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  • 8 mg BDS or TDS orally or IV by slow injection over 15 min
  • It is the prototype of a distinct class of antiemetic drugs developed to control cancer chemotherapy/radiotherapy induced vomiting, and later found to be highly effective in PONV and disease/drug associated vomiting as well.
  • It blocks the depolarizing action of 5-HT exerted through 5-HT3 receptors on vagal afferents in the g.i.t. as well as in NTS and CTZ.
  • Cytotoxic drugs/radiation produce nausea and vomiting by causing cellular damage → release of mediators including 5-HT from intestinal mucosa → activation of vagal afferents in the gut → emetogenic impulses to the NTS and CTZ.
  • Ondansetron blocks emetogenic impulses both at their peripheral origin and their central relay.
  • It does not block dopamine receptors. Apomorphine or

motion sickness induced vomiting is not suppressed.

  • Ondansetron is generally well tolerated
  • The only common side effect is headache and dizziness.
  • Mild constipation and abdominal discomfort occur in few patients.
  • Hypotension, bradycardia, chest pain and allergic reactions are reported, especially after IV injection
  • Before starting chemotherapy especially cisplatin
  • PONV
  • Radiotherapy
  • Vomiting due to uremia, neurological surgery

Metoclopramide (Prokinetic Drug- promote GI transit and speed gastric emptying by enhancing coordinated propulsive motility)

DOSAGE- 10 mg TDS oral or IM



Metoclopramide has more prominent effect on upper g.i.t.; increases gastric peristalsis while relaxing the pylorus and the first part of duodenum → speeds gastric emptying, especially if it was slow. This action is independent of vagal innervation, but is stronger when vagus is intact. Lower esophageal sphincter (LES) tone is increased and gastroesophageal reflux is opposed. It also increases intestinal peristalsis to some extent, but has no significant action on colonic motility and gastric secretion.


Metoclopramide is an effective antiemetic; acting on the CTZ, blocks apomorphine induced vomiting. The gastrokinetic action may contribute to the antiemetic effect. However, it has no chlorpromazine (CPZ) like antipsychotic property, though it does share the extrapyramidal and prolactin secretion augmenting action of CPZ.


Metoclopramide acts through both dopaminergic and serotonergic receptors

D2 antagonism

Dopamine (acting through D2 receptors) is an inhibitory transmitter in the g.i.t. — normally acts to delay gastric emptying when food is present in stomach. It also appears to cause gastric dilatation and LES relaxation attending nausea and vomiting. Metoclopramide blocks D2 receptors and has an opposite effect— hastening gastric emptying and enhancing LES tone by augmenting ACh release. However, clinically this action is secondary to that exerted through 5HT4 receptors. The central antidopaminergic (D2) action of metoclopramide on CTZ is clearly responsible for its antiemetic property. Other manifestations of D2 blockade are antagonism of apomorphine induced vomiting, CPZ like extrapyramidal effects and hyperprolactinaemia.

5-HT4 agonism

Metoclopramide acts in the g.i.t. to enhance ACh release from myenteric motor neurones. This results from 5-HT 4 receptor activation on primary afferent neurones (PAN) of the ENS via excitatory interneurons. The gastric hurrying and LES tonic effects are mainly due to this action which is synergised by bethanechol and attenuated by atropine.

5-HT3 antagonism

At high concentrations metoclopramide can block 5-HT3 receptors present on inhibitory myenteric interneurons and in NTS/ CTZ. The peripheral action can augment ACh release in the gut, but appears to be minor. The central anti 5-HT 3 action appears to be significant only when large doses are used to control CINV.



  • Sedation, dizziness, loose stools, muscle dystonia (especially in children) are the main side effects.
  • Long-term use can cause Parkinsonism, galactorrhea and gynecomastia, but it should not be used to augment lactation.
  • Suckling infant may develop loose motions, dystonia, myoclonus
  • Antiemetic
  • Gastro-kinetic: when emergency GA has to be given, to relieve postvagotomy or diabetic gastroparesis, to facilitate duodenal intubation
  • Dyspepsia and other functional GI distress
  • Persistent hiccups
  • GERD


It is a D2 receptor antagonist, chemically related to haloperidol, but pharmacologically related to metoclopramide.

The antiemetic and prokinetic actions have a lower ceiling. Unlike metoclopramide, its prokinetic action is not attenuated by atropine and is based only on D2 receptor blockade in upper g.i.t. Domperidone crosses blood-brain barrier poorly. Accordingly, extrapyramidal side effects are rare, but hyperprolactinemia can occur.

The antiemetic action is exerted mainly through CTZ which is not protected by blood-brain barrier. Because of poor entry into CNS, it does not block the therapeutic effect of levodopa and bromocriptine in Parkinsonism, but counteracts their dose-limiting emetic action.


Are much less than with metoclopramide.

Dry mouth, loose stools, headache, rashes, galactorrhoea are generally mild. Cardiac arrhythmias have developed on rapid i.v. injection.


Its indications are similar to that of metoclopramide, but it is a less efficacious gastrokinetic and not useful against highly emetogenic chemotherapy.

DOSE: 10–40 mg (Children 0.3–0.6 mg/kg) TDS

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