ISCHEMIC CONDITIONING (DELAY PHENOMENON) IMPROVES ESOPHAGOGASTRIC ANASTOMOTIC WOUND-HEALING IN THE RAT

Citation
Jd. Urschel et al., ISCHEMIC CONDITIONING (DELAY PHENOMENON) IMPROVES ESOPHAGOGASTRIC ANASTOMOTIC WOUND-HEALING IN THE RAT, Journal of surgical oncology, 66(4), 1997, pp. 254-256
Citations number
26
Categorie Soggetti
Surgery,Oncology
ISSN journal
00224790
Volume
66
Issue
4
Year of publication
1997
Pages
254 - 256
Database
ISI
SICI code
0022-4790(1997)66:4<254:IC(PIE>2.0.ZU;2-C
Abstract
Background and Objectives: Esophagogastric anastomotic leaks are a maj or source of morbidity after esophagectomy. Occult ischemia of the mob ilized gastric fundus is an important etiological actor for this failu re of healing. To test the hypothesis that ischemic conditioning (dela y phenomenon) could improve esophagogastric anastomotic healing, anast omotic healing was studied in a rodent model of partial gastric devasc ularization. Methods: Thirty-four Sprague-Dawley rats (two groups of 1 7 rats) underwent partial gastric devascularization and creation of es ophagogastric anastomoses. In the acute ischemia group, devascularizat ion and anastomosis were done at the same laparotomy. In the ischemic conditioned group, devascularization was done 3 weeks before anastomos is. Gastric tissue perfusion was assessed by laser-Doppler flowmetry b efore and after devascularization in both groups, and 3 weeks after de vascularization in the ischemic conditioned group. All rats were kille d 4 days after anastomosis, and the wounds assessed for dehiscence, br eaking strength, and hydroxyproline concentration. Results: Gastric ti ssue perfusion, measured in tissue perfusion units (TPU) decreased imm ediately after devascularization (before: 73.6 +/- 12.1 TPU; after: 25 .0 +/- 6.5 TPU; P < 0.001). After 3 weeks, gastric tissue perfusion re turned to baseline values in the ischemic conditioned rats (before: 72 .3 +/- 11.0 TPU; 3 weeks, 71.1 +/- 15.1 TPU; P < 0.80). Ischemic condi tioned rats had fewer anastomotic leaks (2 vs. 9, P < 0.023) and highe r anastomotic wound breaking strengths (2.35 +/- 1.05 N vs. 1.56 +/- . 76 N, P < 0.02) than the acute ischemic rats. Anastomotic wound hydrox yproline concentration was not significantly different in the two grou ps (acute ischemic-0.111 +/- .033 mu mol/mg, ischemic conditions-0.097 +/- .026 mu mol/mg, P < 0.20). Conclusions: In this rodent model of p artial gastric devascularization, ischemic conditioning (delay phenome non) ameliorated the harmful effect of ischemic on esophagogastric ana stomotic wound healing. (C) 1997 Wiley-Liss, Inc.