Abstract :
Most patients who undergo chemotherapy have noted that nausea and vomiting are the mostfeared and distressing side-effects of cancer treatment (1). Nausea and vomiting from chemotherapy can be classified as acute, delayed, or anticipatory. Acute emesis generally occurs within 24 hours of chemotherapy administration; while delayed nausea and vomiting begin 24 hours after chemotherapy and may continue for up to one week. Anticipatory emesis occurs prior to chemotherapy in patients who anticipate another episode by sight, odors, or memory of the place where acute nausea and vomiting occuned (2,3). Different neurotransmitters found in the gastrointestinal tract (GlT) and central nervous system (CNS) mediate the pathophysiology of chemotherapy-induced nausea and vomiting (CINV).These include dopamine, histamine, acetylcholine, serotonin, and substance P; which act directly and indirectly on the vomiting center located in the lateral reticular formation of the medulla (1,4). Substance P is a member of the tachykinins family of neuropeptides.The hiological activity of this substance is to induce vomiting mediated by neurokinin-l (NKl) receptors located primarily in the GIT and the CNS (5). Both NKl receptors and substance P playa significant role in the pathogenesis of acute and delayed CINV.
