Tay H P, Chaparala R C, Harmon J W, Huesken J, Saini N, Hakki F Z, Schweitzer E J
Department of Surgery, Washington VA Medical Center, DC 20422.
Gut. 1990 Jan;31(1):11-6. doi: 10.1136/gut.31.1.11.
Bismuth subsalicylate was tested in an in vivo perfused rabbit model of oesophagitis for its ability to prevent the mucosal injury caused by pepsin. Treatment efficacy was assessed under both a treatment-before-injury protocol and a treatment-after-injury protocol. Oesophageal mucosal barrier function was evaluated by measuring flux rates of H+, K+, and glucose. The degree of oesophagitis was determined by gross and microscopic examination of the mucosa by several independent observers. Results showed that under both treatment protocols, bismuth subsalicylate significantly reduced the pepsin induced disruption of the mucosal barrier, as well as the morphologic changes. Bismuth subsalicylate when given after exposure to pepsin was also found to protect against the morphologic injury in a dose dependent manner. Experiments in vitro suggested that bismuth subsalicylate inhibits the proteolytic action of pepsin by interacting with pepsin, rather than with the pepsin substrate. We conclude that bismuth subsalicylate can protect the oesophageal mucosa against peptic injury, probably through inactivation of pepsin.
在兔食管灌注的体内食管炎模型中测试碱式水杨酸铋预防胃蛋白酶所致黏膜损伤的能力。在损伤前给药方案和损伤后给药方案下评估治疗效果。通过测量H⁺、K⁺和葡萄糖的通量率来评估食管黏膜屏障功能。由几位独立观察者通过大体和显微镜检查黏膜来确定食管炎的程度。结果表明，在两种治疗方案下，碱式水杨酸铋均能显著减少胃蛋白酶诱导的黏膜屏障破坏以及形态学变化。还发现，在暴露于胃蛋白酶后给予碱式水杨酸铋也能以剂量依赖方式预防形态学损伤。体外实验表明，碱式水杨酸铋通过与胃蛋白酶相互作用而非与胃蛋白酶底物相互作用来抑制胃蛋白酶的蛋白水解作用。我们得出结论，碱式水杨酸铋可能通过使胃蛋白酶失活来保护食管黏膜免受消化性损伤。
