Nux Vomica 200 CH reduced acute hypnotic effect of alcohol in young toads

Potentized Nux Vomica has been reported to produce antialcoholic effect in mice, rats and toads. The effect relates to consumption of alcohol and alcohol-induced loss of righting reflex (RR). RR’s maintain normal erect posture of an animal and are centrally controlled in the midbrain. In the present study young toads, Duttaphrynus melanostictus were first treated with Nux vomica 200 CH and then partially immersed in 209 mM ethanol solution in such a way that their head remained above the level of ethanol solution. Toadlets were removed from the ethanol solution every 10 min, tested for the loss of RR and returned to the ethanol solution. Toadlets were placed in a supine position on a dry flat surface. Failure to right within 60 sec was considered as the loss of RR. The experiment was repeated 10 times. Control toadlets were pretreated with 90% ethanol instead of Nux Vomica 200 CH. The percentages of toadlets showing loss of RR, both in the control as well as in the Nux-treated groups, were shown in graphs against the duration of exposure to ethanol solution. Differences in the percentage distribution between the control and the treatment groups losing RR were tested by χ2 test. All the experiments were conducted at room temperature. The percentage of toadlets losing RR increased with time of exposure to ethanol solution. The increase was significantly higher with the control than with the Nux-treated group. Nux Vomica 200 CH might have influenced the mid-brain of toadlets thereby countering the hypnotic effect of ethanol in the toadlets.

Preliminary evaluation of the efficacy and safety of brimonidine for general anesthesia

Background To determine the hypnotic and analgesic effects of brimonidine, and evaluate its efficacy and safety for general anesthesia. Potentiation of pentobarbital sleeping time following brimonidine administration was observed in mice, as was the analgesic activity of brimonidine. Methods The median effective dose (ED50) and lethal dose (LD50) of intraperitoneally injected brimonidine were determined in hypnotized mice. In addition, the LD50 of intravenously injected brimonidine, and ED50 of intravenously, intramuscularly, and intrarectally injected brimonidine in hypnotized rabbits were determined. Finally, the synergistic anesthetic effect of brimonidine and chloral hydrate was evaluated in rabbits. Results Intraperitoneal injection of 10 mg/kg brimonidine enhanced the hypnotic effect of a threshold dose of pentobarbital. Intraperitoneally injected brimonidine produced dose-related analgesic effects in mice. The ED50 of intraperitoneally administered brimonidine in hypnotized mice was 75.7 mg/kg and the LD50 was 379 mg/kg. ED50 values of intravenous, intramuscular, and intrarectal brimonidine for hypnosis in rabbits were 5.2 mg/kg, 8.8 mg/kg, and 8.7 mg/kg, respectively; the LD50 of intravenous brimonidine was 146 mg/kg. Combined intravenous administration of 0.6 mg/kg brimonidine and 0.03 g/kg chloral hydrate had a synergistic anesthetic effect. Conclusions Brimonidine elicited hypnotic and analgesic effects after systemic administration and exhibited safety. Moreover, brimonidine enhanced the effects of other types of narcotics when combined.

Effect of meloxicam coadministration on the anaesthetic potency of thiopental sodium in a chick model

Few studies have dealt with thiopental sodium-induced anaesthetic action and the effect of combining meloxicam (a high plasma protein-bound) in 10–15 day old chicks. First, the analgesic median effective dose (ED50) was determined as 35.85 mg/kg, IM by up-and-down routine, while the hypnotic ED50 value was 34.40 mg/kg, IM in the chick model. A thiopental sodium injection (18, 36 and 72 mg/kg, IM) produces a significant dose-responsive hypnotic effect in chicks, determined by the beginning of the lack of a righting reflex, duration and recovery time. Thiopental sodium and meloxicam (72 and 1 mg/kg, IM) in combination shortened the beginning of hypnosis, and significantly extended its duration, with a significant increase in recovery time from the hypnotic effect when compared to the group receiving only thiopental sodium. The same combination also elicited a significant increase in the analgesic percentage and efficacy, and significant increase in the voltage current estimated via using electrical stimulation to induce the ache feeling. No significant changes were found in the concentrations of serum glutamate pyruvate trans-aminase (GPT), glutamate oxalo-acetate trans-aminase (GOT) with body temperature between the two groups, with the exception of a significant change in respiratory rate. The outcomes of this study support the prospect of using thiopental sodium as an anaesthetic agent for veterinary surgical procedures in the chicks, in combination with meloxicam, to produce worthy, consistent, and proficient anaesthesia.

