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Chemotherapy-Related Nausea & Vomiting
Author Bio
Introduction
What Causes Nausea & Vomiting?
Automatic Nervous System
Chemotherapy Induced NV
Currently selected section: NV Control
Issues in Research Design
Case Study 1
Case Study 2
Summary


Chapter 11: Chemotherapy-Related Nausea & Vomiting: NV Control
         In order to improve the effectiveness of treatments and the quality of patients' lives, it is important to control, or at least mitigate, the damage wrought by nausea and vomiting. The search for effective pharmacologic and behavioral methods of preventing or alleviating these unpleasant and potentially dangerous treatment complications has been an ongoing one since the serendipitous discovery that compazine relieved emesis following the administration of nitrogen mustard.

Dopamine Receptor Antagonists

Early research showed that antiemetics (typically phenothiazines and butyrophenones) blocked dopamine receptors (Morrow, 1989; Wampler, 1983).

Metoclopramide, a substituted benzamide, has been widely used as an antiemetic drug for more than 27 years and was originally believed to act solely by blocking dopamine receptors in the chemoreceptor trigger zone (Harrington et al., 1983). However, its efficacy against the severe emetogenic effects of chemotherapeutic agents, such as cisplatin, was very limited.

As a consequence, high dose metoclopramide (up to 10 mg/kg/day) was introduced and proved to be more effective against cisplatin-induced emesis (Gralla et al., 1981). This important development led to the conclusion that some mechanism other than dopamine receptor blockade might be producing the antiemetic effect by its action on 5-hydroxytryptamine (5-HT3) receptors located on gut neurons (Miner et al., 1986).

 

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