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目的：观察严重烧伤休克期胃酸分泌功能的改变，为烧伤临床急性胃粘膜损害（ＡＧＭＬ）的防治研究提供依据。方法：采用大鼠３０％体表面积（ＴＢＳＡ）全层皮肤３度烧伤模型，对烧伤休克期胃液量、胃液总酸度和总酸排出量进行动态观察。结果：伤后３小时胃液量、胃液总酸度和总酸排出量均显著低于正常对照组（Ｐ均＜０．０１）；伤后６小时上述指标值继续下降，并于伤后１２小时降至最低值；伤后２４小时，胃液量、胃液总酸度和总酸排出量虽有回升，但伤后４８小时仍显著低于正常对照组。结论：烧伤休克期大鼠胃酸分泌功能出现了显著抑制，这是胃粘膜功能障碍重要表现之一；胃酸在严重烧伤诱发的ＡＧＭＬ中，可能不是主导的和决定性因素；目前临床预防性使用抗酸疗法存在着某些不合理性；烧伤后尽快纠正胃粘膜缺血缺氧，可能是防治ＡＧＭＬ更为有效的措施。
Objective: To observe the changes of gastric acid secretion in severe burn shock stage, and to provide evidence for the prevention and treatment of clinical acute gastric mucosal injury (AGML) in burns. Methods: A total thickness of 30% body surface area (TBSA) rat model of 3-degree skin burn was used to observe the amount of gastric juice, gastric acid total acidity and total acid excretion during burn shock. Results: The volume of gastric juice, the total acidity and the total acid excretion of gastric juice were significantly lower than those of the normal control group at 3 hours after injury (all P <0.01). The index values continued to decline 6 hours after injury and decreased 12 hours after injury To the lowest value. After 24hours of injury, gastric juice volume, total acidity of gastric juice and total acid excretion returned, but still significantly lower than the normal control group 48h after injury. Conclusion: Gastric acid secretion was significantly inhibited in rats during burn shock, which is one of the most important manifestations of gastric mucosal dysfunction. Gastric acid may not be the dominant and decisive factor in severe burns-induced AGML. At present, prophylactic use of acid-fast There are some irrational therapy; to correct gastric ischemia and hypoxia as soon as possible after burns may be more effective measures to prevent AGML.