Fig. 2. Colonic and total gastrointestinal (GI) tract motility are delayed throughout the experimental times. Control and infected groups were evaluated in the acute phase (AP; 11 days) and chronic phases (CP; 3, 7, 12, and 15 months post-infection [m.p.i.]) of Trypanosoma cruzi infection (A) Colonic transit time estimated by measuring the time required to release a glass bead. (B) Total transit time, estimated by measuring the time between carmine red orally administration and the time to excretion of red stools. n = 10 mice, except for infected acute phase (IAP) and infected chronic phase 3 m.p.i. (ICP3) groups, n = 16 and n = 15, respectively. For (A) and (B), statistical analysis: two-way ANOVA and Student–Newman–Keuls. Control (○); Infected (●). The symbols (*) represent differences in the relation to the group (control vs infected) and the letters (a, b, c, and d) represent the difference in the time, considering the same group. aDifferent from AP (ie, ICP15 was different from IAP). bDifferent from CP3 (ie, ICP15 was different from ICP3; CCP15 was different from CCP3). cDifferent from CP7 (ie, ICP15 was different from ICP7). dDifferent from CP12 (ie, ICP15 was different from ICP12). (C) Colonic transit time in 15 m.p.i. mice in the absence (–) or in the presence (+) of pyridostigmine. (D) The GI total transit time in 15 m.p.i mice in the absence (–) or in the presence (+) of pyridostigmine. n = 10, except for CCP 15 and ICP15 groups, n = 9 and n = 8, respectively. For (C) and (D), statistical analysis: Student’s t tests. P ≤ 0.05. Data presented as mean ± SD. The symbols (*) represent differences in the relation to the group (control vs infected).
© J Neurogastroenterol Motil
