Feldman M, Blair A J, Richardson C T, Samloff I M
University of Texas Southwestern Medical School at Dallas.
Dig Dis Sci. 1988 Jul;33(7):824-7. doi: 10.1007/BF01550970.
Acid secretion and basal serum pepsinogen I and II concentrations were measured in 14 duodenal ulcer patients before and at intervals up to six years after proximal gastric vagotomy. Vagotomy led to significant and long-standing reductions in basal, vagally mediated (induced by sham feeding), and peak pentagastrin-stimulated acid secretion. Serum pepsinogen I concentrations also decreased significantly after vagotomy but to a significantly lesser extent than acid secretion. There was no correlation between serum pepsinogen I concentrations and peak acid secretion, either before or after vagotomy. Serum pepsinogen II concentrations decreased only slightly and transiently after vagotomy. Thus, proximal gastric vagotomy reduces acid hypersecretion and pepsinogen I hypersecretion, but not pepsinogen II hypersecretion, in duodenal ulcer patients.
在14例十二指肠溃疡患者中，于近端胃迷走神经切断术前及术后长达6年的时间内定期测量胃酸分泌以及基础血清胃蛋白酶原I和II的浓度。迷走神经切断术导致基础胃酸分泌、迷走神经介导的胃酸分泌（由假饲诱导）以及五肽胃泌素刺激后的胃酸分泌峰值显著且长期降低。迷走神经切断术后血清胃蛋白酶原I浓度也显著降低，但降低程度明显小于胃酸分泌。迷走神经切断术前或术后，血清胃蛋白酶原I浓度与胃酸分泌峰值之间均无相关性。迷走神经切断术后血清胃蛋白酶原II浓度仅轻微且短暂降低。因此，近端胃迷走神经切断术可降低十二指肠溃疡患者的胃酸分泌过多和胃蛋白酶原I分泌过多，但不能降低胃蛋白酶原II分泌过多。
