| Objective:The slow transit constipation is thought as a primary defect that the movement of contents from the proximal to the distal colon and rectum is slower than that of normal. Its' clinical features are infrequent faeces, hard faeces, and a feeling of incomplete evacuation. Incidence of slow transit constipation increases along with the improvement of standard of living. However, the pathophysiology of slow transit constiption is still not delineated. The present study was carried out to establish the model of slow transit constipation by feeding rats with Diphenoxylate, and study the pathogenesis of slow transit constipation by investigating the changes of interstitial cells of Cajal, enteric nerves system and colonic myoelectric activity in rats.Methods: Seventy-four health Wistar rats were used in the study. First, fourty-two rats were used to choose the fittest dosage of Diphenoxylate to establish slow transit constipation model. Then, 32 rats were randomly divided into control group and model group of slow transit constipation. After 120 days, colonic myoelectric activity was recorded and the time of colonic transit was measured. At last the rats were killed, the colonic tissues (1cm apart from cecum and 2cm apart from anus) were dyed with Hematoxylin and eosin (HE). Cholinergic nerves, nitrergic nerves, SP nerves and P nerves were investingted in colonic myenteric plexuses in the rats with histochemistry and immuneohistochemistry, and interstitiall cells of cajal were investingted in colonic myenteric plexuses with ZIO histochemistry in the rats.Results: (1) The movement of contents from the proximal to the distal colon and rectum in model rats was significantly slower than that of normal rats. In model rats group, the time of the first black faeces was 356±50min, it was significantly longer than that of normal rats (249±35 min, p﹤0.01). (2) In some model rats, the frequency of colonic slow wave decreased (5.55±1.20 /min vs control group 13.20±1.09/min, p﹤0.01)and amplitude increased (0.43±0.05 mv vs control group 0.19±0.02 mv, p﹤0.01)compared with the normal rats, and its' slow wave form was irregular. In the other model rats, the frequency of colonic slow wave increased(30.85±3.86 /min vs control group 13.20±1.09 /min, p﹤0.01) and amplitude was variable (0.21±0.03 mv vs control group 0.19±0.02 mv, p﹤0.01), and its slow wave form was also irregular. (3) The chronic inflammation occurred in colonic mucosa of all model rats. (4) In the colonic myenteric plexuses of rats with slow transit constipation, cholinergic nerves and cholinergic cells were significantly decreased with denser immunostainning, but its' volume increased (positive cells were 14.34±4.56 vs control group 27.56±6.64, the ratio of nuclei/cytoplasm was 0.57±0.20 vs control group 0.76±0.18, p﹤0.01); nitriergic nerves was significantly reduced, nitriergic cells decreased and had lighter immunostainning (positive cells were7.10±2.04 vs control group 11.16±2.81, lightly positive cells were 2.21±1.38 vs control group 0.84±0.67, p﹤0.01). (5) In the colonic myenteric plexuses of rats with slow transit constipation, VIP immunoreactive positive nerves and cells were significantly lessened(surface density was 19.35±1.13 vs control group 23.08±1.82, p﹤0.01), SP immunoreactive positive ganglions and fascicles were significantly larger and SP immunoreactive positive cells increased compared with that in normal rats(surface density was 18.14±1.18 vs control group15.45±1.05, p﹤0.01). (6) In the colon of rats with slow transit constipation, interstitial cells of Cajal(ICCs) were not well-distributed, the number of ICCs in some area increased but decrased in other area.Conclusions:1. The model of rats with slow transit constipation was successfully established. 2. Pathological changes of colonic myenteric plexuses occured in rats with slow transit constipation,dysfunction of colonic transit is close related with the changes of colonic myenteric plexuses. 3. Abnormality of distribution and numbers of interstitial... |
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