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Background and Objective: The alteration of mitochondrial functions, especially the opening of the mitochondrial permeability transition pore (mPTP), has been proposed as a key mechanism in the development of lesions in cerebral ischemia, wherefore it is considered as an important target for drugs against ischemic injury. In this study, we aimed to investigate the effects of mitochondrial complex I inhibitors as possible regulators of mPTP using an in vitro brain ischemia model of the pentobarbital/ketamine (PBK)-anesthetized rats. Results: We found that PBK anesthesia itself delayed Ca2+-induced mPTP opening and partially recovered the respiratory functions of mitochondria, isolated from rat brain cortex and cerebellum. In addition, PBK reduced cell death in rat brain slices of cerebral cortex and cerebellum. PBK inhibited the adenosine diphosphate (ADP)-stimulated respiration of isolated cortical and cerebellar mitochondria respiring with complex I-dependent substrates pyruvate and malate. Moreover, pentobarbital alone directly increased the resistance of isolated cortex mitochondria to Ca2+-induced activation of mPTP and inhibited complex I-dependent respiration and mitochondrial complex I activity. In contrast, ketamine had no direct effect on functions of isolated normal cortex and cerebellum mitochondria. Conclusions: Altogether, this suggests that modulation of mitochondrial complex I activity by pentobarbital during PBK anesthesia may increase the resistance of mitochondria to mPTP opening, which is considered the key event in brain cell necrosis during ischemia. [ABSTRACT FROM AUTHOR]

Background and Objective: The alteration of mitochondrial functions, especially the opening of the mitochondrial permeability transition pore (mPTP), has been proposed as a key mechanism in the development of lesions in cerebral ischemia, wherefore it is considered as an important target for drugs against ischemic injury. In this study, we aimed to investigate the effects of mitochondrial complex I inhibitors as possible regulators of mPTP using an in vitro brain ischemia model of the pentobarbital/ketamine (PBK)-anesthetized rats. Results: We found that PBK anesthesia itself delayed Ca2+-induced mPTP opening and partially recovered the respiratory functions of mitochondria, isolated from rat brain cortex and cerebellum. In addition, PBK reduced cell death in rat brain slices of cerebral cortex and cerebellum. PBK inhibited the adenosine diphosphate (ADP)-stimulated respiration of isolated cortical and cerebellar mitochondria respiring with complex I-dependent substrates pyruvate and malate. Moreover, pentobarbital alone directly increased the resistance of isolated cortex mitochondria to Ca2+-induced activation of mPTP and inhibited complex I-dependent respiration and mitochondrial complex I activity. In contrast, ketamine had no direct effect on functions of isolated normal cortex and cerebellum mitochondria. Conclusions: Altogether, this suggests that modulation of mitochondrial complex I activity by pentobarbital during PBK anesthesia may increase the resistance of mitochondria to mPTP opening, which is considered the key event in brain cell necrosis during ischemia.

We previously reported that sodium pentobarbital inhibited the growth of the breast cancer associated with the normalization of microcirculatory hemodynamics and oxygenation. Here, we aimed to screen the key regulatory proteins involved in pentobarbital‐induced normalization of microcirculatory hemodynamics in the breast cancer tissues. A nude mice model of xenograft was established using triple negative breast cancer cell line MDA‐MB‐231. After tumor cell implantation, the mice were subcutaneously injected with 50 mg/kg/day of sodium pentobarbital or an equal volume of solvent adjacent to the tumor for 14 days. Liquid chromatography linked to tandem mass spectrometry (LC–MS/MS) was used to analyze the difference in protein expression profile between the two groups. Ingenuity pathway analysis (IPA) was used to perform the canonical pathway analysis, upstream regulators analysis, and protein–protein interaction networks analysis. Screened proteins were confirmed by real‐time quantitative polymerase chain reaction (RT–qPCR) and Western blot analysis. A total of 101 differentially expressed proteins were revealed between groups. Canonical pathway analysis suggested that acute phase response signaling (z = 1, p =.00208), dilated cardiomyopathy signaling pathway (z = −2, p =.00671), and ILK signaling (z = 1, p =.0172) were key pathways with highlight associations. The mRNA and protein expressions of SMTNL1 were found significantly decreased in pentobarbital‐treated tumor tissues compared with those in controls (both p <.01). Nine important protein–protein interaction networks were identified, and of which, two contained multiple downstream regulatory proteins of SMTNL1. In conclusion, SMTNL1 is revealed as a key protein involved in pentobarbital‐induced growth inhibition signaling in breast cancer. SMTNL1 may become a new potential target for tumor microcirculation research. [ABSTRACT FROM AUTHOR]