Preliminary Evaluation of the Efficacy and Safety of Brimonidine for General Anesthesia

Background:To determine the hypnotic and analgesic effects of brimonidine, and evaluate its efficacy and safety for general anesthesia. Potentiation of pentobarbital sleeping time with brimonidine was observed in mice, as was analgesic activity of brimonidine.Methods:The median effective dose (ED50)and lethal dose (LD50) of intraperitoneally injected brimonidine were determined in hypnotized mice. In addition, LD50 of intravenously injected brimonidine, ED50 of intravenously , intramuscularly and intrarectally injected brimonidine in hypnotized rabbits were determined. The synergistic anesthetic effect of brimonidine and chloral hydrate on rabbits was evaluated. Results:Intraperitoneal injection of 10 mg/kg brimonidine enhanced the hypnotic effect of a threshold dose of pentobarbital. Intraperitoneal injection brimonidine produced dose-related analgesic effects in mice. ED50 of intraperitoneally administered brimonidine in hypnotized mice was 75.7 mg/kg, and LD50 was 379 mg/kg. The ED50 of intravenous, intramuscular and intrarectal brimonidine for hypnosis in rabbits were 5.2 mg/kg, 8.8 mg/kg and 8.7mg/kg, respectively, and LD50 of intravenous brimonidine was 146 mg/kg. Combined intravenous administration of 0.6 mg/kg brimonidine and 0.03 g/kg chloral hydrate had a synergistic anesthetic effects.Conclusions:Brimonidine elicited hypnotic and analgesic effects after systemic administration, and exhibited safety. Brimonidine enhanced the effects of other types of narcotics when combined.

The Anxiolytic effect of salicylic acid is mediated via the GABAergic system

Salicylic acid (SA) is a natural phenolic compound in plants with many beneficial effects for humans. The anxiolytic effect of this compound has been reported in animal models, but its mechanism of action remains unclear. In this study, by using the fear potentiated plus maze test, we evaluated the effect of salicylic acid on the gene expression of the main form of GABA synthesizing enzyme i.e., the enzyme glutamic acid decarboxylase 67 (GAD67), in the ventral subiculum of the hippocampus. Also, the hypnotic effect of Salicylic acid was evaluated. Animals were divided into the solvent, (SA) and diazepam treated groups (n = 6). For evaluating the anxiolytic effect of Salicylic acid, animals were subjected to 2 hours of isolation, before placing them in the elevated plus maze (EPM). Afterward, the ventral part of the hippocampus was removed for evaluating the change in (GAD67) gene expression by the reverse transcription-quantitative polymerase chain reaction (RTqPCR) technique. The hypnotic effect of Salicylic acid was evaluated in the ketamine induced sleeping test. Our results showed that Salicylic acid at 10, 30 (mg/kg) increased time spent and entries to the open arms in the (EPM) (p < 0.05). (RTqPCR) revealed that 30mg/kg of Salicylic acid increased (GAD67) gene expression (p < 0.001). Salicylic acid (30 and 300 mg/kg) also increased the duration of sleep, in ketamine induced sleeping test (p < 0.05). Our results showed that Salicylic acid has anxiolytic and hypnotic effects and it exerts its anxiolytic effect partly, via up regulation of (GAD67) in the ventral part of the hippocampus.