PURPOSE: The effect of prostaglandin E1 (PGE1) and corticosteroids alone and in combination were studied in the healing rat colon to determine whether PGE1 could not only improve healing but reverse the negative effect of steroids on colonic wound healing. METHODS: Colonic anastomoses were performed in 144 male Sprague-Dawley rats divided into four groups. The control group (I) received no further treatment. The steroid group (II) received cortisone acetate (5 mg/kg/day) beginning six days preoperatively and continuing until sacrifice. The PGE1 group (III) received 2 micrograms of PGE1 intra-aortically at surgery and for three days postoperatively. The combination PGE1/steroid group (IV) received both drugs in the same doses as those in Groups II and III. Animals were sacrificed on postoperative days 6, 10, and 14. Wound healing was evaluated by hydroxyproline content, bursting pressures, and histology. RESULTS: The hydroxyproline assay at day 10 revealed that steroid-treated rats have significantly lower levels than any other group. The PGE1 group (III) had the highest level of significance in comparison to the steroid group (II) (P = 0.001). The addition of PGE1 to steroid (Group IV) appeared to abolish the negative effect of the steroid as measured by hydroxyproline content on day 10 (P = 0.038). When measuring bursting pressures, the PGE1 group (III) had significantly higher pressures than any other group at day 10. However, no amelioration of the steroid effect on bursting pressures was seen. Histologic evaluation of the anastomosis did not reveal any significant differences among the four groups. CONCLUSIONS: PGE1 reverses the negative effect of the steroid on hydroxyproline levels at day 10. Furthermore, using bursting pressure as a parameter of wound healing, administration of PGE1 results in significantly improved anastomotic healing at day 10.
PURPOSE: The effect of prostaglandin E1 (PGE1) and corticosteroids alone and in combination were studied in the healing rat colon to determine whether PGE1 could not only improve healing but reverse the negative effect of steroids on colonic wound healing. METHODS: Colonic anastomoses were performed in 144 male Sprague-Dawley rats divided into four groups. The control group (I) received no further treatment. The steroid group (II) received cortisone acetate (5 mg/kg/day) beginning six days preoperatively and continuing until sacrifice. The PGE1 group (III) received 2 micrograms of PGE1 intra-aortically at surgery and for three days postoperatively. The combination PGE1/steroid group (IV) received both drugs in the same doses as those in Groups II and III. Animals were sacrificed on postoperative days 6, 10, and 14. Wound healing was evaluated by hydroxyproline content, bursting pressures, and histology. RESULTS: The hydroxyproline assay at day 10 revealed that steroid-treated rats have significantly lower levels than any other group. The PGE1 group (III) had the highest level of significance in comparison to the steroid group (II) (P = 0.001). The addition of PGE1 to steroid (Group IV) appeared to abolish the negative effect of the steroid as measured by hydroxyproline content on day 10 (P = 0.038). When measuring bursting pressures, the PGE1 group (III) had significantly higher pressures than any other group at day 10. However, no amelioration of the steroid effect on bursting pressures was seen. Histologic evaluation of the anastomosis did not reveal any significant differences among the four groups. CONCLUSIONS:PGE1 reverses the negative effect of the steroid on hydroxyproline levels at day 10. Furthermore, using bursting pressure as a parameter of wound healing, administration of PGE1 results in significantly improved anastomotic healing at day 10.
Authors: Mari Nanna Oines; Peter-Martin Krarup; Lars Nannestad Jorgensen; Magnus Sven Agren Journal: World J Gastroenterol Date: 2014-09-21 Impact factor: 5.742
Authors: Harshad Ladha; Tushar Pawar; Mark R Gilbert; Jacob Mandel; Barbara O-Brien; Charles Conrad; Margaret Fields; Teresa Hanna; Carolyn Loch; Terri S Armstrong Journal: J Neurooncol Date: 2015-08-23 Impact factor: 4.130