Abstract We previously reported that sodium pentobarbital inhibited the growth of the breast cancer associated with the normalization of microcirculatory hemodynamics and oxygenation. Here, we aimed to screen the key regulatory proteins involved in pentobarbital‐induced normalization of microcirculatory hemodynamics in the breast cancer tissues. A nude mice model of xenograft was established using triple negative breast cancer cell line MDA‐MB‐231. After tumor cell implantation, the mice were subcutaneously injected with 50 mg/kg/day of sodium pentobarbital or an equal volume of solvent adjacent to the tumor for 14 days. Liquid chromatography linked to tandem mass spectrometry (LC–MS/MS) was used to analyze the difference in protein expression profile between the two groups. Ingenuity pathway analysis (IPA) was used to perform the canonical pathway analysis, upstream regulators analysis, and protein–protein interaction networks analysis. Screened proteins were confirmed by real‐time quantitative polymerase chain reaction (RT–qPCR) and Western blot analysis. A total of 101 differentially expressed proteins were revealed between groups. Canonical pathway analysis suggested that acute phase response signaling (z = 1, p = .00208), dilated cardiomyopathy signaling pathway (z = −2, p = .00671), and ILK signaling (z = 1, p = .0172) were key pathways with highlight associations. The mRNA and protein expressions of SMTNL1 were found significantly decreased in pentobarbital‐treated tumor tissues compared with those in controls (both p

Copyright of Mycosystema is the property of Mycosystema Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The delivery of sodium pentobarbital as part of assisted suicide requires a doctor's prescription. This prescription must meet the legal and professional requirements as well as the corresponding ethical guidelines. Current legal practice restrictively permits suicide assistance in this form, especially in the case of patients who are willing to die and whose death is foreseeable. The new guidelines of the SAMS (2018) extend the possibility to patients who suffer intolerably due to disease symptoms and/or functional restrictions. The prescription of NaP in other cases or in violation of the duty of care provided for in the guidelines may result in supervisory, professional and criminal consequences. Suicide assistance itself is a decision of conscience, not a medical task, which is why there is no entitlement to it. [ABSTRACT FROM AUTHOR]

In this study, several neuropharmacological effects of methanolic leaf extract of Pandanus odoratissimus (PO) (family; Pandanaceae) were studied in albino mice using various experimental models. The effect of PO on the CNS was studied by using different neuropharmacological paradigms including spontaneous motor activity, rota-rod performance and potentiation of Pentobarbital sodium sleeping time in albino mice. Preliminary phytochemical evaluation and acute toxicity studies were also carried out where LD50 >2000 mg/kg was considered non-toxic through acute exposure in rats by the oral route. The methanolic leaf extract (50,100 and 200 mg/kg i. p.) produced a reduction in spontaneous motor activity, motor coordination and prolonged Pentobarbital sodium sleeping time. Preliminary qualitative chemical studies indicated the presence of steroids, saponins, terpinoids, glycosides, tannins, flavonoids and phenolics in the extract. These observations suggest that the leaf of Pandanus odoratissimus contains some active principles which possess potential CNS-depressant actionEstudaram-se alguns efeitos neurofarmacológicos do extrato metanólico de Pandanus odoratissimus (PO) (família Pandanaceae) em camundongos albinos, usando vários modelos experimentais. O efeito do PO no SNC foi estudado por meio de diferentes paradigmas neurofarmacológicos, como atividade motora espontânea, desempenho na haste rotatória e a potenciação do tempo de sono em camundongos albinos pelo pentobarbital sódico. A avaliação fitoquímica preliminar e os estudos de toxicidade aguda foram realizados e a DL50 >2000 mg/kg é considerada não tóxica, por meio da exposição aguda, por via oral, em ratos. O extrato metanólico de folha (50,100 e 200 mg/kg i. p.) produziu redução da atividade motora espontânea, da coordenação motora e tempo prolongado de sono pelo pentobarbital sódico. Estudos químicos qualitativos preliminares indicaram a presença de esteróide, saponinas, terpenóides, glicosídios, taninos, flavonóides e fenólicos no extrato. As observações sugerem que a folha de Pandanus odoratissimus contém alguns princípios ativos com atividade potencial como depressores do SNC.

