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Related Concept Videos

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...
Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
Phenothiazines, such as prochlorperazine...
Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
Two synthetic agonists of THC,...
Pathophysiology of Vomiting01:22

Pathophysiology of Vomiting

Vomiting is a complex physiological response to expel harmful or irritating substances from the body. It's a defensive mechanism triggered by stimuli like poisons, microbial toxins, cytotoxic drugs, and mechanical abdominal distension. The process is centrally coordinated by the vomiting (or emetic) center located in the medulla of the brainstem. This area, rich in muscarinic M1, histamine H1, neurokinin 1 (NK1), and serotonin 5-HT3 receptors, coordinates the act of vomiting through interaction...
Prevention of Further Absorption of Poison01:14

Prevention of Further Absorption of Poison

In cases of acute poisoning, the primary objective is to prevent further absorption of the toxic substance into the body. Immediate interventions using various decontamination techniques targeting the gastrointestinal (GI) tract can achieve this. Decontamination is crucial to prevent poison from entering the systemic circulation, which involves washing affected areas with water and mild soap and removing contaminated clothing. Once external decontamination is done, attention must be turned to...

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Related Experiment Video

Updated: Jul 14, 2026

Acupoint Application Combined with Acupressure as an Adjunctive Therapy for Chemotherapy-Induced Nausea and Vomiting
05:56

Acupoint Application Combined with Acupressure as an Adjunctive Therapy for Chemotherapy-Induced Nausea and Vomiting

Published on: June 21, 2024

[Substance P and anticancer drug-induced emesis].

Takeshi Yamada1, Noritake Tanaka, Kimiyoshi Yokoi

  • 1Dept. of Surgery,Chiba Hokusoh Hospital.

Gan to Kagaku Ryoho. Cancer & Chemotherapy
|June 15, 2007
PubMed
Summary

Chemotherapy increases substance P (SP) levels, a key factor in delayed emesis (DE). Higher SP level differences post-chemotherapy correlate with experiencing DE, suggesting SP

Related Experiment Videos

Last Updated: Jul 14, 2026

Acupoint Application Combined with Acupressure as an Adjunctive Therapy for Chemotherapy-Induced Nausea and Vomiting
05:56

Acupoint Application Combined with Acupressure as an Adjunctive Therapy for Chemotherapy-Induced Nausea and Vomiting

Published on: June 21, 2024

Area of Science:

  • Oncology
  • Neuroscience
  • Pharmacology

Context:

  • Delayed emesis (DE) remains a significant challenge in chemotherapy despite advances in managing acute emesis.
  • Serotonin antagonists are effective for acute emesis, but DE mechanisms may involve different mediators.
  • Substance P (SP) and its receptor, neurokinin receptor 1 (NK 1), are implicated in emesis development.

Purpose:

  • To investigate the association between delayed emesis (DE) and substance P (SP) levels in cancer patients undergoing chemotherapy.
  • To measure plasma SP levels before and after cytotoxic agent administration.

Summary:

  • Plasma SP levels were measured in 20 digestive and breast cancer patients before and for five days after chemotherapy.
  • SP levels significantly increased on days one and three post-administration.
  • Patients experiencing DE showed a greater increase in plasma SP levels from pre-chemotherapy to day one post-chemotherapy compared to those who did not.

Impact:

  • Chemotherapy transiently elevates plasma SP levels.
  • The magnitude of SP increase post-chemotherapy is a potential indicator for delayed emesis.
  • Findings suggest SP as a potential therapeutic target for managing chemotherapy-induced delayed emesis.