scholarly journals Carbamazepine does not alter the intrinsic cardiac function in rats with epilepsy

2010 ◽  
Vol 68 (4) ◽  
pp. 573-578 ◽  
Author(s):  
Diego B Colugnati ◽  
Ricardo M Arida ◽  
Roberta M Cysneiros ◽  
Vera C Terra ◽  
Eliza Y.F Sonoda ◽  
...  

Among the causes for sudden unexpected death (SUDEP) in epilepsy, the effects of antiepileptic drugs on the heart have been poorly explored. Based on this, the aim of our study was to evaluate the heart rate (in vivo and isolated ex vivo) and ventricular pressure (isolated ex vivo) of rats with and without epilepsy treated with carbamazepine. Four groups of adult, male Wistar rats (200-250 g) were studied: [A] control rats (n=8), received neither pilocarpine nor carbamazepine [B] carbamazepine-treated rats (n=8), received a daily dose of 120 mg/Kg, i.p. of carbamazepine for two weeks; [C] rats with epilepsy that received just saline solution (n=8); [D] rats with epilepsy that received a daily dose of 120 mg/Kg, i.p. of carbamazepine for two weeks (n=8). Our results showed significant increase in heart rate in animals with epilepsy (with and without the use of carbamazepine) when compared to the control groups in vivo. In contrast, we did not find differences during isolated ex vivo experiments comparing animals with and without epilepsy and despite the use of carbamazepine. Our results suggest that, in isolation, carbamazepine may not be a potential risk factor for sudden unexpected death in epilepsy.

2021 ◽  
Vol 8 (28) ◽  
pp. 119-127
Author(s):  
Olney Leite Fontes ◽  
Fátima Cristiane Lopes Goularte Farhat ◽  
Amarilys Toledo Cesar ◽  
Marilisa Guimarães Lara ◽  
Maria Imaculada Lima Montebelo ◽  
...  

Aims: Homeopaths diverge on the concept of dose, i.e. the amount of drug that a patient must take to alter his or her state of disease. In order to stimulate reflections on this concept, this study sought to evaluate in vivo the effect of different concentrations of Arsenicum album 6cH prepared according to homeopathic pharmacotechnics. Methods: male Wistar rats were intoxicated with arsenic and then treated with Arsenicum album 6cH and Arsenicum album 6cH diluted at 1%, administered orally. The amount of arsenic retained in the animals’ organism and that eliminated by urine were measured through atomic absorption spectroscopy. Samples of urine were collected before and after intoxication and during treatment. The positive control group (intoxicated animals) and the negative control group (non-intoxicated animals) received only the vehicle used in the preparation of the medicine. Results: Groups treated with Arsenicum album 6cH and Arsenicum album 6cH diluted at 1% eliminated significant amounts of arsenic when compared to the control groups. The group treated with Arsenicum album 6cH eliminated significantly higher amounts of arsenic than the group treated with the diluted medicine at 1%. Conclusion: results suggest that Arsenicum album 6cH should not be diluted as not to compromise its effectiveness in the treatment of rats intoxicated with arsenic.


Author(s):  
Yasmin Olsson ◽  
Helga Höifödt Lidö ◽  
Klara Danielsson ◽  
Mia Ericson ◽  
Bo Söderpalm

AbstractApproved medications for alcohol use disorder (AUD) display modest effect sizes. Pharmacotherapy aimed at the mechanism(s) by which ethanol activates the dopamine reward pathway may offer improved outcomes. Basal and ethanol-induced accumbal dopamine release in the rat involve glycine receptors (GlyR) in the nucleus accumbens (nAc). Glycine transporter 1 (GlyT-1) inhibitors, which raise extracellular glycine levels, have repeatedly been shown to decrease ethanol intake in the rat. To further explore the rational for elevating glycine levels in the treatment of AUD, this study examined accumbal extracellular glycine and dopamine levels and voluntary ethanol intake and preference in the rat, after systemic treatment with glycine. The effects of three different doses of glycine i.p. on accumbal glycine and dopamine levels were examined using in vivo microdialysis in Wistar rats. In addition, the effects of the intermediate dose of glycine on voluntary ethanol intake and preference were examined in a limited access two-bottle ethanol/water model in the rat. Systemic glycine treatment increased accumbal glycine levels in a dose-related manner, whereas accumbal dopamine levels were elevated in a subpopulation of animals, defined as dopamine responders. Ethanol intake and preference decreased after systemic glycine treatment. These results give further support to the concept of elevating central glycine levels to reduce ethanol intake and indicate that targeting the glycinergic system may represent a pharmacologic treatment principle for AUD.


