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Hesketh reports receiving consulting fees from GlaxoSmithKline, Helsinn, Merck, MGI Pharma, Sanofi-Aventis, Schering-Plough, and Solvay; lecture fees from GlaxoSmithKline and Merck; and grant support from Merck, MGI Pharma, and Sanofi-Aventis. No other potential conflict of interest relevant to this article was reported. I thank Paul L. Andrews and Steven M. Grunberg for their insightful and extraordinarily helpful comments and Sarah Francis for her expert editorial assistance with an earlier draft of the manuscript. Figure 1 Pathways by Which Chemotherapeutic Agents May Produce an Emetic Response.

Antineoplastic agents may cause emesis through effects at a number of sites. The mechanism that is best supported by research involves an effect on the upper small intestine (bottom of figure). Thiyagam Serial Cast. After the administration of chemotherapy, free radicals are generated, leading to localized exocytotic release of 5-hydroxytryptamine (5-HT) from the enterochromaffin cells; 5-HT then interacts with 5-hydroxytryptamine 3 (5-HT 3) receptors on vagal afferent terminals in the wall of the bowel. Vagal afferent fibers project to the dorsal brain stem, primarily to the nucleus tractus solitarius (NTS), and, to a lesser extent, the area postrema (AP), the two parts of the brain referred to collectively here as the dorsal vagal complex. Receptors for a number of neurotransmitters with potentially important roles in the emetic response are present in the dorsal vagal complex. These include the neurokinin-1, 5-HT 3, and dopamine-2 receptors, which bind to substance P, 5-HT, and dopamine, respectively.

Automotive Technology A Systems Approach By Jack Erjavec Pdf Free Download on this page. Efferent fibers project from the dorsal vagal complex to the final effecter of the emetic reflex, the central pattern generator, which is an anatomically indistinct area occupying a more ventral location in the brain stem. Receptors for other locally released mediators, such as substance P, cholecystokinin, and prostaglandins, are also present on the vagal afferent terminals. However, the extent to which these mediators are involved at this peripheral site is unknown. Antineoplastic agents may also induce emesis through an interaction with the area postrema within the dorsal vagal complex. The area postrema is a circumventricular organ located at the caudal end of the floor of the fourth ventricle, which is accessible to blood and cerebrospinal fluid–borne emetic stimuli.

Other potential sources of efferent input that result in emesis after chemotherapy include a number of structures in the temporal lobe, such as the amygdala. Evidence for this pathway is less well established than for other proposed sites of chemotherapeutic action.