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Surgical Facilities, Peri-Operative Care, Anesthesia, and Surgical Techniques
Published in Yuehuei H. An, Richard J. Friedman, Animal Models in Orthopaedic Research, 2020
Alison C. Smith, M. Michael Swindle
Barbiturate anesthesia is used in all species. However, it requires iv access for most species. They may be administered as an ip injection for rodents. The barbiturates are potent cardiorespiratory depressants which are dose dependent in their activity. In large animals, they are best administered as iv infusion protocols. Pentobarbital is relatively long acting in most animals and may provide 30-45 min. of anesthetic activity following a single iv injection. It requires hepatic metabolism and excretion for biodegradation. Thiobarbiturates, such as thiopental and thiamylal, are primarily excreted by the kidneys and have much shorter anesthetic times of 5-20 min. The dosage of barbiturates are reduced 1/3-1/2 by administration of tranquilizers or other preanesthetic agents.11-16
Sedative and Hypnotic Drugs
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Arup Kumar Misra, Pramod Kumar Sharma
Barbiturate poisoning varies with its lethal dose. Severe poisoning with barbiturate happens when the dose is more than the 10 times of its therapeutic dose for hypnosis. If other depressant drugs or another sedative–hypnotics drugs are given concomitantly then the quantity of drug to be lethal is lowered. Barbiturate poisoning is most commonly seen in children due to accidental poisonings, suicidal bid, and drug abusers (Eugene et al., 1952). The patient is comatose with respiratory system affected early in severe barbiturate poisoning. Rapid and shallow or slow breathing pattern are characteristic of barbiturate poisoning. The lethal dose decreases the cardiac contractility leading to fall of blood pressure due to the depressive effect on the cardiovascular system. The medullary vasomotor centers and sympathetic ganglia are depressed by barbiturates leading to hypoxia (Eugene et al., 1952). Severe barbiturate poisoning may cause to kidney failure and pulmonary complications like atelectasis, edema, and bronchopneumonia. Management of barbiturate poisoning consists of supportive procedures like maintaining airway, breathing, and circulation. Forced diuresis, urine alkalinization, and maintaining of hydration will increase the renal excretion of barbiturate. In barbiturate poisoning, use of CNS stimulants are contraindicated (Santos and Olmedo, 2017).
Therapeutic Potential of Ocimum tenuiflorum L.: Metabolic and Mental Disorders
Published in Megh R. Goyal, Hafiz Ansar Rasul Suleria, Ademola Olabode Ayeleso, T. Jesse Joel, Sujogya Kumar Panda, The Therapeutic Properties of Medicinal Plants, 2019
Nishikant A. Raut, Dadasaheb M. Kokare, Gail B. Mahady
Benzodiazepines are regularly prescribed CNS depressants that are considered relatively safe when compared with the barbiturates. Some commonly prescribed benzodiazepines are: Alprazolam;Clonazepam;Diazepam;Lorazepam;Triazolam;Temazepam;Chlordiazepoxide.
A primer on sleeping, dreaming, and psychoactive agents
Published in Journal of Social Work Practice in the Addictions, 2023
Synthesized depressants including barbiturates and benzodiazepines were created in part with the goal of aiding sleep. These drugs, that with chronic use produce both a physical and psychological dependency, are also able to relieve anxiety, tension, and convulsions by producing calmness and muscular relaxation through their inhibition of GABA. However, individuals not requiring these drugs for therapeutic use experience a significant sense of euphoria when self-administering. Barbiturates, which are no longer prominently dispensed or used illicitly, disrupt both the sleep and dream cycles; thus, while people often took these drugs to aid in sleeping, it is now known that they do not produce normal sleep patterns, with users feeling tired and irritable upon waking, regardless of what early advertising of the drugs promoted. Barbiturates are among the few psychoactive agents that are not readily flushed from the human body, as they accumulate in body fat. With regular use, tolerance develops to their effects; it develops more slowly to the harmful effects than to the sleep-inducing or intoxicating effects. At high doses or when mixed with other CNS depressants, particularly alcohol, respiratory depression, and/or cardiovascular depression leading to death are possible. Temporary sleep disturbances may lead a user to incorrectly decide that more of the drug is required, also leading to a risk of overdose. There is a high cross-tolerance between barbiturates and other depressants, particularly alcohol (Hancock & McKim, 2018).