Biomarkers ◽  
2021 ◽  
pp. 1-15
Author(s):  
Akpotu E. Ajirioghene ◽  
Samuel I. Ghasi ◽  
Lawrence O. Ewhre ◽  
Olusegun G. Adebayo ◽  
Jerome N. Asiwe

Author(s):  
Carlos Edmundo Rodrigues FONTES ◽  
Ana Paula de ABREU ◽  
Aretuza Zaupa GASPARIM

ABSTRACT Background: Researches on Chagas disease still use several animals and rats, due to size and susceptibility were preferred by many authors. Aim: To develop an experimental model of megacolon in rats inoculated with the strain Y of Trypanosoma cruzi. Methods: Thirty male Wistar rats were distributed in three groups inoculated with different inoculants: Group A: 600000, Group B: 1000000 and Group C: 1500000 blood trypomastigotes of T. cruzi. Animals were sedated intramuscularly at zero inoculation time (T0) and 60 days after inoculation (T60), to perform the barium enema in order to evaluate the dilatation of the different segments of colon in a comparative study of the measurements obtained, using a digital caliper. Evidence of infection was performed by blood smear collected from the animal’s tail 18 days after inoculation with observation of blood forms. Results: Comparing the intestinal diameter of the inoculated animals with 60,0000 trypomastigotes in the T0 of infection with T60 days after the inoculation, significant dilatation was observed between the proximal, medial and distal segments (p<0.01), indicating the establishment of the megacolon model. In addition, comparing intestinal diameter between the different segments, with in the T0 of infection and the T60 after inoculation, significant alterations were observed (p<0.05). Conclusion: The proposed model was possible for in vivo studies of alterations due to infection by T. cruzi and functional alterations of the colon. In addition, the changes manifested in the colon are not directly proportional to the size of the inoculum, but to the time of infection that the animals were submitted, since the animals inoculated with 60,0000 blood forms were the ones which presented the most significant alterations.


2015 ◽  
Vol 1 (1) ◽  
pp. 25
Author(s):  
Laila Fitrotuz Zahroh ◽  
Rahmawati Sri Praptiningsih ◽  
Moh. Baehaqi

Background: Oral mucosa ulceration which often occurs usually in the form of white-yellowish spot with concave surface, reddish edge and pain. Based on previous research, Aloe vera process anti-inflammation substance that could help quickening ulceration healing process. This research aims to know the effect of Aloe vera flesh extract on Male wistar rats oral mucosa ulceration in-vivo. Method: this research was quasi experimental research with the post-test only control group design using Male wistar rats as the testing animal. In the research, there were three treatment groups: The first groups which was given aquadest treatment, second groups with Aloe vera flesh extract, and third groups which was given chlorhexidine gluconate 0,2% treatment. The data collecting was based on histopathology observation concerning the increase of fibroblast quantity. Result: The research result based on comparison test among the three groups with One Way Anova showed that on Day 3th, the average quantity of fibroblast didn't have significant difference between the treatment group and control group positive that was p>0,05, meanwhile on Day 7th every group showed significant difference p<0,05. Conclusion: It concluded that Aloe vera flesh extract has influence on the healing of Male wistar rats oral mucosa ulceration as shown by fibroblast increasing quantity.


2015 ◽  
Vol 32 (04) ◽  
pp. 231-235
Author(s):  
R. Dantas ◽  
K. Souza ◽  
D. Santos ◽  
V. Feitosa ◽  
E. Fioretto ◽  
...  