Background: Galphimia glauca is an evergreen shrub found across peninsular India, belonging to family Malpighiaceae. Objective: The objective of this study was to assess the in vivo depressant effects and muscle coordination activity of G. glauca stem methanol extract (GGSME). Materials and Methods: The stem methanol extract was administered in Swiss albino mice in 1 day to study the central nervous system (CNS) depressant and muscle coordination activity employing animal models such as sodium pentobarbital-induced sleep test, hole-board test, open field test, pentylenetetrazole (PTZ)-induced convulsions, picrotoxin-induced convulsions, grip strengthening test in mice, and Rota-rod test. Results: The LD50 of GGSME was found to be >2000 mg/kg body weight (b.w.). Mice treated with stem methanol extract at 100, 200, and 400 mg/kg, b.w. doses extended the sleeping time induced by sodium pentobarbital (40 mg/kg. b.w., i.p.). The stem methanol extract at 400 mg/kg dose showed a significant (P = 0.001) dose-dependent decrease in the number of rears and head dipping number in the hole-board test. The extract exhibited a significant (P = 0.001) effect on the ambulatory behavior of mice in the open field test and also extended the onset of seizures induced by PTZ (90 mg/kg b.w., i.p.) and picrotoxin (10 mg/kg, b.w., i.p.). The extract also exhibited significant (P = 0.001) effects on muscle coordination in rota-rod and grip strengthening test in mice. Conclusion: The study results conclude that the GGSME has a potential CNS depressant and muscle relaxant effects compared to the standard drugs. [ABSTRACT FROM AUTHOR]

Directive 2010/63/EU on the protection of animals used for scientific purposes requires that the killing of mammal foetuses during the last third of their gestational period should be accomplished through effective and humane methods. The fact that murine foetuses are resistant to hypoxia-mediated euthanasia renders the current euthanasia methods ineffective or humane for the foetuses when these methods are applied to pregnant female mice. We have assessed the time to death of foetuses after performing either indirect (dam euthanasia) or direct (via intraplacental injection – a new approach to euthanasia) euthanasia methods in order to determine a euthanasia method that is appropriate, ethical and efficient for the killing of mouse foetuses. The respective times to death of foetuses after performing the three most commonly used euthanasia methods (namely cervical dislocation, CO2 inhalation and intraperitoneal sodium pentobarbital administration) were recorded. Absence of foetal heartbeat was monitored via ultrasound. We consider that the most effective and humane method of foetal euthanasia was the one able to achieve foetal death within the shortest possible period of time. Among the indirect euthanasia methods assessed, the administration of a sodium pentobarbital overdose to pregnant female mice was found to be the fastest for foetuses, with an average post-treatment foetal death of approximately 29.8 min. As for the direct euthanasia method assessed, foetal time to death after intraplacental injection of sodium pentobarbital was approximately 14 min. Significant differences among the different mouse strains employed were found. Based on the results obtained in our study, we consider that the administration of a sodium pentobarbital overdose by intraplacental injection to be an effective euthanasia method for murine foetuses. [ABSTRACT FROM AUTHOR]