Ultrasound stress compromises the correlates of emotional-like states and brain AMPAR expression in mice: effects of antioxidant and anti-inflammatory herbal treatment
Published in Stress, 2020
João Pedro Costa-Nunes, Anna Gorlova, Dmitrii Pavlov, Raymond Cespuglio, Anna Gorovaya, Andrei Proshin, Aleksei Umriukhin, Eugene. D. Ponomarev, Alan. V. Kalueff, Tatyana Strekalova, Careen A. Schroeter
The incidence of anxiety disorders is currently the highest of all mental disorders (Kessler, Petukhova, Sampson, Zaslavsky, & Wittchen, 2012; Bandelow & Michaelis, 2015). As for instance, 20% of adults are diagnosed with generalized anxiety alone (Grenier et al., 2019). Anxiety disorders are frequently accompanied by increased aggression, violence, self-harm, and suicide (Stone, 2016). “Psychological” or “emotional” stress resulting from the adverse experience of non-material nature is the most common cause of these conditions (Fontes et al., 2014). At the same time, side effects of traditional anti-anxiety drugs are well-documented: benzodiazepines, the most widely used anxiolytics, cause rebound anxiety, insomnia and memory impairments (Uzun, Kozumplik, Jakovljević, & Sedić, 2010); barbiturates induce drowsiness and balance problems, disrupt learning and reproductive functions (Anderson & Hakimian, 2018), selective serotonin re-uptake inhibitors (SSRIs) evoke irritability and restlessness (Orsolini & Bellantuono, 2015), as well as fatigue, nausea and insomnia (Quagliato et al., 2019). That said, there is a need for an effective and safe pharmacological treatment, and herbal medicine appears as an attractive solution (Bystritsky et al., 2012) affordable for low-income patients (Oyebode, Kandala, Chilton, & Lilford, 2016). However, with an increase in self-medication with herbal remedies, there is a need for better understanding of their mechanisms of action to prevent potential adverse effects (McIntyre, Saliba, & Moran, 2015).
Pharmacogenomics of drugs used to treat brain disorders
Published in Expert Review of Precision Medicine and Drug Development, 2020
At least 13 categories of CNS drugs can be differentiated: (i) general anesthetics; (ii) analgesics and antipyretics (nonsteroidal anti–inflammatory agents, opiate agonists, opiate partial agonists); (iii) opiate antagonists; (iv) anticonvulsants (barbiturates, benzodiazepines, hydantoins, succinimides); (v) psychotherapeutic agents (antidepressants: monoamine oxidase inhibitors, selective serotonin and norepinephrine-reuptake inhibitors, selective serotonin-reuptake inhibitors, serotonin modulators, tricyclics and other norepinephrine-reuptake inhibitors; antipsychotics: atypical antipsychotics, butyrophenones, phenothiazines, thioxanthenes); (vi) anorexigenic agents and respiratory and cerebral stimulants (amphetamines); (vii) anxiolytics, sedatives, and hypnotics (barbiturates, benzodiazepines, and miscellaneous anxiolytic, hypnotic and sedative agents); (viii) antimanic agents; (ix) antimigraine agents (selective serotonin agonists); (x) antiparkinsonian agents (adamantanes, anticholinergic agents, catechol-O-methyltransferase (COMT) inhibitors, dopamine precursors, dopamine receptor agonists, monoamine oxidase B inhibitors); (xi) anti-dementia agents (cholinesterase inhibitors, nootropics, neuroprotective agents, vasoactive agents, immunotrophins, anti-atherogenic compounds, other anti-dementia drugs); (xii) fibromyalgia agents; and (xiii) miscellaneous CNS agents [8, 9].