BACKGROUND: Chronic administration of sucralfate (SCR), a non-systemic ulcer-healing drug, exerts a trophic action on the gastric mucosa and prevents or reduces ulcer recurrence. The aim of this study was to determine whether SCR and/or the acid inhibiting drug omeprazole (OME) may affect the quality of ulcer healing, i.e., restoration of mucosal architecture. METHODS: Gastric ulcers were produced in male rats by serosal application of acetic acid. Rats were gavaged twice daily for 14 days with 2 ml of: (a) Placebo (PLA), (b) SCR 500 mg/kg, or (c) OME, 50 mg/kg starting 48 h after ulcer induction. We determined ulcer size under a dissecting microscope, and performed quantitative histologic assessment of quality of healing score (QS) on a scale from 0 (normal) to 5 (most abnormal). RESULTS: Ulcer size was 1.4 +/- 0.15 mm in the PLA group, 0.61 +/- 0.1 mm in the SCR group and 0.86 +/- 0.13 mm in the OME group (both OME and SCR p < 0.01 versus PLA). In the PLA group, histology showed (in rats with ulcers) a well-developed ulcer margin with cystically dilated glands. The QS of the ulcer scar in the PLA group was 3.3 +/- 0.22. IN the SCR-treated group, within the scar gastric glands were less dilated, more vertically oriented and the healing zone and granulation tissue were well developed and organized. The QS was 1.6 +/- 0.2, p < 0.001 versus PLA and OME. In the OME group, the ulcer margin and the scar were thinner-reduction of mucosal thickness by 43 +/- 2% (p < 0.005) and 18 +/- 1%, respectively, versus SCR and PLA groups. The number of dilated glands and connective tissue components in the scar was increased by 60%. The QS was 3.6 +/- 0.3. CONCLUSIONS: (1) Both SCR and OME significantly reduced the size of the experimental gastric ulcer. (2) Restoration of mucosal architecture, assessed quantitatively, was much better in the SCR than in the OME and PLA-treated groups. (3) a trophic action of SCR on the gastric mucosa may be the basis of better quality of ulcer healing with SCR.
BACKGROUND: Chronic administration of sucralfate (SCR), a non-systemic ulcer-healing drug, exerts a trophic action on the gastric mucosa and prevents or reduces ulcer recurrence. The aim of this study was to determine whether SCR and/or the acid inhibiting drug omeprazole (OME) may affect the quality of ulcer healing, i.e., restoration of mucosal architecture. METHODS: Gastric ulcers were produced in male rats by serosal application of acetic acid. Rats were gavaged twice daily for 14 days with 2 ml of: (a) Placebo (PLA), (b) SCR 500 mg/kg, or (c) OME, 50 mg/kg starting 48 h after ulcer induction. We determined ulcer size under a dissecting microscope, and performed quantitative histologic assessment of quality of healing score (QS) on a scale from 0 (normal) to 5 (most abnormal). RESULTS:Ulcer size was 1.4 +/- 0.15 mm in the PLA group, 0.61 +/- 0.1 mm in the SCR group and 0.86 +/- 0.13 mm in the OME group (both OME and SCR p < 0.01 versus PLA). In the PLA group, histology showed (in rats with ulcers) a well-developed ulcer margin with cystically dilated glands. The QS of the ulcer scar in the PLA group was 3.3 +/- 0.22. IN the SCR-treated group, within the scar gastric glands were less dilated, more vertically oriented and the healing zone and granulation tissue were well developed and organized. The QS was 1.6 +/- 0.2, p < 0.001 versus PLA and OME. In the OME group, the ulcer margin and the scar were thinner-reduction of mucosal thickness by 43 +/- 2% (p < 0.005) and 18 +/- 1%, respectively, versus SCR and PLA groups. The number of dilated glands and connective tissue components in the scar was increased by 60%. The QS was 3.6 +/- 0.3. CONCLUSIONS: (1) Both SCR and OME significantly reduced the size of the experimental gastric ulcer. (2) Restoration of mucosal architecture, assessed quantitatively, was much better in the SCR than in the OME and PLA-treated groups. (3) a trophic action of SCR on the gastric mucosa may be the basis of better quality of ulcer healing with SCR.
Authors: M D Basson; Z Rashid; G A Turowski; A B West; N J Emenaker; S A Sgambati; F Hong; D M Perdikis; S Datta; J A Madri Journal: Yale J Biol Med Date: 1996 Mar-Apr
Authors: C M Polo; T M Moraes; C H Pellizzon; M O Marques; L R M Rocha; C A Hiruma-Lima Journal: Evid Based Complement Alternat Med Date: 2012-11-01 Impact factor: 2.629