Urschel J D, Antkowiak J G, Delacure M D, Takita H
Department of Thoracic Surgery, Roswell Park Cancer Institute, Buffalo, New York 14263-0001, USA.
J Surg Oncol. 1997 Dec;66(4):254-6. doi: 10.1002/(sici)1096-9098(199712)66:4<254::aid-jso6>3.0.co;2-a.
Esophagogastric anastomotic leaks are a major source of morbidity after esophagectomy. Occult ischemia of the mobilized gastric fundus is an important etiological factor for this failure of healing. To test the hypothesis that ischemic conditioning (delay phenomenon) could improve esophagogastric anastomotic healing, anastomotic healing was studied in a rodent model of partial gastric devascularization.
Thirty-four Sprague-Dawley rats (two groups of 17 rats) underwent partial gastric devascularization and creation of esophagogastric anastomoses. In the acute ischemia group, devascularization and anastomosis were done at the same laparotomy. In the ischemic conditioned group, devascularization was done 3 weeks before anastomosis. Gastric tissue perfusion was assessed by laser-Doppler flowmetry before and after devascularization in both groups, and 3 weeks after devascularization in the ischemic conditioned group. All rats were killed 4 days after anastomosis, and the wounds assessed for dehiscence, breaking strength, and hydroxyproline concentration.
Gastric tissue perfusion, measured in tissue perfusion units (TPU) decreased immediately after devascularization (before: 73.6 +/- 12.1 TPU; after: 25.0 +/- 6.5 TPU; P < 0.001). After 3 weeks, gastric tissue perfusion returned 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 conditioned rats had fewer anastomotic leaks (2 vs. 9, P < 0.023) and higher anastomotic wound breaking strengths (2.35 +/- 1.05 N vs. 1.56 +/- .76 N, P < 0.02) than the acute ischemic rats. Anastomotic would hydroxy-proline concentration was not significantly different in the two groups (acute ischemic--0.111 +/- .033 mumol/mg, ischemic conditions--0.097 +/- .026 mumol/mg, P < 0.20).
In this rodent model of partial gastric devascularization, ischemic conditioning (delay phenomenon) ameliorated the harmful effect of ischemic on esophagogastric anastomotic wound healing.
食管胃吻合口漏是食管切除术后发病的主要原因。游离胃底的隐匿性缺血是导致愈合失败的重要病因。为验证缺血预处理（延迟现象）可改善食管胃吻合口愈合的假说，在部分胃去血管化的啮齿动物模型中研究了吻合口愈合情况。
34只Sprague-Dawley大鼠（两组，每组17只）接受部分胃去血管化并创建食管胃吻合口。在急性缺血组，去血管化和吻合在同一次剖腹手术中进行。在缺血预处理组，去血管化在吻合前3周进行。两组在去血管化前后以及缺血预处理组去血管化3周后，通过激光多普勒血流仪评估胃组织灌注。所有大鼠在吻合后4天处死，评估伤口的裂开情况、断裂强度和羟脯氨酸浓度。
以组织灌注单位（TPU）衡量，去血管化后胃组织灌注立即下降（术前：73.6±12.1 TPU；术后：25.0±6.5 TPU；P<0.001）。3周后，缺血预处理大鼠的胃组织灌注恢复到基线值（术前：72.3±11.0 TPU；3周后：71.1±15.1 TPU；P<0.80）。与急性缺血大鼠相比，缺血预处理大鼠的吻合口漏较少（2例对9例，P<0.023），吻合口伤口断裂强度较高（2.35±1.05 N对1.56±0.76 N，P<0.02）。两组的吻合口羟脯氨酸浓度无显著差异（急性缺血组——0.111±0.033 μmol/mg，缺血预处理组——0.097±0.026 μmol/mg，P<0.20）。
在这个部分胃去血管化的啮齿动物模型中，缺血预处理（延迟现象）改善了缺血对食管胃吻合口伤口愈合的有害影响。
