: To investigate the effects of chronic ethanol consumption on the reactivity of detrusor smooth muscle. MATERIALS AND METHODS: Eight male rats received ethanol (7.2% v/v) in a modified liquid diet for 4 weeks. Two control groups were assessed; eight rats in one group were fed sucrose and received a liquid diet, and 12 rats in the second group received standard rat chow and water for 4 weeks. The reactivity of detrusor smooth muscle strips from ethanol-fed animals and control animals was evaluated in organ chambers. RESULTS: The relaxation response elicited by isoprenaline or adenosine was unaffected in the both control groups while it was significantly inhibited, with decreased maximum responses and pD2 values, in the ethanol-fed group. Contractile responses of detrusor smooth muscle to carbachol or 80 mmol/L KCl and relaxant responses to papaverine were similar in the control groups and the ethanol-fed group. There was no change in agonist potency among the groups. CONCLUSION: Chronic ethanol consumption impairs beta-adrenoceptor- and purinoceptor-mediated relaxation but not cholinoceptor-mediated contraction of the rat detrusor smooth muscle. Thus, it appears that different regulatory mechanisms are involved in ethanol-induced alterations in beta-adrenergic, purinergic and muscarinic receptors in detrusor strip.

Blood pressure and vascular reactivity to endothelin-1, phenylephrine, serotonin, KCl and acetylcholine following chronic alcohol consumption in vitro.

Ethanol has been reported to cause hypertension, the mechanism of which is unknown. Therefore, the effect of chronic ethanol consumption on vascular responsiveness and blood pressure was investigated. Systolic blood pressure was recorded weekly by tail-cuff method. Aortic rings from rats fed chow ad libitum or pair-fed liquid diets containing either ethanol (7.2% v/v) or isocaloric carbohydrate for 4 weeks were placed in organ chambers for isometric tension measurement. There was a mild but significant elevation of the systolic blood pressure in the alcohol-fed rats by week 1 compared to baseline measurements and this remained higher. No significant changes in reactivity of rat isolated aortas to phenylephrine, serotonin, endothelin-1 (ET-1) and KCl were seen in chronic ethanol consumption. In addition, the sensitivity (i.e. pD2) of alcohol-fed aortic rings to the vasoconstrictors was also unchanged compared to controls. Chronic ethanol consumption, however, increased relaxation to acetylcholine with increased pD2 values, but did not alter relaxation to sodium nitroprusside, a cyclic guanosine monophosphate (cGMP)-dependent direct smooth muscle dilator. The results indicate that chronic ethanol consumption significantly potentiates endothelium-dependent relaxations in aortic rings, probably through interference with the production and/or the release of nitric oxide (NO) or adaptive alterations in muscarinic receptors on the endothelial cells, and that increased vascular responsiveness to several vasoconstrictors is not a mechanism responsible for the blood pressure elevation in the chronic alcohol consumption in rats.

The effect of long-term ethanol feeding on Brucella melitensis infection of rats.

The adverse effects of ethanol on Brucella melitensis have not been studied previously. In this study, a new model of B. melitensis infection was used in the setting of chronic ethanol administration in rats. It was found that the chronically ethanol-receiving rats exposed to B. melitensis infection had significantly greater numbers of B. melitensis in their spleen and liver than the rats in the control group.

Antidepressant, anxiogenic, and antinociceptive properties of levofloxacin in rats and mice.

Levofloxacin, an optically active isomer of ofloxacin, is a fluorinated quinolone with a broad spectrum of antibacterial activity. Fluoroquinolones have been used for the treatment of bacterial infections for many years. Although they were considered as relatively safe drugs, various adverse effects have recently been reported along with increase in the usage of new-generation fluoroquinolones. In the present study, some of the central nervous system (CNS)-related side effects of levofloxacin were clarified in animals. Our results suggested that: levofloxacin (10-20-40 mg/kg i.p.) had no depression-like effect in the forced swimming test (FST) in rats; exerted anxiety-like effect in the elevated plus maze test in rats; did not alter the locomotor activity in rats; had no apparent effect on sleep latency but shortened the sleeping time on pentobarbital sleeping time in mice; and showed analgesic activity in acetic acid writhing and hot plate test in mice.

Impaired neurogenic and endothelium-dependent relaxant responses of corpus cavernosum smooth muscle from hyperthyroid rabbits.

We investigated the effect of hyperthyroidism on the responsiveness of the rabbit corpus cavernosum smooth muscle. In male albino rabbits, hyperthyroidism was established by oral feeding of L-thyroxine at increasing dosages (150-450 microg/kg) over an 8-week period. This treatment produced a stable hyperthyroid state as indicated by the increased serum T4 levels. The reactivity of corpus cavernosum tissue from hyperthyroid animals and euthyroid control animals was studied in organ chambers. Hyperthyroidism caused impaired neurogenic and endothelium-dependent relaxant responses with decreased Emax and pD2 values. However, hyperthyroidism had no effect on both phenylephrine- and KCl-induced contractile responses and sodium nitroprusside- and papaverine-induced endothelium-independent relaxant responses, and there was no change in agonist potency. These data indicate that hyperthyroidism may impair both neurogenic and endothelium-dependent relaxation of corporal smooth muscle, and may contribute to the etiology of impotence.

Dextromethorphan attenuates ethanol withdrawal syndrome in rats.

The effects of dextromethorphan (DM), a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptors, have been investigated on ethanol withdrawal signs in rats. Ethanol (7.2% v/v) was given to rats in a liquid diet for 16 days. DM (10, 20, and 40 mg/kg) and saline were injected intraperitoneally at the third hour of ethanol withdrawal. DM (40 mg/kg) and ethanol dependent saline were also administered to ethanol naive rats. DM (40 mg/kg) did not produce any significant change in locomotor activity in ethanol naive rats. The effects of DM on locomotor activity and total ethanol withdrawal score were evaluated at the fourth and sixth hours of ethanol withdrawal. DM inhibited locomotor hyperactivity at these periods. DM also reduced total ethanol withdrawal score from the fourth hour to the sixth hour, and it significantly decreased audiogenic seizures. Seizure susceptibility after chronic ethanol exposure may be dependent upon sensitization or upregulation of NMDA processes and NMDA receptors. Our results suggest that inhibition of NMDA receptors by DM alleviates signs of ethanol withdrawal.