Colonic Activities Before Administration of Luminal Prucalopride
HAPWs were not present at baseline nor postprandially while SPWs were observed at baseline (n=1) and after meal intake (n=3) (Figure 1A,B). At baseline, a pan-colonic SPW with a mean amplitude of 8.7 mmHg, maximum pressure of 24.0 mmHg and a duration of 3.7 s was observed, not associated with gas or liquid expulsion. After the meal, pan-colonic SPWs were observed with an amplitude of 7.2 ± 0.8 mmHg and duration of 12.2 ± 2.5 s which entered the rectum but were not associated with gas nor liquid expulsion (Table 1). The SPW observed at baseline was associated with 69% relaxation of the anal sphincter while SPWs evoked postprandially were associated with 87% relaxation. The anal sphincter showed an intrinsic rhythmicity of 5.5 cpm (Figures 1A,B).

Effects of Intraluminal Prucalopride on Propulsive Motor Patterns

Administration of intraluminal prucalopride in the proximal colon introduced HAPWs and HAPW-SPWs whereas none were present during the preceding 180 min of baseline and meal response (Figures 1C,D). Moreover, intraluminal prucalopride resulted in a significant increase of the SPW amplitude compared to both baseline and meal response (Table 1, Figure 2A). These effects were observed only 6 mins after administration of intraluminal prucalopride.
During the 30 min period after prucalopride administration, six HAPWs were generated, all belonging to category 2, that is, they started in the ascending colon and propagated to the transverse or descending colon with or without a change into an SPW. We have previously classified HAPWs based on their origin and place of termination in three distinct categories as described in Milkova et al. (37). The average amplitude of the HAPWs was 81.5 mmHg and the average HAPW Index was 2200 mmHg.m.s. The HAPW Index assesses the vigor with which a contraction occurs, and it was calculated as the multiplication of average amplitude within the 20-mmHg isobar, the length of the HAPW and the duration, expressed as mmHg.m.s. (37). The HAPWs here propagated with an average velocity of 0.53 ± 0.4 cm s-1. One HAPW was associated with urge to defecate (Figures 2B,C & 3). Two HAPWs without SPWs, were associated with significant, 78%, anal sphincter relaxation, lasting 26.5 ± 7 s.
Among the six HAPWs, two were HAPW-SPWs with the SPWs entering the rectum with an average amplitude of 18.4 ± 9.8 mmHg (Table 2), they were associated with liquid expulsion, urge to defecate and nausea (Figures 1, 2B, 3). These motor patterns were associated with 48% anal sphincter relaxation, from 63 to 33 mmHg.
Five pan- colonic SPWs were evoked with an average amplitude of 13.0 ± 6.4 mmHg ranging between 7.3 – 24.0 mmHg with an average duration of 6.2 ± 2 s (Table 1). Vomiting associated pressure transients occurred at the end of the recording (Figure 1).
A SPW-cluster consisting of 4 pan-colonic SPWs was associated with significant anal sphincter relaxation. Anal sphincter did not recover in between the four SPWs. Before relaxation, the mean amplitude of the sphincter was 31.6 mmHg with maximum and minimum amplitudes of 56.0 and 15.4 mmHg respectively. During the relaxation phase, the anal sphincter amplitude decreased to 13.1 mmHg with maximum pressure of 45 and minimum pressure of 3.6 mmHg resulting in 60% relaxation (Table 2). One pan colonic SPW overlapped with an HAPW; therefore, anal sphincter relaxation could not be reliably attributed to either of the motor patterns.
The degree of relaxation associated with SPWs during baseline, meal and intraluminal prucalopride did not show any significant difference.