The bibliometric analysis of most cited 100 papers in anesthesia-induced neurotoxicity.

Anesthesia-induced neurotoxicity is a major concern for anesthetists for more than 20 years. Many experimental and clinical studies have been conducted on this topic since late 1990s. However, bibliometric analysis of these papers has not been reported. In this study, we aimed to analyze the 100 most cited articles on anesthesia-induced neurotoxicity. It was planned as cross-sectional study. On January 30, 2023, we searched the "Web of Science (WOS)" database for anesthesia-induced neurotoxicity and most cited 100 papers about this topic were obtained. Data such as authors' names, year of publication, name of the journal, type of paper, and citation numbers were analyzed. The most cited 100 papers were read by the investigators, and the anesthetic, animal type in experimental studies, any protective agent and the method for detecting neurotoxicity used in the studies were also noted. There were 75 articles and 22 reviews in the 100 most cited articles. We found that most of the papers in most cited 100 list were published between 2010 to 1024. Most of the papers (11%) were from Harvard University and almost half of the papers (49%) were published in Anesthesiology. A great number of studies were performed in newborns or early childhood (85.5%) and inhalational anesthetics (54.7%) were the most studied anesthetic type. Most of the most cited 100 papers were published in Q1 journals (P = .012) and the continent of the most journals in this list was America (P = .014). The median total and annual citation numbers of funded papers were statistically significantly higher (P < .001 and P < .001 respectively). Anesthesia-induced neurotoxicity is very important, especially for pediatric anesthetists. This study is the first to conduct a bibliometric analysis of the most cited 100 publications on this field. Although there was a gap in the publications about this topic during COVID-19 pandemic, we believe that there will be many more publications on anesthesia-induced neurotoxicity since the mechanism, outcome and possible protection are still unknown.

The effects of intra-cerebroventricular administered rocuronium on the central nervous system of rats and determination of its epileptic seizure-inducing dose / Efeitos da administração intracerebroventricular de rocurônio sobre o sistema nervoso central de ratos e determinação da dose indutora de crise epiléptica

Abstract 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 ± 0.009 µmoL. The seizure threshold, as a function of the body weight of rats, was calculated as 0.286 µmoL/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.

Resumo Justificativa: O objetivo deste estudo foi investigar os efeitos do brometo de rocurônio administrado intracerebroventricularmente sobre o sistema nervoso central, determinar a dose do limiar convulsivo de rocurônio em ratos e investigar os efeitos de rocurônio no sistema nervoso central em diluições de 1/5, 1/10 e 1/100 da dose do limiar convulsivo determinada. Métodos: Uma cânula permanente foi colocada no ventrículo lateral do cérebro dos animais. O estudo foi projetado em duas fases. Na primeira, a dose do limiar convulsivo do brometo de rocurônio foi determinada. Na segunda, o Grupo R 1/5 (n = 6), o Grupo 1/10 (n = 6) e Grupo 1/100 (n = 6) foram formados com doses de 1/5, 1/10 e 1/100, respectivamente, da dose do limiar convulsivo de brometo de rocurônio obtida. Resultados: Descobrimos que o valor do limiar convulsivo de brometo de rocurônio é 0,056 ± 0,009 µmoL. O limiar convulsivo, como uma função do peso corporal dos ratos, foi calculado como 0,286 µmoL/kg-1. Uma dose de 1/5 da dose do limiar convulsivo causou principalmente abertura postural dos membros e tremores em todo o corpo, enquanto uma dose de 1/10 da dose do limiar convulsivo causou agitação e tremores. Uma dose de 1/100 da dose do limiar convulsivo foi associada à diminuição da atividade locomotora. Conclusões: Este estudo mostrou que o brometo de rocurônio tem efeitos deletérios relacionados com a dose sobre o sistema nervoso central e pode produzir efeitos excitatórios dependentes da dose e convulsões.

[The effects of intra-cerebroventricular administered rocuronium on the central nervous system of rats and determination of its epileptic seizure-inducing dose]. / Efeitos da administração intracerebroventricular de rocurônio sobre o sistema nervoso central de ratos e determinação da dose indutora de crise epiléptica.

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.

The effects of intra-cerebroventricular administered rocuronium on the central nervous system of rats and determination of its epileptic seizure-inducing dose.

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.

Effect of Day and Night Desflurane Anaesthesia on Melatonin Levels in Rats.

OBJECTIVE: The aim of this study is to investigate the effect of day and night administration of desflurane anaesthesia on melatonin levels in rats. METHODS: Twenty-four 15-day-old rats were included in the study and were divided into four groups. The rats were anaesthetised between 19:00-01:00 (night group) and 07:00-13:00 (day group) with 5.7% desflurane concentration in 6 L min-1 100% oxygen. 6 L min-1 oxygen was administered to the control groups. At the end of 6 h of anaesthesia, blood samples were taken, and rats were sacrificed. Blood samples were centrifuged and melatonin levels from plasma samples were measured with radioimmunoassay. RESULTS: There was a statistically significant difference between the groups (p=0.007). Between group day control and group night control there was a statistically significant difference (p=0.042). Further, there was a significant difference between group day control and night desfluran as well (p=0.024). We could not find any difference between other groups. CONCLUSION: This study showed that 6 hours of 5.7% desflurane anaesthesia during day and night hours did not significantly change melatonin levels.

