Sagor G R, Bryant M G, Ghatei M A, Kirk R M, Bloom S R
Br Med J (Clin Res Ed). 1981 Feb 14;282(6263):507-10. doi: 10.1136/bmj.282.6263.507.
To determine the effect of gastric surgery on the plasma vasoactive intestinal peptide (VIP) concentration, 13 patients with gastrectomy and seven controls were given an oral hypertonic load (200 ml 50% glucose solution). Blood was taken at intervals during the test for measurement of VIP and blood glucose concentrations and packed cell volume. At the same time observations were made on the occurrence of dumping symptoms and a record kept of the pulse rate. VIP values in the patients with gastrectomy were significantly increased by glucose ingestion, while these did not alter in controls (p less than 0.001). There was a highly significant correlation between the rate of rise in plasma VIP concentration and the rates of rise in packed cell volume (r = 0.85; p less than 0.001) and blood glucose concentration (r = 0.76; p less than 0.01) in patients with gastrectomy. Changes in packed cell volume and blood glucose values and the occurrence of dumping symptoms during the test were significantly different when postoperative patients were compared with controls (p less than 0.001, p less than 0.005, and p less than 0.001 respectively). Furthermore, when the patients with gastrectomy were divided into those without symptoms and those with dumping after meals the latter group showed a significantly greater rise of VIP (p less than 0.05). Despite the increased plasma VIP concentrations observed during dumping, VIP cannot be taken as the sole factor in the pathogenesis of the dumping syndrome.
为了确定胃部手术对血浆血管活性肠肽(VIP)浓度的影响,对13例胃切除患者和7例对照者给予口服高渗负荷(200 ml 50%葡萄糖溶液)。在测试期间每隔一段时间采集血液,以测量VIP、血糖浓度和血细胞比容。同时观察倾倒症状的发生情况,并记录脉搏率。胃切除患者摄入葡萄糖后VIP值显著升高,而对照组则无变化(p<0.001)。胃切除患者血浆VIP浓度的上升速率与血细胞比容的上升速率(r = 0.85;p<0.001)和血糖浓度的上升速率(r = 0.76;p<0.01)之间存在高度显著的相关性。与对照组相比,术后患者在测试期间血细胞比容和血糖值的变化以及倾倒症状的发生情况有显著差异(分别为p<0.001、p<0.005和p<0.001)。此外,将胃切除患者分为无症状组和餐后有倾倒症状组,后一组的VIP升高更为显著(p<0.05)。尽管在倾倒期间观察到血浆VIP浓度升高,但VIP不能被视为倾倒综合征发病机制中的唯一因素。