Sodium pentobarbital, a euthanasia drug, can persist in animal carcasses following euthanasia and can cause secondary toxicosis to animals that consume the remains. This experiment was conducted to observe the effects of composting on euthanized horse carcass degradation and sodium pentobarbital residues in compost material up to 367 d. Six separate compost bins were constructed on pastureland. Three bins served as the control while 3 served as the treatment. The carbonaceous material, or bulking agent, consisted of hardwood chips mixed with yard waste wetted to approximately 50% moisture content. Bulking agent was added to each bin at a depth of 0.46 m, creating the pad. A licensed veterinarian provided 6 horse carcasses for use in the experiment. These horses had required euthanasia for health reasons. All horses were weighed and then sedated with an intravenous injection of 8 mL of xylazine. After sedation the 3 horses in the treatment group were euthanized by intravenous injection of 60 mL of sodium pentobarbital. The 3 control group horses were anesthetized by intravenous injection of 15 mL of ketamine hydrochloride and then humanely euthanized by precise gunshot to the temporal lobe. Following euthanasia, each carcass was placed on the center of the pad and surrounded with 0.6 m of additional bulking agent. Serum and liver samples were obtained immediately following death. Compost samples were obtained on d 7, 14, 28, 56, 84, 129, 233, and 367 while soil samples were obtained on d -1 and 367. Each sample was analyzed for sodium pentobarbital concentration. Compost pile and ambient temperatures were also recorded. Composting successfully degraded soft tissue with only large bones remaining. Data illustrate that sodium pentobarbital was detectable up to 367 d in compost piles with no clear trend of concentration reduction. Drug residues were detected in soil samples indicating that sodium pentobarbital leached from the carcass and through the pad. These findings confirm the persistence of sodium pentobarbital from equine mortality compost piles and emphasize the importance of proper carcass management of animals euthanized with a barbiturate to reduce environmental impact and secondary toxicosis. [ABSTRACT FROM AUTHOR]

• Equine mortality composting is effective during spring and fall in Minnesota. • Mostly large bones remained in compost piles after 6 months of composting. • Composting reduced estimated sodium pentobarbital quantities. • Physicochemical characteristics of compost were suitable for land application. Recent changes in rendering availability for chemically-euthanized animals have created a need to explore composting as an equine mortality management method. The objectives of this study were to evaluate equine mortality composting in the Upper Midwest during fall and spring, document sodium pentobarbital concentrations throughout the process, and determine nutrient content of finished compost. During each season, four horses were euthanized by intravenous administration of sodium pentobarbital. Carcasses were positioned at the center of a woodchip and shavings base and covered with a 2:1 mixture of horse stall waste and cattle feedlot waste. Data loggers were placed at 46- and 91cm depths to record pile temperatures every 8 hours. At turning (44–50 days) and trial conclusion (181–216 days), compost piles were sampled for sodium pentobarbital and nutrient composition. Piles contained large bones after 6 months of composting. Sodium pentobarbital remained detectable at trial conclusion (<0.002–1.49 mg kg1 dry matter); however, composting reduced the estimated quantities of sodium pentobarbital by ≥94% (P ≤.001). Compost from each season met ideal land application values for organic matter (45%–48%), pH (7.3–7.6), and electrical conductivity (3.3–3.4 mm hos cm−1). Low NPK and high C:N ratio (20–30) indicate compost could partially replace synthetic fertilizers when land applied. These findings suggest equine mortality composting is an effective management practice during fall and spring in the Upper Midwest. While remaining sodium pentobarbital residues were minimal, further research is needed to determine environmental implications of composting chemically-euthanized equines. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the effects of three commonly used general anesthetics on intraocular pressure (IOP) in mouse. Methods: Fifteen 2-3-month-old C57BL/6J mice were randomly divided into three groups (each group, n = 5). A non-invasive TonoLab tonometer (Icare LAB, Icare Finland Oy, Espoo, Finland) was used to measure IOP at 0, 5, 10, 15, 20, 30 min after mice were anesthetized, respectively, by intraperitoneal injection of sodium pentobarbital (150 mg/kg), chloral hydrate (500 mg/kg) and a mixture of ketamine and xylazine (75 mg/kg and 13.6 mg/kg). IOP were obtained in the daytime and nighttime. Anterior segment was photographed and palpebral fissure height was measured offline. Results: Immediately after anesthesia, the averaged IOPs in the three groups were 17.2 ± 1.5, 16.7 ± 1.4 and 17.3 ± 2.4 mmHg in the daytime and 19.3 ± 2.1, 21.3 ± 1.1 and 21.7 ± 1.5 mmHg in the nighttime. Thereafter, the averaged IOPs in sodium pentobarbital and chloral hydrate groups showed a trend of decline. Then IOPs became stable at 10-15 min after anesthesia. In contrast, the IOPs of ketamine and xylazine injected group increased to 23.7-25.1 mmHg at 10-15 min in the daytime and 26.1-27.7 mmHg in the nighttime. Compared to chloral hydrate and sodium pentobarbital treated mice (2.4 ± 0.1 mm, 1.7 ± 0.0 mm), ketamine and xylazine injected animals had significantly increased palpebral fissure height (3.6 ± 0.3 mm, p < 0.01). Conclusion: General anesthetics have a large impact on mouse IOP. Sodium pentobarbital and chloral hydrate reduce but the ketamine and xylazine mixture increases mouse IOP. IOP levels become stabilized at 10 to 15 min after anesthesia. The ketamine and xylazine cocktail mediated elevation of palpebral fissure height may be associated with an increasing of intraorbital pressure. Measurement performs at 10-15 min after anesthesia may obtain more reliable IOPs. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To explore effect of different anesthesia methods and different anesthetics on erythrocyte immune function in mice. Methods: The mice were anesthetized by isoflurane and ether inhalation, and also under intraperitoneal anesthesia with sodium pentobarbital and chloral hydrate. Blood was collected from the ventro-cardinal vein. Automatic blood cell analyzer was used for routine blood examination, and the canthine oxidase method was used to measure the superoxide dismutase (SOD) activity. Lipid peroxidation product malondialdehyde (MDA) was measured with TBA, and glutathione peroxidase (GSH-Px) was measured with DTNB, and then the effect of different anesthesia methods and different anesthetics on erythrocyte immune function in mice was observed. Results: Hct level of chloral hydrate intraperitoneal injection group was significantly higher than the other three groups (P<0.05). And the MDA levels in the pentobarbital sodium group were significantly higher than the other three groups (P<0.05). SOD and GSH-Px of the chloral hydrate and sodium pentobarbital intraperitoneal injection group were significantly lower than the other two groups; RBC-C 3bRR and RBC-ICR of the chloral hydrate and sodium pentobarbital intraperitoneal injection group were significantly lower than the other two groups. Conclusions: Different drugs can induce changes in immune function of mice at different levels. Isoflurane and ether have less damage to animal body, while chloral hydrate and sodium pentobarbital intraperitoneal injection have a certain inhibitory effect on the animal body respiratory system and can cause greater damage to the body. Therefore, the reasonable selection and control of anesthetics are very important in order to avoid the experimental errors caused by anesthesia. [Copyright &y& Elsevier]