Abstract Introduction: The objective of this study was to analyze the morphological structure of the heart and aorta of rats treated with the synthetic glucocorticoid dexamethasone. Material and Methods: Male Wistar rats were divided into two groups: 08 control rats undergoing treatment with a 0.9% saline solution for 10 days and 08 rats treated for 10 days with dexamethasone (2mg/kg animal weight). Results: Histological analysis detected a mild cardiac hypertrophy and 15% reduction of collagen located in the aorta of animals treated with glucocorticoid when compared to the control group. Conclusion: We conclude that treatment with dexamethasone for a period of 10 consecutive days is able to promote morphological changes in the structure of the heart chamber and, impair morphological structure of aorta.


2020 ◽  
Vol 3 (1) ◽  
pp. 31-44
Author(s):  
Bermansyah ◽  
Gama Satria ◽  
Ahmad Umar

Introduction.Pulmonary contusions can cause a progressive inflammatory response. Activation of TNF-α cytokines and reactive oxygen species (ROS) can cause pulmonary cell death. Antioxidants can have the potential to neutralize ROS. The purpose of this study is to determine the effectiveness of antioxidant administration in maintaining pulmonary cell function in wistar rats that have been induced to experience pulmonary contusions through caspase-3 levels. Methods.This study was an in vivo experimental study conducted on thirty male wistar rats and divided into five groups (n = 6): control, pulmonary contusion + asthaxanthine 5 mg/kgBW, pulmonary contusion + vitamin C and E 50 mg/kgBW, pulmonary contusion + vitamin C and E 100 mg/kgBW, pulmonary contusion + vitamin C and E 200 mg/kgBW. The value of Caspase-3 is evaluated by the IHC. All data analyzes used SPSS 18. Results. Low doses of antioxidants have the potential to reduce pulmonary cell death in wistar rats induced by pulmonary contusions.Conclussion. Vitamin C and E effective to reduce polmonary cell death in pulmonary contusion.Keywords: antioxidants, vitamin C, vitamin E, pulmonary contusions animal model, apoptosis, caspase-3


Author(s):  
Zhipeng Sun ◽  
Luqi Wang ◽  
Lu Han ◽  
Yue Wang ◽  
Yuan Zhou ◽  
...  

Background: Calsequestrins (Casqs), comprising the Casq1 and Casq2 isoforms, buffer Ca 2+ and regulate its release in the sarcoplasmic reticulum (SR) of skeletal and cardiac muscle, respectively. Human inherited diseases associated with mutations in CASQ1 or CASQ2 include malignant hyperthermia/environmental heat stroke (MH/EHS) and catecholaminergic polymorphic ventricular tachycardia. However, patients with an MH/EHS event often suffer from arrhythmia for which the underlying mechanism remains unknown. Methods: Working hearts from conventional ( Casq1 -KO) and cardiac-specific ( Casq1 -CKO) Casq1 knockout mice were monitored in vivo and ex vivo by electrocardiogram and electrical mapping, respectively. MH was induced by 2% isoflurane and treated intraperitoneally with dantrolene. Time-lapse imaging was used to monitor intracellular Ca 2+ activity in isolated mouse cardiomyocytes or neonatal rat ventricular myocytes (NRVMs) with knockdown, over-expression or truncation of the Casq1 gene. Conformational change in both Casqs was determined by crosslinking Western blot analysis. Results: Like MH/EHS patients, Casq1 -KO and Casq1 -CKO mice had faster basal heart rate, and ventricular tachycardia upon exposure to 2% isoflurane, which could be relieved by dantrolene. Basal sinus tachycardia and ventricular ectopic electrical triggering also occurred in Casq1 -KO hearts ex vivo . Accordingly, the ventricular cardiomyocytes from Casq1 -CKO mice displayed dantrolene-sensitive increased Ca 2+ waves and diastole premature Ca 2+ transients/oscillations upon isoflurane. NRVMs with Casq1-knockdown had enhanced spontaneous Ca2+ sparks/transients upon isoflurane, while cells over-expressing Casq1 exhibited decreased Ca2+ sparks/transients that were absent in cells with truncation of 9 amino acids at the C-terminus of Casq1. Structural evaluation showed that most of the Casq1 protein was present as a polymer and physically interacted with RyR2 in the ventricular SR. The Casq1 isoform was also expressed in human myocardium. Mechanistically, exposure to 2% isoflurane or heating at 41ºC induced Casq1 oligomerization in mouse ventricular and skeletal muscle tissues, leading to a reduced Casq1/RyR2 interaction and increased RyR2 activity in the ventricle. Conclusions: Casq1 is expressed in the heart, where it regulates SR Ca 2+ release and heart rate. Casq1 deficiency independently causes MH/EHS-like ventricular arrhythmia by trigger-induced Casq1 oligomerization and a relief of its inhibitory effect on RyR2-mediated Ca 2+ release, thus revealing a new inherited arrhythmia and a novel mechanism for MH/EHS arrhythmogenesis.


