Fig. 4: Optimization of Electrical Stimulation for Oesophageal and Gastric Motility.

a Disease-specific controller scheme of the myenteric neuroprosthesis highlighting the proof-of-concept model for hypomotility. b–e The ES parameters of (b) amplitude, (c) frequency and (d) pulse train length were optimized for oesophageal contraction time using ex vivo and in vivo models. (n = 4 animals | 10 repetitions of each condition, mean and standard deviations are plotted) e An amplitude sweep of the ES parameters (with a set frequency of 40 Hz, and pulse train length of 0.5 s) elicited a monotonically increasing electromyographic (EMG) responses in the smooth muscle. (n = 4 animals | 10 repetitions of each condition, mean and standard deviations are plotted) f, g Endoscopic views of the oesophagus during titration of muscle activation and contraction duration enabling graded control of closure. Endoscopic visualization of the opening (h) and (i) closing of the pylorus was utilized to characterize gastric peristalsis. j Panel of ES parameters evaluated for stomach motility. k All stimulation conditions yielded an increase in peristaltic rate (pyloric cycles/time), with setting C optimizing activity with minimal energy. Mean and standard deviations are plotted. (* p < 0.01, p <= 0.001, student’s two-sided t-test, n = 4 animals) l Changes in impedances at 500 Hz (green), 1000 Hz (blue), and 2000 Hz (purple) of proximal electrodes of the neuroprosthesis implanted in the swine oesophagus enable detection of ingested boluses, applying forces greater than 0.2 N. (n = 3 samples, 11 repetitions- mean and standard deviations are plotted) m EMG signals recorded from implanted neuroprosthesis can be used to monitor the peristaltic waves.