Isoflurane is a preferred anesthetic, due to its properties that allow a precise concentration to be delivered continually during in vivo experimentation. The major mechanism of action of isoflurane is modulation of the γ-amino butyric acid (GABAA) receptor-chloride channel, mediating inhibitory synaptic transmission. Animal studies have shown that isoflurane does not cause cell death, but it does inhibit cell growth and causes long-term hippocampal learning deficits. As there are no studies characterizing the effects of isoflurane on electrophysiological aspects of long-term potentiation (LTP) in the hippocampus, it is important to determine whether isoflurane alters the characteristic responses of hippocampal afferents to cornu ammonis region 3 (CA3). We investigated the effects of isoflurane on adult male rats during in vivo induction of LTP, using the mossy fiber pathway, the lateral perforant pathway, the medial perforant pathway, and the commissural CA3 (cCA3) to CA3, with intracranial administration of Ringer's solution, naloxone, RS-aminoindan-1, 5-dicarboxylic acid (AIDA), or 3-[(R)-2-carboxypiperazin-4-yl]-propo-2-enyl-1-phosphonic acid (CPP). Then, we compared these responses to published electrophysiological data, using sodium pentobarbital as an anesthetic, under similar experimental conditions. Our results showed that LTP was exhibited in animals anesthetized with isoflurane under vehicle conditions. With the exception of AIDA in the lateral perforant pathway, the defining characteristics of the four pathways appeared to remain intact, except for the observation that LTP was markedly reduced in animals anesthetized with isoflurane compared to those anesthetized with sodium pentobarbital. The results suggest that isoflurane may affect amplitude through activation of GABAA receptors or mechanisms important to LTP in CA3 afferent fibers. [ABSTRACT FROM AUTHOR]

