Analeptic
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Analeptic

An analeptic, in medicine, is a type of central nervous system (CNS) stimulant. The term analeptic typically refers to respiratory stimulants (e.g., doxapram). Analeptics include a wide variety of medications used to treat depression, attention deficit hyperactivity disorder (ADHD), and respiratory depression. Analeptics can also be used as convulsants, with low doses causing patients to experience heightened awareness, restlessness, and rapid breathing. The primary medical use of these drugs is as an anesthetic recovery tool or to treat emergency respiratory depression. Other drugs of this category are prethcamide, pentylenetetrazole, and nikethamide. Nikethamide is now withdrawn due to risk of convulsions. Analeptics have recently been used to better understand the treatment of a barbiturate overdose. Through the use of agents, researchers were able to treat obtundation and respiratory depression.

Analeptics have been used throughout history for two main purposes, to help patients recover from anesthesia more efficiently and to manage respiratory distress and apnea, particularly in infants.[citation needed]

Analeptics can be used to increase the speed of recovery from propofol, remifentanil, and sevoflurane. In clinical settings, analeptics such as doxapram have been used to help patients recover from anesthesia better, as well as to remove some of the potential negative side effects of potent anesthetics.[citation needed]

The three most prevalent clinical analeptic uses of caffeine are in the treatment of asthma, apnea of prematurity, and bronchopulmonary dysplasia in newborn infants. Caffeine is a weak bronchodilator, which explains the relief of the effects of asthma. Some preliminary research indicates that caffeine reduces the incidence of cerebral palsy and cognitive delay, but additional research is needed. Apnea of prematurity is officially described as a cessation of breathing for more than 15–20 seconds, usually accompanied by bradycardia and hypoxia. This cessation of breathing is due to the underdevelopment of the body's respiratory control center, the medulla oblongata, in premature infants.[citation needed]

Ample research also suggests that caffeine significantly reduces the occurrence of bronchopulmonary dysplasia, which is a chronic lung disorder defined by the need for supplemental oxygen after a postmenstrual age of 36 weeks. Bronchopulmonary dysplasia is common in infants with low birth weight (<2500 g) and very low birth weight (<1500 g) who received mechanical ventilator machines to help manage respiratory distress syndrome. Currently, no treatment is known for bronchopulmonary dysplasia, as the risks of treatment are generally thought to outweigh the necessity for using a mechanical ventilator. Caffeine only reduces occurrence.[citation needed]

Theophylline is no longer used as a respiratory stimulant in newborn infants. Theophylline has a very narrow therapeutic index, so its dosages must be supervised by direct measurement of serum theophylline levels to avoid toxicity.[citation needed]

Analeptics are a diverse group of medications that work through a variety of chemical pathways; analeptic medications work through four main mechanisms to stimulate respiration. Analeptics can act as potassium channel blockers, ampakines, serotonin receptor agonists, and adenosine antagonists.

Two common potassium channel blockers are doxapram and GAL-021. Both act on potassium channels in carotid bodies. These cells are responsible for sensing low concentrations of oxygen and transmitting information to the CNS, ultimately leading to an increase in respiration. Blocking the potassium channels on the membranes of these cells effectively depolarizes the membrane potential, which in turn leads to opening of voltage-gated calcium channels and neurotransmitter release. This begins the process of relaying the signal to the CNS. Doxapram blocks leaky potassium channels in the tandom pore domain family of potassium channels, while GAL-021 blocks BK channels, or big potassium channels, which are activated by a change in membrane electron potential or by an increase in internal calcium.

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