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SUMMARY:Disruptions of Pacemaker Activity in the Human Stomach: A Model of
  Nausea? - Gareth Sanger - Professor of Neuropharmacology\, Queen Mary Uni
 versity\, London
DTSTART:20200305T110000Z
DTEND:20200305T120000Z
UID:TALK140410@talks.cam.ac.uk
CONTACT:Kirsty Shepherd
DESCRIPTION:The use of anti-emetic drugs means that vomiting and in partic
 ular\, the severe vomiting experienced by cancer patients during chemother
 apy\, can be controlled. However\, nausea is harder to control. This is tr
 ue for the cancer patients and for several common disorders in which nause
 a is a major symptom. Examples include the gastrointestinal disorders\, ga
 stroparesis and functional dyspepsia.\nMovements of the stomach are regula
 ted by pacemaker cells in the stomach wall\, which spontaneously generate 
 slow waves of electrical activity that in a syncytium of cells\, pass circ
 umferentially 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 interpret
 ation as nausea.  These are hard to study.  Mostly\, this is because roden
 ts (mice\, rats) cannot vomit and the capacity of any mammal to experience
  nausea cannot be ascertained. For this reason\, we have established proto
 cols for studying spontaneous movements of human isolated stomach so that 
 dysrhythmia can be modelled\, potentially of relevance to the genesis of n
 ausea and to methods of control.\nMuscle 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 du
 ring nausea and able to induce nausea) increase the rate\, frequency and a
 mplitude of contraction and act in synergy (vasopressin and adrenaline\, i
 ncreased during motion sickness) whereas others break the regularity of co
 ntractions 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 musc
 le or the pacemaker cells\, that the movements can be ‘reverse translate
 d’ to the overall electrical activity of the muscle (a composite of pace
 maker cells and muscle) and that rodents cannot be used as surrogates. Fur
 ther\, the model being developed may make it possible to design ways to co
 rrect gastric dysrhythmia and potentially\, nausea.\n
LOCATION:Electrical Engineering\, Department of Engineering - EED Seminar 
 Room - 9 JJ Thomson Avenue\, Cambridge\, CB3 0FA
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