Rationale: Previous studies have shown that adenosine A receptors are colocalized with dopamine D receptors on striatal neurons. Activation of these two receptors has antagonistic effects under a number of conditions suggesting that stimulation of adenosine A receptors may have behavioral effects resembling those produced by blockade of dopamine D receptors, but this possibility has been investigated in a limited number of situations. Objective: We compared the effects of the adenosine A agonist CGS-21680 and the preferential D dopamine antagonist haloperidol in a situation in which dopamine blockade produces a distinctive pattern of behavioral effects. Materials and methods: Six rats were trained to lever press for food reward on a fixed ratio 15 schedule of reinforcement and then tested after being injected with various doses of CGS-21680 (0.064, 0.128, and 0.25 mg/kg) and haloperidol (0.25 and 0.1 mg/kg). Results: Haloperidol produced a dose-dependent suppression of lever pressing with mean response rates declining across the duration of the test session. CGS-21680 also produced a dose-dependent suppression of responding, but this effect was not temporally graded, and responding was equivalently suppressed across the duration of the session. Additionally, CGS-21680 increased post-reinforcement pause duration to a much greater extent than did haloperidol. Conclusions: On this task, the behavioral effects of CGS-21680 do not resemble those produced by haloperidol. Several explanations of this discrepancy are possible, the most likely being that the observed behavioral effects of CGS-21680 result from an action at a site other than D receptor-expressing striatal neurons. [ABSTRACT FROM AUTHOR]

The superior colliculus (SC) is a midbrain structure that plays a central role in the integration of information from different sensory modalities and the generation of orienting responses. Its normal function is thought to be governed by a strictly held balance between excitation and inhibition. This hypothesis was tested by recording from the same single units in the SC of cats before the injection of anesthetics, while anesthetics took effect, and after the injections during recovery. Sodium pentobarbital and ketamine, two agents commonly used in sensory physiology, were used. The results show a plethora of dose-dependent and nonlinear effects: the magnitude of evoked responses, receptive field properties, first spike latency, and bimodal integration were affected by both anesthetics in all units tested. Notably, prominent facilitation was observed at low levels of anesthesia, and inhibitory responses were changed into excitatory. Overall, the results challenge a fundamental tenet of sensory physiology: anesthesia, while decreasing single-unit responsiveness, leaves unaltered basic physiological properties. [ABSTRACT FROM AUTHOR]

In the present study we observed that mice anesthetized with sodium pentobarbital were far more susceptible to gastrointestinal challenge with Listeria monocytogenes than were unanaesthetized mice. The effect of pentobarbital anesthesia was transient (gone within 2 h) and did not alter the severity of infection following i.v. challenge with L. monocytogenes. Treatment with pharmacological inhibitors of gastric acidity (i.e. cimetidine and omeprazole), or intestinal motility (loperamide), did not duplicate the effect of pentobarbital on gastrointestinal listeriosis. These findings suggest that sodium pentobarbital anesthesia causes a short-lived but striking diminution in resistance to gastrointestinal listeriosis in mice, via an undefined mechanism. [Copyright &y& Elsevier]

Four experiments were conducted to determine the effects of sodium pentobarbital (0, 3, 9, and 15 mg/kg) on the acquisition of the rabbit's classically conditioned nictitating membrane response (NMR) and to determine the locus of the drug's effects on sensory, motor, associative, and nonassociative processes. In experiment 1, classical conditioning of the NMR was accomplished by pairing tone and light conditioned stimuli (CSs) with paraorbital shock as the unconditioned stimulus (US). The experiment revealed that pentobarbital retarded the acquisition of conditioned responses (CRs) to both tone and light CSs. Experiment 2, employing unpaired CS, UCS presentations, indicated small but significant drug effects on NMR base rate and nonassociative NMRs to the CS. Experiment 3 revealed no significant drug effect on the psychophysical functions relating UCS intensity to UCR frequency or amplitude, nor on the UCS intensity threshold for eliciting UCRs. On the other hand, in experiment 4, the drug significantly impaired CR frequency over an extended range of CS intensities and raised CS intensity threshold. It was concluded that pentobarbital's attenuation of CS intensity also operated to impair CR acquisition. [ABSTRACT FROM AUTHOR]

