Maitra R S, Edgerton E A, Majumdar A P
Research Service, Veterans Administration Medical Center, Allen Park, Michigan 48101.
Exp Gerontol. 1988;23(6):463-72. doi: 10.1016/0531-5565(88)90058-7.
Changes in basal- and pentagastrin-stimulated gastric acid, pepsin secretion as well as gastric mucosal histidine decarboxylase activity were examined in 4- to 21-month-old pyloric ligated Fischer-344 rats. In addition, serum gastrin levels, gastric mucosal DNA, and RNA content were determined in these rats. The results revealed that whereas acid secretion decreased progressively with age, pepsin output increased between 4 and 14 months of age and then decreased sharply. Serum gastrin levels decreased progressively with age, and 3 h of pyloric obstruction produced no apparent change in serum gastrin levels in any of the age groups. Gastric mucosal weight, DNA, and RNA content in 4-month-old rats were not significantly different from those of 14-month-old animals. However, in 21-month-old rats, each of these values were found to be significantly lower than in their 4- or 14-month-old counterparts. A single injection of pentagastrin (250 micrograms/kg) significantly stimulated acid and pepsin secretion (45-52%) in 4-month-old rats, but not in 14- and 21-month-old animals, when compared with the corresponding saline-injected controls. Gastric mucosal histidine decarboxylase activity increased steadily between 4 and 21 months of age. Pentagastrin caused a significant 78% stimulation in histidine decarboxylase activity in 4-month-old rats, but had no effect on the enzyme activity in 14-month-old animals, when compared with the corresponding saline-injected controls. However, in 21-month-old rats, pentagastrin inhibited histidine decarboxylase activity by 55% when compared with the saline-injected controls. It is concluded that a) aging decreases capacity of the gastric mucosa to secrete acid and pepsin, b) in aged rats, decreased acid and pepsin output could in part be attributed to mucosal atrophy; c) responsiveness of the gastric mucosa to pentagastrin decreases with age; and d) in aged animals, gastric acid secretion is not regulated by histamine.
在4至21月龄的幽门结扎Fischer-344大鼠中，检测了基础胃酸分泌、五肽胃泌素刺激的胃酸分泌、胃蛋白酶分泌以及胃黏膜组氨酸脱羧酶活性。此外，还测定了这些大鼠的血清胃泌素水平、胃黏膜DNA和RNA含量。结果显示，虽然胃酸分泌随年龄增长而逐渐减少，但胃蛋白酶分泌量在4至14月龄之间增加，然后急剧下降。血清胃泌素水平随年龄增长而逐渐降低，幽门梗阻3小时后，各年龄组的血清胃泌素水平均无明显变化。4月龄大鼠的胃黏膜重量、DNA和RNA含量与14月龄动物无显著差异。然而，21月龄大鼠的这些值均显著低于4月龄或14月龄的大鼠。与相应的生理盐水注射对照组相比，单次注射五肽胃泌素（250微克/千克）能显著刺激4月龄大鼠的胃酸和胃蛋白酶分泌（45%-52%），但对14月龄和21月龄动物无此作用。胃黏膜组氨酸脱羧酶活性在4至21月龄之间稳步增加。与相应的生理盐水注射对照组相比，五肽胃泌素能使4月龄大鼠的组氨酸脱羧酶活性显著提高78%，但对14月龄动物的酶活性无影响。然而，在21月龄大鼠中，与生理盐水注射对照组相比，五肽胃泌素使组氨酸脱羧酶活性降低了55%。结论是：a）衰老会降低胃黏膜分泌胃酸和胃蛋白酶的能力；b）在老年大鼠中，胃酸和胃蛋白酶分泌减少部分可归因于黏膜萎缩；c）胃黏膜对五肽胃泌素的反应性随年龄增长而降低；d）在老年动物中，胃酸分泌不受组胺调节。
