J D Urschel1, H Takita, J G Antkowiak. 1. Division of Thoracic Surgery, Roswell Park Cancer Institute, Buffalo, New York 14263-0001, USA.
Abstract
BACKGROUND: Esophagectomy, with gastric pull up replacement, is not uncommonly complicated by leakage from the esophagogastrostomy anastomosis. Occult ischemia of the mobilized gastric fundus is a major etiological factor for anastomotic leakage. Gastric tissue perfusion can be improved by ischemic conditioning ("delay" phenomenon). OBJECTIVE: To test the hypothesis that ischemic conditioning will improve gastric wound healing, and reduce the incidence of anastomotic dehiscence, in a rodent model of partial gastric devascularization. EXPERIMENTAL DESIGN: Laboratory study of gastric wound healing in rats. ANIMALS: Forty-five Sprague-Dawley rats (3 groups of 15 rats). INTERVENTIONS: All animals underwent laparotomy on day 0. Group 1 (control) and group 3 (acute ischemia) rats had sham laparotomies done. Group 2 (ischemic conditioning) rats underwent laparotomy and left gastric artery ligation. On postoperative day 14, all animals underwent repeat laparotomy; gastrotomy wounds were created and sutured. Group 1 (control) and group 2 (ischemic conditioning) rats had gastrotomy alone, while group 3 (acute ischemia) rats also underwent left gastric artery ligation. All rats were sacrificed 5 days after gastrotomy and wound healing was assessed. MEASURES: Gastrotomy wounds were assessed for dehiscence, bursting strength, and hydroxyproline concentration. RESULTS: Anastomotic dehiscence did not occur in group 1 (control) or group 2 (ischemic conditioning) rats. Four of 15 rats (27%) in group 3 (acute ischemia) suffered anastomotic dehiscence (p = 0.028). Wound bursting pressure in the three groups was not significantly different (group 1--96.3 +/- 8.3 mmHg, group 2--91.1 +/- 4.8 mmHg, group 3--70.9 +/- 12.7 mmHg, p = 0.13). Wound hydroxyproline concentration in the control group was significantly higher than in the other 2 groups (group 1--0.124 +/- 0.005 mumol/mg, group 2--0.113 +/- 0.007 mumol/mg, group 3--0.102 +/- 0.006 mumol/ mg, p = 0.04), but there was no difference between the acute ischemia and the ischemic conditioning groups (p = 0.24). CONCLUSIONS: In this rodent model of partial gastric devascularization, ischemic conditioning reduced the incidence of anastomotic dehiscence. Wound bursting strength and hydroxyproline concentration were not affected by ischemic conditioning. Therefore, the harmful effect of ischemia, and the beneficial effect of ischemic conditioning, are probably not primarily related to synthesis of wound collagen. Ischemic conditioning of the stomach is a concept that may prove clinically useful in reducing the incidence of leakage from esophagogastrostomy anastomoses.
BACKGROUND: Esophagectomy, with gastric pull up replacement, is not uncommonly complicated by leakage from the esophagogastrostomy anastomosis. Occult ischemia of the mobilized gastric fundus is a major etiological factor for anastomotic leakage. Gastric tissue perfusion can be improved by ischemic conditioning ("delay" phenomenon). OBJECTIVE: To test the hypothesis that ischemic conditioning will improve gastric wound healing, and reduce the incidence of anastomotic dehiscence, in a rodent model of partial gastric devascularization. EXPERIMENTAL DESIGN: Laboratory study of gastric wound healing in rats. ANIMALS: Forty-five Sprague-Dawley rats (3 groups of 15 rats). INTERVENTIONS: All animals underwent laparotomy on day 0. Group 1 (control) and group 3 (acute ischemia) rats had sham laparotomies done. Group 2 (ischemic conditioning) rats underwent laparotomy and left gastric artery ligation. On postoperative day 14, all animals underwent repeat laparotomy; gastrotomy wounds were created and sutured. Group 1 (control) and group 2 (ischemic conditioning) rats had gastrotomy alone, while group 3 (acute ischemia) rats also underwent left gastric artery ligation. All rats were sacrificed 5 days after gastrotomy and wound healing was assessed. MEASURES: Gastrotomy wounds were assessed for dehiscence, bursting strength, and hydroxyproline concentration. RESULTS: Anastomotic dehiscence did not occur in group 1 (control) or group 2 (ischemic conditioning) rats. Four of 15 rats (27%) in group 3 (acute ischemia) suffered anastomotic dehiscence (p = 0.028). Wound bursting pressure in the three groups was not significantly different (group 1--96.3 +/- 8.3 mmHg, group 2--91.1 +/- 4.8 mmHg, group 3--70.9 +/- 12.7 mmHg, p = 0.13). Wound hydroxyproline concentration in the control group was significantly higher than in the other 2 groups (group 1--0.124 +/- 0.005 mumol/mg, group 2--0.113 +/- 0.007 mumol/mg, group 3--0.102 +/- 0.006 mumol/ mg, p = 0.04), but there was no difference between the acute ischemia and the ischemic conditioning groups (p = 0.24). CONCLUSIONS: In this rodent model of partial gastric devascularization, ischemic conditioning reduced the incidence of anastomotic dehiscence. Wound bursting strength and hydroxyproline concentration were not affected by ischemic conditioning. Therefore, the harmful effect of ischemia, and the beneficial effect of ischemic conditioning, are probably not primarily related to synthesis of wound collagen. Ischemic conditioning of the stomach is a concept that may prove clinically useful in reducing the incidence of leakage from esophagogastrostomy anastomoses.
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