Sodium pentobarbital and chlorpromazine were evaluated for the degree to which they differentially reduce the speed or efficiency with which sensory information can be processed. Rhesus monkeys were tested under comparable doses of sodium pentobarbital and CPZ on a visual discrimination problem with varying durations of tachistoscopically presented stimulus information. When unlimited stimulus information was available, no effects of the two drugs were observed at the doses used, but as the duration of stimulus presentation was progressively decreased, the effects of sodium pentobarbital became more severe, whereas CPZ did not differ from the saline control at any presentation duration. While previously published literature indicates that CPZ impairs performance by intermittantly blocking sensory input or transmission, the present data provide the first direct behavioral confirmation that barbiturates impair performance by retarding the rate at which sensory stimuli can be processed and utilized. [ABSTRACT FROM AUTHOR]

The immediate and persistent effects of single oral doses of sodium pentobarbital 20 mg/kg, nitrazepam 25 mg/kg and imipramine 25 mg/kg, were compared on behavioural patterns as well as on quantitative aspects of diurnal EEG patterns in rhesus monkeys. Consecutive pre-drug EEG recordings on agar treated monkeys, showed no significant variations in day to day EEG levels of wakefulness, drowsiness, sleep and the REM state. Both the sedative-hypnotic agents, sodium pentobarbital and nitrazepam, significantly reduced wakefulness and the REM state and increased slow wave sleep. They reduced the latency to onset of slow wave sleep but significantly increased the latency to onset of the REM state. The antidepressant agent imipramine, did not influence any of the EEG parameters to a significant extent. Significantly enhanced REM levels persisted during the 7-day post-drug period after cessation of medication of all three psychoactive agents. The effect on the macaque EEG of an increase in slow wave sleep with concomitant decreased levels of wakefulness and REM with respect to baseline levels, provides a quantitative basis for comparing sedative-hypnotic agents in monkeys. Residual drug-induced EEG changes, reflected by enhanced REM levels, may prove a sensitive indicator of persistent drug effects in subhuman primates. [ABSTRACT FROM AUTHOR]

The state dependent learning paradigm was used with a one-trial, passive avoidance task. Forty male rats were equally distributed among four groups: One group received intrathoracic injections of sodium pentobarbital immediately after the acquisition trial and immediately before the retention test trial; a second group received equivalent injections of 0.9% saline; a third group was drugged after acquisition and given saline prior to retention testing and the fourth group was given saline after acquisition and drug prior to retention testing. All groups showed increased latencies on the retention trial but marked group differences in retention test latencies indicate that there was significantly more retention of training when drug states were the same during the memory storage interval and the memory retrieval interval. Intrathoracic injection proved to be a practical substitute for intravenous injection in assuring rapid onset of drug effect. [ABSTRACT FROM AUTHOR]

Acute hypothermia was surface-induced in unrestrained conscious rats at two different levels, moderate (30°C T) and severe (20°C T). Data reflecting the acid/base status were determined. The values obtained for moderate hypothermia were compared with the acid/base pattern observed during hypothermia induced by two different anaesthetics, sodium pentobarbital and urethane, at room temperature. Conscious, hypothermic animals developed an apparent respiratory alkalosis, with an increase in pH (from 7.476 to 7.546 in moderate hypothermia and from 7.484 to 7.563 in severe hypothermia) correlated with a decrease in arterial bicarbonate levels (from 22.9 to 16.8 mmol 1 and from 20.7 to 14.9 mmol 1 respectively). Lactate increased slightly in conscious, severely hypothermic rats (1.02 mmol 1). This acid/base pattern was clearly different from that seen in sodium pentobarbital (mild respiratory acidosis) and urethane-induced hypothermia (metabolic acidosis). These results suggest that conscious rats follow a pattern closer to that underlying the relative alkalinity shown by many poikilotherms than to that underlying the constant pH shown in hibernating mammals. This latter pattern, nevertheless, approaches that observed during moderate pentobarbital hypothermia and the acid/base pattern during shallow hypothermia in birds. Anaesthesia may interfere with the development of the processes that lead to the acid/base pattern observed in conscious animals. [ABSTRACT FROM AUTHOR]

