Kim S W, Parekh D, Townsend C M, Thompson J C
Department of Surgery, University of Texas Medical Branch, Galveston 77550.
Ann Surg. 1990 Sep;212(3):332-7; discussion 337-8. doi: 10.1097/00000658-199009000-00011.
The incidence of duodenal ulcer increases with age, but acid secretion does not. We have investigated the effects of aging on a mechanism of duodenal mucosal defense. Basal and acid-stimulated bicarbonate secretions were measured in the proximal duodenum in anesthetized rats of three different age groups (3 months, 1 year, and 2 years). The proximal duodenum was cannulated in situ between two plastic tubes that extend downward from a titrating chamber, and bicarbonate secretion was measured by the method of Flemström et al. Although there was no significant difference in basal secretion among three groups, bicarbonate secretion in response to luminal acid (100 mmol/L [millimolar] HCl) was diminished in 1-year-old and 2-year-old rats (1-hour integrated bicarbonate secretions; 3 months = 5.8 +/- 0.7; 1 year = 3.1 +/- 1.0*; 2 years = 2.0 +/- 0.7*). We also studied the effects of two mediators for acid-stimulated duodenal bicarbonate secretion, vasoactive intestinal polypeptide (VIP), and prostaglandin E2 (PGE2). Intravenous infusion of VIP (0.4, 4, 40 nmol/kg/hr) and intraluminal administration of PGE2 (10(-5) mol/L [molar] and 10(-4) mol/L) induced duodenal bicarbonate secretion in a dose-dependent manner in all three groups, without significant difference between groups. These findings suggest that the release of mediator(s) in response to acid is decreased in the duodenum of the aging rats. The progressive breakdown in mucosal defense mechanisms with increasing age may explain, at least in part, the age-related increase of incidence of duodenal ulcer disease.
十二指肠溃疡的发病率随年龄增长而增加,但胃酸分泌却不然。我们研究了衰老对十二指肠黏膜防御机制的影响。在三种不同年龄组(3个月、1年和2年)的麻醉大鼠的十二指肠近端测量基础和酸刺激下的碳酸氢盐分泌。在从滴定室向下延伸的两根塑料管之间将十二指肠近端原位插管,并用Flemström等人的方法测量碳酸氢盐分泌。尽管三组之间基础分泌无显著差异,但1岁和2岁大鼠对腔内酸(100 mmol/L盐酸)刺激的碳酸氢盐分泌减少(1小时综合碳酸氢盐分泌;3个月 = 5.8±0.7;1年 = 3.1±1.0*;2年 = 2.0±0.7*)。我们还研究了两种酸刺激十二指肠碳酸氢盐分泌的介质,血管活性肠肽(VIP)和前列腺素E2(PGE2)的作用。静脉输注VIP(0.4、4、40 nmol/kg/小时)和腔内给予PGE2(10⁻⁵ mol/L和10⁻⁴ mol/L)在所有三组中均以剂量依赖方式诱导十二指肠碳酸氢盐分泌,组间无显著差异。这些发现表明,衰老大鼠十二指肠中对酸反应的介质释放减少。随着年龄增长黏膜防御机制的逐渐破坏可能至少部分解释了十二指肠溃疡疾病发病率与年龄相关的增加。