2018 ◽  
Vol 96 (9) ◽  
pp. 898-901 ◽  
Author(s):  
Mariana Rinaldi ◽  
Aline Cristina Batista Rodrigues Johann ◽  
Patrícia Vida Cassi Bettega ◽  
Fábio Rocha ◽  
Sérgio Aparecido Ignácio ◽  
...  

To evaluate the apoptosis in parotid glands of rats treated with midazolam associated or not with pilocarpine, 60 Wistar rats were assigned to 6 groups: control groups received saline solution for 30 days (S30) and 60 days (S60) and the other groups received pilocarpine for 60 days (P60), midazolam for 30 days (M30), midazolam for 30 days and 30 days of saline (M30 + S30), and finally midazolam for 30 days and 30 days of midazolam and pilocarpine (M30 + MP30). Histological sections were subjected to the TdT-mediated dUTP-biotin nick and labeling technique. The number of positive and negative cells was quantified, calculating the apoptotic index. ANOVA at 2 criteria and Tukey’s test were used. A greater apoptotic index was observed in the M30 (52.79 ± 9.01) and M30 + S30 (62.43 ± 8.52) groups when compared with the S30 (37.94 ± 5.94) and S60 (31.85 ± 9.18) groups, respectively (p < 0.05). There was no difference between M30 + MP30 (30.98 ± 6.19) and S60 (31.85 ± 9.18) groups regarding apoptotic index. Chronic administration of midazolam has been shown to increase the number of apoptotic cells in the parotid glands of rats. However, pilocarpine inhibited this effect, thus inhibiting the apoptosis.


1990 ◽  
Vol 259 (4) ◽  
pp. H1038-H1043 ◽  
Author(s):  
G. Julou-Schaeffer ◽  
G. A. Gray ◽  
I. Fleming ◽  
C. Schott ◽  
J. R. Parratt ◽  
...  

The involvement of L-arginine-dependent nitric oxide (NO) production in the vascular failure observed in endotoxemia was investigated in male Wistar rats treated with Escherichia coli lipopolysaccharide (LPS). Contractile responses to norepinephrine (NE) were measured ex vivo in aortas isolated from rats treated with LPS (20 mg/kg ip, 4 h before experiments) and pressor responses to NE were recorded in vivo in rats infused with LPS (5 mg.kg-1.h-1 iv). LPS pretreatment induced a rightward shift of the concentration-response curve to NE and a reduction of the maximal contraction by approximately 43% and 54% (P less than 0.05) in aortic rings with and without functional endothelium, respectively. This was not modified by the presence of indomethacin (10 microM) during the contractile experiments. In contrast, in the presence of NG-monomethyl-L-arginine (L-NMMA, 300 microM) or methylene blue (10 microM), maximal contractions to NE were restored to control values whether functional endothelium was present or not. The effects of L-NMMA were reversed by L- but not by D-arginine. Additionally, the effects of LPS pretreatment on vascular contractility were potentiated by L-arginine. In vivo, LPS infusion produced a reduction in pressor responsiveness to NE (0.1-10 mg/kg), which was also abolished by L-NMMA (30 mg/kg iv). This effect of L-NMMA was reversed by L- but not by D-arginine (100 mg/kg iv). These results demonstrate that activation of the L-arginine pathway has a major role in the production of vascular hyporeactivity in endotoxemia, ex vivo as well as in vivo. Additionally, they suggest that endothelium-independent vascular production of NO may be involved.


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