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BACKGROUND: The aim of this study was to investigate the effects of intracerebroventricularly administered rocuronium bromide on the central nervous system, determine the seizure threshold dose of rocuronium bromide in rats, and investigate the effects of rocuronium on the central nervous system at 1/5, 1/10, and 1/100 dilutions of the determined seizure threshold dose. METHODS: A permanent cannula was placed in the lateral cerebral ventricle of the animals. The study was designed in two phases. In the first phase, the seizure threshold dose of rocuronium bromide was determined. In the second phase, Group R 1/5 (n=6), Group 1/10 (n=6), and Group 1/100 (n=6) were formed using doses of 1/5, 1/10, and 1/100, respectively, of the obtained rocuronium bromide seizure threshold dose. RESULTS: The rocuronium bromide seizure threshold value was found to be 0.056±0.009µmoL. The seizure threshold, as a function of the body weight of rats, was calculated as 0.286µmoL/kg-1. A dose of 1/5 of the seizure threshold dose primarily caused splayed limbs, posturing, and tremors of the entire body, whereas the dose of 1/10 of the seizure threshold dose caused agitation and shivering. A dose of 1/100 of the seizure threshold dose was associated with decreased locomotor activity. CONCLUSIONS: This study showed that rocuronium bromide has dose-related deleterious effects on the central nervous system and can produce dose-dependent excitatory effects and seizures.

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BACKGROUND: The aim of this study was to investigate the effects of intracerebroventricularly administered rocuronium bromide on the central nervous system, determine the seizure threshold dose of rocuronium bromide in rats, and investigate the effects of rocuronium on the central nervous system at 1/5, 1/10, and 1/100 dilutions of the determined seizure threshold dose. METHODS: A permanent cannula was placed in the lateral cerebral ventricle of the animals. The study was designed in two phases. In the first phase, the seizure threshold dose of rocuronium bromide was determined. In the second phase, Group R 1/5 (n=6), Group 1/10 (n=6), and Group 1/100 (n=6) were formed using doses of 1/5, 1/10, and 1/100, respectively, of the obtained rocuronium bromide seizure threshold dose. RESULTS: The rocuronium bromide seizure threshold value was found to be 0.056±0.009µmoL. The seizure threshold, as a function of the body weight of rats, was calculated as 0.286µmoL/kg-1. A dose of 1/5 of the seizure threshold dose primarily caused splayed limbs, posturing, and tremors of the entire body, whereas the dose of 1/10 of the seizure threshold dose caused agitation and shivering. A dose of 1/100 of the seizure threshold dose was associated with decreased locomotor activity. CONCLUSIONS: This study showed that rocuronium bromide has dose-related deleterious effects on the central nervous system and can produce dose-dependent excitatory effects and seizures.

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BACKGROUND: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS: Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1µg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS: There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION: Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.

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BACKGROUND: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS: Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1µg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS: There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION: Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.

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BACKGROUND: It is known that hypoxic pulmonary vasoconstriction increases as a result of intermittent regional hypoxic challenges. The aim of this study was to compare the effects of sevoflurane and propofol on oxygenation and shunt fraction during one-lung ventilation in a novel model of hypoxic preconditioning before one-lung ventilation. METHODS: Sixteen Wistar-albino rats were anesthetized intra-peritoneally before venous and arterial cannulations and tracheotomized. The animals were randomly allocated to receive either sevoflurane 2% or 10mg/kg/h propofol infusion and ventilated with 100% oxygen at an inspiratory rate of 80 breaths/min for 30min. Three cycles of one-lung ventilation and two-lung ventilation were performed and one-lung ventilation was continued for 15min. Arterial blood gas samples were obtained as follows: after cannulation and tracheotomy, following 30min of treatment with sevoflurane or propofol, and at the 5th and 15th min of one-lung ventilation. RESULTS: The PaO2 levels were higher and shunt fractions were lower in rats receiving propofol compared to rats treated with sevoflurane but the difference was not significant; the two groups were comparable in terms of PaCO2. CONCLUSIONS: The similar effects of sevoflurane and propofol on PaO2 during one-lung ventilation following hypoxic preconditioning may be due to other causes beside the inhibition of hypoxic pulmonary vasoconstriction. Gradual transition to one-lung ventilation is a novel technique for preconditioning experiments for one-lung ventilation.

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Justificativa e objetivo: sabe-se que a vasoconstrição pulmonar hipóxica aumenta como resultado de desafios hipóxicos regionais intermitentes. O objetivo deste estudo foi comparar os efeitos de sevoflurano e propofol na oxigenação e fração de shunt durante a ventilação monopulmonar em um novo modelo de hipóxia pré-condicionado antes da ventilação monopulmonar. Métodos: foram anestesiados intraperitonealmente antes das canulações venosa e arterial e traqueostomizados 16 ratos albinos Wistar. Os animais foram randomicamente distribuídos para receber perfusão de sevoflurano a 2% ou 10 mg/kg/h de propofol e ventilados com oxigênio a 100%, a uma taxa inspiratória de 80 respirações/minuto por 30 minutos. Três ciclos de ventilação monopulmonar e ventilação de ambos os pulmões foram feitos e a ventilação monopulmonar foi continuada por 15 min. Amostras de gasometria arterial foram obtidas da seguinte forma: após punção e traqueotomia, após 30 minutos de tratamento com sevoflurano ou propofol e aos cinco e 15 minutos de ventilação monopulmonar. Resultados: os níveis de PaO2 foram maiores e as frações de shunt menores nos ratos que receberam propofol em comparação com os ratos tratados com sevoflurano, mas a diferença não foi significante. Os dois grupos foram comparáveis em termos de PaCO2. Conclusões: os efeitos similares de sevoflurano e propofol na PaO2 durante a ventilacão monopulmonar após pré-condicionamento hipóxico podem ter resultado de outras causas além da inibição da vasoconstrição pulmonar hipóxica. A transição gradual para a ventilação monopulmonar é uma técnica nova de pré-condicionamento de experimentos para ...

