Dissociation Of Toxic And Behavioral Effects Of Chronic Treatment With Lithium In Rats [dissociacao Entre Efeitos Toxicos E Comportamentais Do Tratamento Cronico Com Litio Em Ratos]

[No abstract available]33642743

Histopathologic Study On The Effects Of Tenoxicam With Bidistilled Water Or With 0.9% Sodium Chloride In Rabbits Venous Endothelium [estudo Histopatológico Do Efeito Do Tenoxicam Com água Bidestilada Ou Com Cloreto De Sódio A 0,9% No Endotélio Venoso De Coelhos]

Background and Objectives - After exposure to indomethacin, human umbilical vein endothelial cells have shown increased procoagulant activity. Thrombosis in rabbit auricular veins has been observed after injection of tenoxicam with its diluent or of the diluent alone. Human studies evaluating venous endothelium after tenoxican injection were not found in the literature. This study aimed at evaluating whether tenoxicam with 0.9% sodium chloride changes the venous endothelium of rabbits as it is observed when associated to its diluent (bidistilled water). Methods - The study involved 90 rabbits (2000 and 3500 grams) divided in two groups: Control group, which received 0.9% NaCl; Experimental group, which received tenoxicam (20 mg) with bidistilled water or with 0.9% NaCl. A constant volume of 2 ml was administered to both groups. Anesthesia was induced with acepromazine maleate, ketamine hydrochloride and xylazine hydrochloride, and the puncture of right and left caudal auricular veins was performed with a 27G butterfly needle. Animals were confined for 6 hrs, 12 hrs, and 24 hrs, when they were once more anesthetized and sacrificed, with extraction of the auriculae at their base, followed by microscopic venous study. Results - Thrombosis was observed in 19.4% of the Experimental Group after the administration of tenoxicam with bidistilled water and in 22.2% after the administration of tenoxicam with 0.9% sodium chloride. In the Control group, which has only received 0.9% sodium chloride, no thrombosis was observed. Conclusions - It was possible to conclude that tenoxicam, either with bidistilled water or 0.9% sodium chloride, has induced thrombosis in the veins it was injected.522223230Nygard, G., Hudson, M., Mazure, G., Procoagulant and prothrombotic responses of human endothelium to indomethacin and endotoxin in vitro. Relevance to non-steroidal anti-inflammatory drug enteropathy (1995) Scand J Gastroenterol, 30, pp. 25-32Schnaider, T.B., Andrade, C.H.V., Juliano, Y., Estudo histopatológico do efeito do tenoxicam e do seu diluente no endotélio venoso, em coelhos (2000) Acta Cir Bras, 15, pp. 118-123Cotran, R.S., Kumar, V., Robbins, S., (1996) Robbins Patologia Estrutural e Funcional, 5 a Ed., pp. 84-109. , Rio de Janeiro, Guanabara KooganWhittle, B.J.R., Morishita, T., Ohya, Y., Microvascular actions of platelet-activating factor on rat gastric mucosa and submucosa (1986) Am J Physiol, 251, pp. G772-G778Wallace, J.L., Keenan, C.M., Granger, D.N., Gastric ulceration induced by nonsteroidal anti-inflammatory drugs is a neutrophil-dependent process (1990) Am J Physiol, 259, pp. G462-G467Wallace, J.L., Lipid mediators of inflammation in gastric ulcer (1990) Am J Physiol, 21, pp. G1-G11Rang, H.P., Dale, M.M., Ritter, J.M., (2001) Farmacologia, 2 a Ed., pp. 255-269. , Rio de Janeiro, Guanabara Kooga

Estrogenic activity of tamoxifen on normal mammary parenchyma in the luteal phase of the menstrual cycle

Objectives: Tamoxifen, an anti-estrogenic drug used in the adjuvant treatment of breast cancer, deserves more investigation for the determination of its efficacy as a prophylactic agent against breast cancer in high risk women. Thus, the action of tamoxifen on the human mammary gland was studied by measuring the number of lysosomes in normal mammary epithelium during the administration of tamoxifen. Methods: Tamoxifen was administered only during the luteal phase of the menstrual cycle to avoid interference with corpus luteum formation. A fragment of breast tissue adjacent to a fibroadenoma was obtained during surgery from 35 premenopausal women aged 15 to 37 years who had been eumenorrheic for at least 6 months; 18 of these patients were treated with tamoxifen and 17 were used as controls. Lysosome counts were performed under the light microscope on slides submitted to the acid phosphatase cytochemical technique and the data were analyzed statistically by the Mann-Whitney test. Results: the fragments from the group treated with tamoxifen showed a significant decrease in lysosome numbers. Conclusions. Tamoxifen administered after ovulation significantly decreases the number of lysosomes in the cells of normal mammary epithelium, demonstrating the antiestrogenic effect of the drug on this target tissue. (C) 1997 International Federation of Gynecology and Obstetrics.Universidade Federal de São Paulo,DEPT GYNECOL,ESCOLA PAULISTA MED,São Paulo,BRAZILUniversidade Federal de São Paulo,DEPT GYNECOL,ESCOLA PAULISTA MED,São Paulo,BRAZILWeb of Scienc

Effect of lung resection and sham surgery on the frequency of infection in alloxan-diabetic rats

The present study was carried out in order to determine the effect of lung resection on the frequency of infections in alloxan-diabetic rats. Adult female Wistar rats were injected with alloxan (40 mg/kg, iv) to induce diabetes mellitus (group D; N = 45) or with vehicle (1.0 ml/kg, iv) to be used as controls (group C; N = 45). Thirty-six days after receiving alloxan both groups were randomly divided into three subgroups: no operation (NO; N = 15), sham operation (SO; N = 15), and left pneumonectomy (PE; N = 15). The rats were sacrificed 36 days after surgery and their lungs were examined microscopically and macroscopically. The occurrence of thoracic wall infection, thoracic wall abscess, lung abscess and pleural empyema was similar in groups D and C. In contrast, the overall infection rate was higher (P<0.05) in the diabetic rats (SO-D and PE-D subgroups, but not in the NO-D subgroup). Considering that the overall infection rate was similar in the SO-D and PE-D subgroups, we suggest that surgery but not pneumonectomy was related to the higher prevalence of infection in diabetic rats

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)