Abstract
Gastric slow wave dysrhythmias are accompanied by deviations in frequency, velocity, and extracellular amplitude, but the inherent association between these parameters in normal activity still requires clarification. This study quantified these associations using a joint experimental-theoretical approach.
Gastric pacing was conducted in pigs with simultaneous high-resolution slow wave mapping (32-256 electrodes; 4-7.6 mm spacing). Relationships between period, velocity, and amplitude were quantified and correlated for each wavefront. Human data from two existing mapping control cohorts were analyzed to extract and correlate these same parameters. A validated biophysically based ICC model was also applied in silico to quantify velocity-period relationships during entrainment simulations and velocity-amplitude relationships from membrane potential equations.
Porcine pacing studies identified positive correlations for velocity-period (0.13 mm s
per 1 s, r
=.63, P<.001) and amplitude-velocity (74 μV per 1 mm s
, r
=.21, P=.002). In humans, positive correlations were also quantified for velocity-period (corpus: 0.11 mm s
per 1 s, r
=.16, P<.001; antrum: 0.23 mm s
per 1 s, r
=.55; P<.001), and amplitude-velocity (94 μV per 1 mm s
, r
=.56; P<.001). Entrainment simulations matched the experimental velocity-period relationships and demonstrated dependence on the slow wave recovery phase. Simulated membrane potential relationships were close to these experimental results (100 μV per 1 mm s
).
These data quantify the relationships between slow wave frequency, velocity, and extracellular amplitude. The results from both human and porcine studies were in keeping with biophysical models, demonstrating concordance with ICC biophysics. These relationships are important in the regulation of gastric motility and will help to guide interpretations of dysrhythmias.