Background: It is known that hypoxic pulmonary vasoconstriction increases as a result of intermittent regional hypoxic challenges. The aim of this study was to compare the effects of sevoflurane and propofol on oxygenation and shunt fraction during one-lung ventilation in a novel model of hypoxic preconditioning before one-lung ventilation. Methods: Sixteen Wistar-albino rats were anesthetized intra-peritoneally before venous and arterial cannulations and tracheotomized. The animals were randomly allocated to receive either sevoflurane 2% or 10 mg/kg/h propofol infusion and ventilated with 100% oxygen at an inspiratory rate of 80 breaths/min for 30 min. Three cycles of one-lung ventilation and two-lung ventilation were performed and one-lung ventilation was continued for 15 min. Arterial blood gas samples were obtained as follows: after cannulation and tracheotomy, following 30 min of treatment with sevoflurane or propofol, and at the 5th and 15th min of one-lung ventilation. Results: The PaO2 levels were higher and shunt fractions were lower in rats receiving propofol compared to rats treated with sevoflurane but the difference was not significant; the two groups were comparable in terms of PaCO2. Conclusions: The similar effects of sevoflurane and propofol on PaO2 during one-lung ventilation following hypoxic preconditioning may be due to other causes beside the inhibition of hypoxic pulmonary vasoconstriction. Gradual transition to one-lung ventilation is a novel technique for preconditioning experiments for one-lung ventilation. .

Justificación y objetivo: se conoce que la vasoconstricción pulmonar hipóxica aumenta como resultado de los retos hipóxicos regionales intermitentes. El objetivo de este estudio fue comparar los efectos del sevoflurano y del propofol en la oxigenación y fracción de shunt durante la ventilación monopulmonar, en un nuevo modelo de hipoxia preacondicionado antes de la ventilación monopulmonar. Métodos: dieciséis ratones albinos Wistar fueron anestesiados intraperitonealmente antes de las canalizaciones venosa y arterial, y fueron traqueostomizados. Los animales fueron aleatoriamente distribuidos para recibir una perfusión de sevoflurano al 2% o 10 mg/kg/h de propofol y ventilados con oxigeno al 100%, a una tasa inspiratoria de 80 rpm durante 30min. Se realiza-ron 3 ciclos de ventilación monopulmonar y ventilación de ambos pulmones y la ventilación monopulmonar se continuó durante 15 min. Se obtuvieron muestras de gasometría arterial de la siguiente forma: posteriormente a la punción y a la traqueotomia, y después de 30 min de tratamiento con sevoflurano o propofol, y a los 5 y 15 min de ventilación monopulmonar. Resultados: los niveles de PaO2 fueron más elevados y las fracciones de shunt menores en los ratones que recibieron propofol en comparación con los ratones tratados con sevoflurano, pero la diferencia no fue significativa, ya que los 2 grupos fueron comparables en términos de PaCO2. Conclusiones: los efectos similares de sevoflurano y propofol en la PaO2 durante la ventilación monopulmonar después del preacondicionamiento hipóxico pueden deberse a otras causas ade-más de por la inhibición de la vasoconstricción pulmonar hipóxica. La transición gradual hacia la ventilación monopulmonar es una técnica nueva de preacondicionamiento de experimentos para la ventilación ...

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INTRODUCTION: Peroxisome proliferator-activated receptor gamma (PPAR-gamma) and retinoic acid receptors (RAR/RXR) belong to the nuclear steroid receptor family. In vitro studies have suggested that PPAR-gamma ligands are highly effective in preventing mammary tumours and these effects are enhanced by some retinoids. However, in vivo anti-initiator and anti-promoter efficacies of this combination are not clear. AIM AND METHODS: The present study aimed to investigate the chemopreventive efficacies of the PPAR-gamma ligand rosiglitazone (200 microg/kg/day), synthetic retinoid fenretinide (0.3 mg/kg/day) and their combination on a DMBA-induced rat mammary carcinogenesis model. RESULTS: In the rosiglitazone group, no malignant tumour developed, apart from the lowest proliferative mammary lesions. In the fenretinide group, 30% developed a malignant tumour but there were no benign tumours. Cancer incidences were 61.5% and 10% in the control and combination groups respectively. CONCLUSIONS: Our results showed that the PPAR-gamma ligand rosiglitazone and synthetic retinoid fenretinide have potent chemopreventive properties against in vivo mammary carcinogenesis; however, the efficacies were not enhanced by their combination.

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