Pentobarbital (previously known as pentobarbitone in Britain and Australia) is a short-acting barbiturate typically used as a sedative, a preanesthetic, and to control convulsions in emergencies. It can also be used for short-term treatment of insomnia but has been largely replaced by the benzodiazepine family of drugs. In high doses, pentobarbital causes death by respiratory arrest. It is used for veterinary euthanasia and is used by some U.S. states and the U.S. federal government for executions of convicted criminals. In some countries and states, it is also used for physician-assisted suicide.Pentobarbital was widely abused and sometimes known as "yellow jackets" due to the yellow capsule of the Nembutal brand. Pentobarbital in oral (pill) form is no longer commercially available. Uses
Medical
Typical applications for pentobarbital are sedative, short term hypnotic, preanesthetic, insomnia treatment, and control of convulsions in emergencies. Abbott Pharmaceutical discontinued manufacture of their Nembutal brand of Pentobarbital capsules in 1999, largely replaced by the benzodiazepine family of drugs. Pentobarbital was also widely abused, known on the street as "yellow jackets". They were available as 30, 50, and 100-milligram capsules of yellow, white-orange, and yellow colors, respectively.It is also used as a veterinary anesthetic agent.Pentobarbital can reduce intracranial pressure in Reyes syndrome, treat traumatic brain injury and induce coma in cerebral ischemia patients. Pentobarbital-induced coma has been advocated in patients with acute liver failure refractory to mannitol. Euthanasia
Pentobarbital can cause death when used in high doses. It is used for euthanasia for humans as well as animals.
These harmful chemicals can be inhaled (in the case of air fresheners) or applied (in the case of perfumes). The substances diffuse into the brain rapidly, as they are lipophilic and readily transported across the blood–brain barrier. This is a result of increased membrane solubility and local blood flow, with central nervous system (CNS) solvent uptake being further increased with high levels of physical activity. When they are not detoxified immediately, the symptoms of toxic encephalopathy begin to emerge. However, in chronic situations, these effects may not become severe enough to be noticed until much later. Increased exposure time and increased concentration of the chemicals will worsen the effects of toxic encephalopathy, due to the associated structural CNS damage and direct functional impairment consequences.Subacute toxic encephalopathies are challenging to identify due to their often insidious tempo of evolution, nonspecific manifestations, relative infrequency as individual entities, and frequent lack of specific diagnostic testing. Yet they are crucial to recognize in aggregate, subacute toxic encephalopathies are a common problem that can lead to severe, irreversible harm if not diagnosed and treated efficiently. This article reviews the clinically relevant aspects of some of the more important subacute toxic encephalopathy syndromes caused by inorganic toxins, carbon monoxide (CO), anti- biotics, antineoplastic agents, and psychiatric medications.All therapeutic interventions are double-edged swords with benefits and adverse effects, and pharmacotherapy is not an exception.