Effect of day/night administration of three different inhalational anesthetics on melatonin levels in rats.

The nocturnal peak of melatonin can be altered after anesthesia and surgery. We aimed to examine the melatonin levels during the day and night after anesthesia with three commonly used inhalational anesthetics. Forty-eight male Wistar albino rats were randomized into eight groups. Rats were administered anesthesia between 7:00 am and 1:00 pm (day groups) or 7:00 pm and 1:00 am (night groups) for 6 hours. At the end of the anesthesia, blood samples were collected for assessing melatonin levels. Mean values of melatonin levels after 6 hours of anesthesia during daytime were 43.17±12.95 for control, 59.79±27.83 for isoflurane, 50.75±34.28 for sevoflurane and 212.20±49.56 pg/mL for desflurane groups. The night groups' mean melatonin levels were 136.12±33.20 for control, 139.85±56.29 for isoflurane, 117.48±82.39 for sevoflurane and 128.70±44.63 pg/mL for desflurane groups. Desflurane anesthesia between 7:00 am and 1:00 pm significantly increased melatonin levels (p<0.001). Sevoflurane and desflurane anesthesia between 7:00 pm and 1:00 am decreased the melatonin levels but there were no significant differences (p=0.904 and p>0.99, respectively). Isoflurane anesthesia did not significantly change melatonin levels during day or night (p=0.718 and p>0.99, respectively). Our results demonstrate that during daytime desflurane anesthesia can alter melatonin levels. Altered melatonin rhythm following inhalational anesthesia can be related to sleep disorders observed after anesthesia.

Cardioprotective Effects of Remifentanil in a Sympathetic Hyperactivity Model in Rabbits.

OBJECTIVE: In this study, the antiarrhythmic and anti-ischemic effects of a 6 µg kg(-1) min(-1) infusion dose of remifentanil are investigated in a central sympathetic hyperactivity model in rabbits. METHODS: In this study, 18 New Zealand rabbits were used. The subjects were randomly divided into three groups (n=6) and received 10 µmol L(-1) glutamate intracerebroventricularly to provide the central sympathetic hyperactivity. In group 1, 10 µmol L(-1) glutamate was used; in group 2, 1 h before L-glutamate injection, 40 mg kg(-1) N (omega)-nitro-L-arginine methyl ester was intravenously (iv) administered; and in group 3, also 1 h before L-glutamate injection, 40 mg kg(-1) N (omega)-nitro-L-arginine methyl ester was iv administered. A 6 µg kg(-1) min(-1) dose of remifentanil infusion was administered 5 min before L-glutamate injection. Heart rate, systolic arterial pressure and mean arterial pressure were measured and recorded. Within 15 min of the intracerebroventricular L-glutamate injection, premature ventricular complexes, bigeminy ventricular arrhythmia, ventricular tachycardia, ST-segment shift and T-wave inversions were recorded. RESULTS: When incidences of heart rate, rate pressure product, premature ventricular complexes and bigeminy ventricular arrhythmia were compared between groups, significant differences were not determined. Mean arterial pressure was more significantly increased in group 2 than in the other groups (p<0.05). Ventricular tachycardia, ST-segment shift and T-wave inversions were significantly lower in group 3 than in groups 1 and 2 (p<0.05). CONCLUSION: Remifentanil (6 µg kg(-1) min(-1) for 5 min of infusion) prevented life-threatening ventricular tachycardia and electrocardiographic signs of myocardial ischemia in a model of arrhythmia resulting from the association of central sympathetic overactivity.

Massive pulmonary embolism and cardiac arrest; thrombolytic therapy in a patient with recent intracranial surgery and glioblastoma multiforme.

Treatment options for pulmonary embolism are increasing, but the scale of the treatments and their availability in the emergency department (ED) are limited. Thrombolytic therapy remains the most commonly used treatment in patients who present a massive pulmonary embolism in the ED. However, systemic thrombolysis is contraindicated in certain cases, such as a known intracranial tumor or a history of cranial surgery.In this case report, we report a 63-year-old man with a history of intracranial surgery due to glioblastoma multiforme 20 days prior to being admitted to the ED. Multidetector-row computed tomography angiography revealed embolisms in both main pulmonary arteries.There was a progression of cardiac arrest while preparing for catheterization; thus, cardiopulmonary resuscitation was initiated.After administering 10 minutes of cardiopulmonary resuscitation, a50-mg alteplase bolus was given. Within minutes, a pulse has returned. No complications associated with the thrombolytic therapy were observed.Our aim was to discuss the management of massive pulmonary embolism with a contraindication to systemic thrombolytic therapy.