The averaged visual evoked response (VER) amplitude in some subjects at the greatest depths of modulation of sine wave light is the same or less than at lesser depths of modulation. This phenomenon is referred to as 'reducing' and is measured by computing the slope of VER amplitudes as a function of the four greatest modulations. Previous studies reported that 'reducing' varies between test and retest sessions, possibly due to changes in the subjects' level of arousal. In order to test this hypothesis, various drugs were employed to alter level of arousal. It was found that the two depressants (sodium pentobarbital and ethyl alcohol) both significantly decreased the slope of the VER amplitude at the four highest depths of modulation, i.e. subjects 'reduce' more. Stimulants (methamphetamine and caffeine) and placebo, on the other hand, had no effect on the slopes. The lack of change in slope after the stimulants is discussed and possible explanations are advanced. It is concluded that level of arousal is one factor in determining the 'augmenting/reducing' level of subjects. [ABSTRACT FROM AUTHOR]

Copyright of Acta Diabetologica Latina is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The anesthetic effect of some water-soluble anesthesic or narcotic drugs currently used in mice was tested in molluscs of the Biomphalaria genus. Sodium thiopental was very toxic to the snails resulting in high rates of mortality in all the treatment schedules tested. Cetamine base, at concentration of 0.25 mg/ml of water, resulted in partial snail anesthesia (40% of snails were anesthetized) only after 20 h of exposition. The association of Cetamine base with Tiazine chloridrate did not improve the anesthesic effect, and higher concentrations of these drugs were toxic to the snails. Sodium pentobarbital at 0.4 mg/ml in water for 8 h was the best treatment schedule to anesthetize Biomphalaria snails. In this schedule, the snails were anesthetized without any toxic effect. The procedure provides a powerful tool for in vivo studies that demande a complete state of snail anesthesia.

Composting is an environmentally friendly, economical, and bio secure method for livestock mortality disposal. Recent changes in availability of rendering for chemically-euthanized animals has created a need to explore composting. The objectives of this study were to demonstrate successful equine mortality composting in the winter and document sodium pentobarbital concentrations throughout the process. The authors hypothesized composting would degrade carcasses and reduce pentobarbital concentrations. On 26 September 2019, 4 horses (451 ± 36 kg) were euthanized for terminal medical reasons by intravenous administration of sodium pentobarbital (88 ± 2 mg/kg; Fatal-Plus, Vortech Pharmaceuticals, LTD, Dearborn, MI). Carcasses were transported immediately to a private composting site. Four separate compost piles were constructed on a 6.1- by 27.4-m concrete pad. Each pile consisted of 46 cm of playground woodchips, 8 cm of dry pine shavings, a horse carcass, and 61 cm of a 2:1 mixture of horse stall waste and cattle feedlot waste. Data loggers were placed at 46- and 91-cm depths to record pile temperatures every 8 h. Compost piles were topped with manure mixture at d 9 to cover cracks, turned at d 50 when pile temperatures were ≤54.4°C, and concluded on d 216 following approximately 5 mo. of curing (≤43.3°C). On d 50 and 216 piles were cut into 3 mirrored cross sections and subsampled (n = 36) to form one composite sample per cross section. Samples were analyzed for sodium pentobarbital (on an "as is" basis) and nutrient content. Carcass degradation was scored on a subjective scale (1 = discernable carcass, 5 = few large brittle bones). Pentobarbital concentrations were compared using a 2-way ANOVA with cross section and day as fixed effects. P -values < 0.05 were considered significant. Three piles received a carcass degradation score of 2 at d 50 with soft tissue, hair, and hide present. By d 216, all piles received scores of 3 (n = 2) or 4 (n = 2) with some hide and large bones remaining. Pentobarbital concentrations declined between d 50 and d 216; however, remained detectable at d 216. On average, pentobarbital concentrations tended to be higher (9.05 mg/kg) at the center of the compost pile on d 50 (P < 0.05); however, on d 216 concentrations were similar (0.432 to 0.735 mg/kg; P > 0.05) among cross sections. While pentobarbital concentrations at d 216 were minimal, further research is needed to determine environmental implications of composting chemically-euthanized equines. These findings suggest mortality composting is an effective method for disposing of equine carcasses. [ABSTRACT FROM AUTHOR]