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在部分胃血管离断的啮齿动物模型中,胃扩张会加重局部缺血。

Gastric distention exacerbates ischemia in a rodent model of partial gastric devascularization.

作者信息

Urschel J D, Antkowiak J G, Takita H

机构信息

Department of Thoracic Surgery, Roswell Park Cancer Institute, Buffalo, New York 14263-0001, USA.

出版信息

Am J Med Sci. 1997 Nov;314(5):284-6. doi: 10.1097/00000441-199711000-00002.

DOI:10.1097/00000441-199711000-00002
PMID:9365328
Abstract

Occult ischemia of the mobilized gastric fundus is an important etiologic factor for esophagogastric anastomotic leaks after esophagectomy. Postoperative gastric distention is another possible predisposing factor for anastomotic leakage. We hypothesized that gastric distention could worsen gastric ischemia. To test this hypothesis, gastric tissue perfusion was studied in 20 Sprague-Dawley rats. Baseline serosal gastric tissue perfusion was measured by laser-Doppler flowmetry at a point 10 mm distal to the gastroesophageal junction. Perfusion was measured after left gastric artery occlusion, gastric distention to 20 cm water pressure, and combined left gastric artery occlusion and gastric distention. Gastric tissue perfusion (in tissue perfusion units, TPU) was 64.2 +/- 9.1 TPU at baseline measurement, 18.6 +/- 4.3 TPU after left gastric artery occlusion, 22.0 +/- 4.1 TPU after gastric distention, and 7.8 +/- 1.8 TPU after combined left gastric artery occlusion and gastric distention. Distention (P < 0.0001) and arterial occlusion (P < 0.0001) both reduced gastric tissue perfusion; of the two, arterial occlusion produced the greatest reduction in perfusion (P < 0.021). The combination of distention and arterial occlusion caused greater reduction in gastric perfusion than either factor alone (P < 0.0001). In this model, gastric distention exacerbated the ischemia produced by partial gastric devascularization. In clinical esophageal surgery, postoperative gastric distention may similarly potentiate the ischemic effects of gastric transposition for esophageal reconstruction.

摘要

游离胃底的隐匿性缺血是食管切除术后食管胃吻合口漏的重要病因。术后胃扩张是吻合口漏的另一个可能的诱发因素。我们推测胃扩张会加重胃缺血。为了验证这一假设,对20只Sprague-Dawley大鼠的胃组织灌注进行了研究。通过激光多普勒血流仪在胃食管交界处远端10毫米处测量基线浆膜胃组织灌注。在左胃动脉闭塞、胃扩张至20厘米水柱压力以及左胃动脉闭塞与胃扩张联合作用后测量灌注。胃组织灌注(以组织灌注单位,TPU计)在基线测量时为64.2±9.1 TPU,左胃动脉闭塞后为18.6±4.3 TPU,胃扩张后为22.0±4.1 TPU,左胃动脉闭塞与胃扩张联合作用后为7.8±1.8 TPU。扩张(P<0.0001)和动脉闭塞(P<0.0001)均降低了胃组织灌注;在这两者中,动脉闭塞导致的灌注降低最大(P<0.021)。扩张与动脉闭塞的联合作用导致的胃灌注降低比单独任何一个因素都更大(P<0.0001)。在这个模型中,胃扩张加剧了部分胃血管离断所产生的缺血。在临床食管手术中,术后胃扩张可能同样会增强胃移位用于食管重建时的缺血效应。

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