X Fu1, Z Sheng, Y Wang, Y Ye, M Xu, T Sun, B Zhou. 1. Trauma Center of Postgraduate Medical College, 304th Hospital, Beijing, People's Republic of China.
Abstract
OBJECTIVE: To explore the possible effects of basic fibroblast growth factor (bFGF) on ischemic gut and liver injuries after trauma. METHODS: Animal models of superior mesenteric artery occlusion (45 minutes) and reperfusion (3 days) were used in this study. Seventy-two Wistar rats were divided into three groups of 24 rats each. The animals in bFGF-treated group were injected with 4 microg bFGF/rat in 0.15 mL normal saline solution containing heparin 0.1% (w/v) through the jugular vein at the onset of reperfusion. In the normal saline control group, all rats received the same vehicle, but without bFGF. Group 3 (sham-operated) underwent the same laparotomy procedure, but without superior mesenteric artery occlusion. Liver function parameters, the levels of serum tumor necrosis factor alpha, nitric oxide, superoxide dismutase, malondialdehyde (MDA), tissue bacterial examination, and pathologic study were used to evaluate the results. RESULTS: In bFGF-treated rats, the amounts of serum alanine transaminase and aspartate aminotransferase and serum tumor necrosis factor-alpha were reduced significantly at 6, 24, and 48 hours when compared with normal saline-treated rats. However, the changes in nitric oxide, superoxide dismutase, and MDA varied from each other as a function of time after injury. The amounts of nitric oxide were increased significantly at 6 hours in intestine in normal saline-treated rats and in liver in bFGF-treated rats (p < 0.05). At 6 hours after reperfusion, the activity of superoxide dismutase in normal saline-treated rats were much lower in liver than those in bFGF-treated and sham-operated rats (p < 0.05), but the levels of MDA were increased in intestine in bFGF-treated rats and in liver in normal saline-treated rats when compared with sham-operated rats (p < 0.05). At 24 hours, the levels of MDA in normal saline-treated rats were much higher than those in both bFGF and sham-operated rats (p < 0.05). Bacterial examination revealed that the ratio and the amounts of bacterial translocation from gut to liver, spleen, and mesenteric lymph nodes in bFGF-treated rats were much lower than those in normal saline-treated rats. The results of pathologic study support the assumption that bFGF provided protective effects against reperfusion injury. CONCLUSIONS: Intravenous administration of bFGF may benefit in reducing gut and liver injuries after ischemia and reperfusion. The mechanisms of those effects may involve mitogenic and nonmitogenic effects of bFGF.
OBJECTIVE: To explore the possible effects of basic fibroblast growth factor (bFGF) on ischemic gut and liver injuries after trauma. METHODS: Animal models of superior mesenteric artery occlusion (45 minutes) and reperfusion (3 days) were used in this study. Seventy-two Wistar rats were divided into three groups of 24 rats each. The animals in bFGF-treated group were injected with 4 microg bFGF/rat in 0.15 mL normal saline solution containing heparin 0.1% (w/v) through the jugular vein at the onset of reperfusion. In the normal saline control group, all rats received the same vehicle, but without bFGF. Group 3 (sham-operated) underwent the same laparotomy procedure, but without superior mesenteric artery occlusion. Liver function parameters, the levels of serum tumor necrosis factor alpha, nitric oxide, superoxide dismutase, malondialdehyde (MDA), tissue bacterial examination, and pathologic study were used to evaluate the results. RESULTS: In bFGF-treated rats, the amounts of serum alanine transaminase and aspartate aminotransferase and serum tumor necrosis factor-alpha were reduced significantly at 6, 24, and 48 hours when compared with normal saline-treated rats. However, the changes in nitric oxide, superoxide dismutase, and MDA varied from each other as a function of time after injury. The amounts of nitric oxide were increased significantly at 6 hours in intestine in normal saline-treated rats and in liver in bFGF-treated rats (p < 0.05). At 6 hours after reperfusion, the activity of superoxide dismutase in normal saline-treated rats were much lower in liver than those in bFGF-treated and sham-operated rats (p < 0.05), but the levels of MDA were increased in intestine in bFGF-treated rats and in liver in normal saline-treated rats when compared with sham-operated rats (p < 0.05). At 24 hours, the levels of MDA in normal saline-treated rats were much higher than those in both bFGF and sham-operated rats (p < 0.05). Bacterial examination revealed that the ratio and the amounts of bacterial translocation from gut to liver, spleen, and mesenteric lymph nodes in bFGF-treated rats were much lower than those in normal saline-treated rats. The results of pathologic study support the assumption that bFGF provided protective effects against reperfusion injury. CONCLUSIONS: Intravenous administration of bFGF may benefit in reducing gut and liver injuries after ischemia and reperfusion. The mechanisms of those effects may involve mitogenic and nonmitogenic effects of bFGF.