Disruptions of Pacemaker Activity in the Human Stomach: A Model of Nausea?

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• Gareth Sanger - Professor of Neuropharmacology, Queen Mary University, London
• Thursday 05 March 2020, 11:00-12:00
• Electrical Engineering, Department of Engineering - EED Seminar Room - 9 JJ Thomson Avenue, Cambridge, CB3 0FA.

If you have a question about this talk, please contact Kirsty Shepherd.

The use of anti-emetic drugs means that vomiting and in particular, the severe vomiting experienced by cancer patients during chemotherapy, can be controlled. However, nausea is harder to control. This is true for the cancer patients and for several common disorders in which nausea is a major symptom. Examples include the gastrointestinal disorders, gastroparesis and functional dyspepsia. Movements of the stomach are regulated by pacemaker cells in the stomach wall, which spontaneously generate slow waves of electrical activity that in a syncytium of cells, pass circumferentially and ‘down’ the stomach to promote gastric emptying. In gastroparesis these appear to be disrupted so the electrical activity is ‘dysrhythmic’, argued to disrupt stomach movements that are detected by the extrinsic vagus nerve for projection to the brainstem and interpretation as nausea. These are hard to study. Mostly, this is because rodents (mice, rats) cannot vomit and the capacity of any mammal to experience nausea cannot be ascertained. For this reason, we have established protocols for studying spontaneous movements of human isolated stomach so that dysrhythmia can be modelled, potentially of relevance to the genesis of nausea and to methods of control. Muscle movements of different regions of the human stomach are captured electronically and measured using bespoke python software so different parameters of the movements can be visualised by RADAR plots; we are attempting to correlate with electrical activity by use of surface electrodes. Some ‘nauseogenic hormones’ (released during nausea and able to induce nausea) increase the rate, frequency and amplitude of contraction and act in synergy (vasopressin and adrenaline, increased during motion sickness) whereas others break the regularity of contractions so different amplitudes occur alternately (motilin and others). We hypothesise that the different responses to ‘nauseogenic stimuli’ depend on expression of their relevant receptors by either the smooth muscle or the pacemaker cells, that the movements can be ‘reverse translated’ to the overall electrical activity of the muscle (a composite of pacemaker cells and muscle) and that rodents cannot be used as surrogates. Further, the model being developed may make it possible to design ways to correct gastric dysrhythmia and potentially, nausea.

This talk is part of the Electrical Engineering series.

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• Electrical Engineering
• Electrical Engineering, Department of Engineering - EED Seminar Room - 9 JJ Thomson Avenue, Cambridge, CB3 0FA

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