Vomiting center, central

MOA Antagonism of the S-HT, receptor prevents stimulation of the chemoreceptor trigger zone and triggering of the vomiting center. Central dopaminergic blockade prevents stimulation of the chemoreceptor trigger zone and triggering of the vomit center... 

Benzodiazepines, especially lorazepam, are used to prevent and treat CINV.5,10 Lorazepam is thought to prevent input from the cerebral cortex and limbic system from reaching the central vomiting center in the brain stem.10 Sedation and amnesia are common side effects. Respiratory depression can occur with high doses or when other central depressants such as alcohol are combined with benzodiazepines. 

Selective 5-HT3 receptor antagonists have potent antiemetic properties that are mediated mainly through peripheral 5-HT3 receptor blockade on intestinal vagal afferents. In addition, central 5-HT3 receptor blockade in the vomiting center and chemoreceptor trigger zone probably plays an important role. The antiemetic action of these agents is restricted to emesis attributable to vagal stimulation other emetic stimuli such as motion sickness are poorly controlled. 

The effects of the ergot alkaloids on the central nervous system are very diverse as sites of action are situated in the vasomotor center and the cardiac inhibitory center in the medulla oblongata as well as in the sympathetic structures of the diencephalon, particularly the hypothalamus. The inhibition of the vasomotor center and of tire baroceptive reflexes and the stimulation of the vagal nuclei are resppfisible for the vasodilator, hypotensive, and bradycardic effects, especially in the case of the peptide type of alkaloid. Some also have a stimulating effect on the vomiting center. 

Tobacco smoke includes 4000 chemical species with varying potential which cause adverse effects. Nicotine is stimulating to the autonomic nervous system ganglia and neuromuscular junction. The most prominent effects relate to stimulation of the adrenal medulla, central nervous system (CNS), cardiovascular system (release of catecholamines), gastrointestinal tract (parasympathetic stimulation), salivary and bronchial glands, and the medullary vomiting center. There is subsequent blockade of autonomic ganglia and the neuromuscular junction transmission, inhibition of catecholamine release from the adrenal medulla, and CNS depression. 

Emesis was also induced in cats given 5-10 mL of fluid pokeroot extract diluted in water via stomach tube (Macht, 1937). These effects were attributed to a nonspecific irritant effect, rather than to a central effect on the vomiting center. 

The action which nicotine exerts on the respiratory center is seen also in the vagal center (71), the vomiting center (72), and the vasomotor center (73). These central actions, which are associated with the peripheral effects of nicotine, manifest themselves in complex cardio-circulatory phenomena. 

There are two primary classes of emetics those that work on the vomiting centers in the medulla (central emetics), and those that act directly on the stomach itself (gastric emetics). There are botanical emetics that fall into each class, although the mechanism of action of most botanical emetics is not fully understood. Central emetics act by affecting a section of the brain stem known as the chemoreceptor... 

It inhibits peripheral dopamine D receptors resulting in increased Gl motility and tone. Its antagonism of the central D receptors raises the threshold of aaivity in the CTZ and decreases the sensitivity of visceral nerves supplying afferents to the vomiting center. It also antagonizes 5- FIT3 receptors at high dose... 

The clinical picture of carbaryl intoxication results from inactivation of cholinesterase, resulting in the accumulation of acetylcholine at synapses in the nervous system, skeletal and smooth muscle, and secretory glands. Signs and symptoms of overexposure may include (1) muscarinic manifestations such as miosis, blurred vision, lacrimation, excessive nasal discharge or salivation, sweating, abdominal cramps, nausea, vomiting, and diarrhea (2) nicotinic manifestations including fasiculation of fine muscles and tachycardia and (3) central nervous system manifestations characterized by headache, dizziness, mental confusion, convulsions, coma, and depression of the respiratory center. 

In most patients, the ergot alkaloids have little or no significant effect on bronchiolar or urinary smooth muscle. The gastrointestinal tract, on the other hand, is quite sensitive. Nausea, vomiting, and diarrhea may be induced even by low doses in some patients. The effect is consistent with action on the central nervous system emetic center and on gastrointestinal serotonin receptors. 

Since volatile solvents depress the central nervous system, including the respiratory center of the brain, prolonged use can be hazardous. Respiratory depression can progress to respiratory arrest, in which the user stops breathing and dies. Death by choking is another possibility. Some users of inhalants have choked to death on their own vomit. 

The general processes are manifested by various mechanisms, determined by the type and characteristics of the toxic noxa. Most often met with are a) heavy dehydratation by copious vomiting and diarrheas related to the local damages b) affection of the acid-alkaline and water-electrolytic balance c) acute blood circulation disorders as a consequence of the dehydratation, as well as of the direct injury by some poisons of the vasomotor centers d) syndromes of the central nervous system (consciousness disorders, convulsions, coma, etc.), the liver, the kidneys, the blood, etc., depending on the chemical character of the poison. 

Nicotine induces vomiting by both central and peripheral actions. The primary sites of action of nicotine in the CNS are prejunctional, causing the release of other transmitters. Accordingly, the stimulatory and pleasure-reward actions of nicotine appear to result from release of excitatory amino acids, DA, and other biogenic amines from various CNS centers. Release of excitatory amino acids may account for much of nicotine s stimulatory action. Chronic exposure to nicotine increases the density or number of nicotinic receptors. 

The first experimental study of a crude infusion of Erythrophlemn by Brunton and Pye (101) established most of the pharmacologic actions. In cats, nausea and vomiting were observed and a central locus established, because emesis occurred after subcutaneous administration and was diminished if both vagi were severed. They also observed that the initial action on the heart was mediated via the medullary vagal centers. First there... 

Central effects are weak, and late in appearance. Vasomotor paralysis is first apparent, and leads to dyspnea the emetic center is stimulated causing nausea and vomiting. 

Hydromorphone binds to mu and delta opiod receptors in the central nervous system. It has no effect at the kappa, sigma, or epsilon opioid receptors. Activity at the mu receptors causes analgesia, but also miosis, urinary retention, constipation, hyperthermia, and euphoria. Other side effects such as respiratory depression, pruritus, nausea, vomiting, and development of tolerance are due to binding at both mu and delta receptors. Hydromorphone, unlike other opioids, also has a direct depressant effect on the respiratory brainstem center and the cough center in the medulla. 

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