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作 者:陈建[1] 李君曼[1] 李学会[1] 郝洪升[1] 付淑花[1]
机构地区:[1]山东医科大学附属医院消化内科
出 处:《新消化病学杂志》1997年第11期717-718,共2页
基 金:山东省卫生厅科研基金
摘 要:目的探讨胃肠激素及胃排空的变化在消化性溃疡发病机制中的作用.方法胃溃疡(GU)30例,男18例,女12例,年龄25岁~66岁,平均5095岁;十二指肠溃疡(DU)29例,男18例,女11例,年龄25岁~62岁,平均4005岁;健康人12例为对照组,男9例,女3例,年龄25岁~63岁,平均465岁.采用RIA法测定空腹血浆生长抑素(SS)、血管活性肠肽(VIP)和P物质(SP)水平,同时应用放射性核素法检测胃排空功能.结果GU患者胃排空(min)明显迟缓(659±148vs533±43,P<001),空腹血浆VIP水平(ng/L)较对照组明显升高(375±107vs184±59,P<005),且与胃半排空时间(GET1/2)呈显著性正相关(r=055,P<001);SS和SP水平与对照组无明显变化(P>005).DU患者胃排空明显亢进(417±102vs533±43,P<001),SS水平(ng/L)显著降低(64±25vs119±34,P<001),并与GET1/2呈显著性正相关(r=056,P<001);SP水平(ng/L)显著升高(544±12?IM To study the plasma level of gastrointestinal hormones and gastric emptying in patients with peptic ulcer. METHODS Thirty patients with gastric ulcer (GU), and 29 duodenal ulcer (DU) and 12 controls were studied. Plasma levels of SS, VIP and SP were measured by radioimmunoassay, and gastric emptying half time (GET1/2) was determined with TC99mresin solid meal method. RESULTS GET1/2(min) was significantly longer in GU than that in controls (659±148 vs 533±43, P<001) and plasma VIP levels (ng/L) were significantly higher than in controls (375±107 vs 184±59, P<005). There was a significant positive correlation between GET1/2 and plasma VIP levels (r=055,P<001). No significant changes were found in SS and SP in GU compared with controls (P>005). GET1/2 in DU was markedly shorter than the control group (417±102 vs 533±43, P<001), and plasma SS levels (ng/L) significantly lower than those in controls (64±25 vs 119±34,P<001), there was a significant positive correlation between GET1/2 and SS levels (r=056,P<001). Plasma SP levels (ng/L) in DU were significantly higher than the controls (544±127 vs 416±58,P<001),there was a significant negative correlation between GET1/2 and SP levels (r=-068,P<001). No significant difference was found in the plasma VIP levels between DU and controls (P>005).CONCLUSION VIP elevation may contribute to the GET1/2 delay and the occurrence of GU. The increased SP and lowered SS may play important roles in the GET1/2 acceleration and the pathogensis of DU.
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