OBJETIVO: O deflazacort é um novo corticóide com os mesmos efeitos antiinflamatórios dos demais, porém com menos efeitos colaterais. O objetivo deste estudo foi investigar os efeitos do deflazacort na cicatrização de anastomoses colônicas. MATERIAL E MÉTODO: 75 ratos Wistar foram randomizados em três grupos para receberem os seguintes tratamentos por gavagem: grupo controle (N=24)= solução fisiológica; grupo deflazacort (N=25)= 0,1 mg/Kg/dia dessa droga e, grupo dexametasona (N=26)= 0,5 mg/Kg/dia substância. Após seis dias de tratamento, os animais foram submetidos à secção colônica, seguida de anastomose primária em um ponto situado a 2 cm acima da reflexão peritoneal. O tratamento com as soluções foi mantido até o sacrifício, que ocorreu no 3º ou no 6º dia de PO. Observou-se na necrópsia sinais de peritonite e deiscência de sutura. Realizou-se o teste de pressão de ruptura das anastomoses e dosou-se nessa região a concentração de hidroxiprolina e proteinas. RESULTADOS: Não houve diferença em relação à ocorrência de deiscência e peritonite. A pressão de ruptura foi semelhante no 3º dia. No 6º dia, ela foi maior (p <0.05) no grupo controle (180 [150-230] mmHg) que nos grupos deflazacort (150 [120-180] mmHg) e dexametasona (140 [100-180] mmHg). Não ocorreu diferença entre os grupos na dosagem de hidroxiprolina. A dosagem de protéinas foi maior no grupo dexametasona que nos controles no 3º PO. CONCLUSÕES: O uso de corticóides determina queda na resistência da anastomose colônica. O deflazacort apresenta os mesmos efeitos deletérios da dexametasona na cicatrização de anastomoses intestinais.

BACKGROUND: Deflazacort, a new corticosteroid is claimed to induce less collateral effects than other corticoids. The aim of this study was to investigate the effect of this drug on the healing of colonic anastomosis. MATERIAL AND METHOD: 75 Wistar rats were randomized to receive daily by gavage, one of the following treatments: control group (N=24) - 1 ml of saline; deflazacort (N=25) - 1 ml of this drug containing 0.15mg/ml (0,1 mg/kg/day), and dexamethasone (N=26) - 1 ml containing 0.03 mg/ml of this drug (0.5 mg/kg/day). After 6 days of treatment, the animals underwent laparotomy followed by section and immediate colonic anastomoses in a point 2 cm above peritoneal reflexion. Treatment in each group was carried out until the animals were killed on the third of a six postoperative day. At necroscopy, signs of peritonitis and anastomotic dehiscence were registered. Anastomotic site was tested for tensile rupture and biopsies containing all layers were sent for hydroxyproline and protein measurements. RESULTS: There was no difference in the peritonitis and anastomotic dehiscence rates among the groups. Bowel rupture pressure was similar at day 3 but significantly higher in controls (180 [150-230] mmHg) than in deflazacort (150 [120-180] mmHg) and dexamethasone groups (140 [100-180] mmHg) at day 6. No difference occurred in the hydroxyproline concentration. Protein content was higher in dexamethasone group than in controls on the third postoperative day. CONCLUSIONS: Corticosteroids may impair colonic anastomotic resistance and deflazacort may have similar deleterious effects of dexamethasone in anastomotic healing.

The short chain fatty acids (SCFA) are the best nutrients for the colonocytes. Glucose is poorly used as a fuel but may be transformed into SCFA by colonic bacteria. The aim of this study was to investigate the effect of SCFA or glucose on experimental colitis. Colitis was induced in 30 Wistar rats by colonic instillation of 4% acetic acid. Five days later they were randomized to receive twice a day colonic lavage containing saline (controls, N = 10), 10% hypertonic glucose (N = 10) or SCFA (N = 10) until day 8 when they were killed. At autopsy, the colon was removed and weighed and the mucosa was evaluated macro- and microscopically and stripped out for DNA assay. Data are reported as mean ± SD or median [range] as appropriate. All animals lost weight but there was no difference between groups. Colon weight was significantly lower in the SCFA group (3.8 ± 0.5 g) than in the control (5.3 ± 2.1 g) and glucose (5.2 ± 1.3 g) groups (P<0.05). Macroscopically, the severity of inflammation was less in SCFA (grade 2 [1-5]) than in control (grade 9 [4-10]) and glucose-treated (grade 9 [2-10]) animals (P<0.01). Microscopically, ulceration of the mucosa was more severe in the glucose and control groups than in the SCFA group. The DNA content of the mucosa of SCFA-treated animals (8.2 [5.0-20.2] mg/g of tissue) was higher than in glucose-treated (5.1 [4.2-8.5] mg/g of tissue; P<0.01) and control (6.2 [4.5-8.9] mg/g of tissue; P<0.05) animals. We conclude that SCFA may enhance mucosal re-epithelialization in experimental colitis, whereas hypertonic glucose is of no benefit.