Hopman W P, Jansen J B, Lamers C B
Ann Surg. 1984 Mar;199(3):276-80. doi: 10.1097/00000658-198403000-00005.
The present study was undertaken to determine whether bypassing the duodenum in patients with Billroth II gastrectomy affects plasma cholecystokinin (CCK) release in response to ingestion of fat. Plasma CCK concentrations were measured by radioimmunoassay using two antibodies; antibody 1703 binds to all carboxyl-terminal CCK-peptides containing at least 14 amino acid residues, while antibody T204 is specific for the sulphated tyrosine region of CCK. There were no significant differences among fasting plasma CCK concentrations in seven patients with Billroth II gastrectomy (1.3 +/- 0.4 fmol/ml, antibody 1703; 2.6 +/- 0.4 fmol/ml, antibody T204), six patients with Billroth I gastrectomy (0.6 +/- 0.3 fmol/ml, antibody 1703; 2.9 +/- 0.5 fmol/ml, antibody T204), and nine normal subjects (0.7 +/- 0.1 fmol/ml, antibody 1703; 1.9 +/- 0.3 fmol/ml, antibody T204). Ingestion of 250 ml 20% Intralipid induced similar increases in plasma CCK in patients with Billroth II gastrectomy (11.2 +/- 2.0 fmol/ml, antibody 1703; 10.1 +/- 2.4 fmol/ml, antibody T204) as in patients with Billroth I gastrectomy (11.8 +/- 2.0 fmol/ml, antibody 1703; 8.4 +/- 1.1 fmol/ml, antibody T204). However, the increments in plasma CCK in patients with gastrectomy (11.5 +/- 1.4 fmol/ml, antibody 1703; 9.3 +/- 1.4 fmol/ml, antibody T204) were significantly (p less than 0.01) greater than those in normal subjects (4.7 +/- 0.8 fmol/ml, antibody 1703; 4.1 +/- 0.7 fmol/ml). Similarly, the integrated plasma CCK secretion in patients with Billroth II gastrectomy (510 +/- 58 fmol/ml X 120 min, antibody 1703; 458 +/- 69 fmol/ml X 120 min, antibody T204) and in patients with Billroth I gastrectomy (457 +/- 143 fmol/ml X 120 min, antibody 1703; 365 +/- 61 fmol/ml X 120 min, antibody T204) were significantly (p less than 0.05) greater than in normal subjects (230 +/- 49 fmol/ml X 120 min, antibody 1703; 162 +/- 24 fmol/ml X 120 min, antibody T204). It is concluded that the plasma CCK response to oral fat is significantly greater in patients with partial gastrectomy than in normal subjects, and that patients with Billroth I and Billroth II gastrectomy have similar increases in plasma CCK after ingestion of fat.
本研究旨在确定毕罗Ⅱ式胃切除患者绕过十二指肠是否会影响摄入脂肪后血浆胆囊收缩素（CCK）的释放。使用两种抗体通过放射免疫分析法测定血浆CCK浓度；抗体1703与所有含有至少14个氨基酸残基的羧基末端CCK肽结合，而抗体T204对CCK的硫酸化酪氨酸区域具有特异性。7例毕罗Ⅱ式胃切除患者（抗体1703：1.3±0.4fmol/ml；抗体T204：2.6±0.4fmol/ml）、6例毕罗Ⅰ式胃切除患者（抗体1703：0.6±0.3fmol/ml；抗体T204：2.9±0.5fmol/ml）和9例正常受试者（抗体1703：0.7±0.1fmol/ml；抗体T204：1.9±0.3fmol/ml）的空腹血浆CCK浓度之间无显著差异。摄入250ml20%英脱利匹特后，毕罗Ⅱ式胃切除患者（抗体1703：11.2±2.0fmol/ml；抗体T204：10.1±2.4fmol/ml）血浆CCK的升高幅度与毕罗Ⅰ式胃切除患者（抗体1703：11.8±2.0fmol/ml；抗体T204：8.4±1.1fmol/ml）相似。然而，胃切除患者（抗体1703：11.5±1.4fmol/ml；抗体T204：9.3±1.4fmol/ml）血浆CCK的升高幅度显著（p<0.01）大于正常受试者（抗体1703：4.7±0.8fmol/ml；抗体T204：4.1±0.7fmol/ml）。同样，毕罗Ⅱ式胃切除患者（抗体1703：510±58fmol/ml×120min；抗体T204：458±69fmol/ml×120min）和毕罗Ⅰ式胃切除患者（抗体1703：457±143fmol/ml×120min；抗体T204：365±61fmol/ml×120min）的血浆CCK综合分泌量显著（p<0.05）高于正常受试者（抗体1703：230±49fmol/ml×120min；抗体T204：162±24fmol/ml×120min）。研究得出结论，部分胃切除患者口服脂肪后血浆CCK反应显著高于正常受试者，且毕罗Ⅰ式和毕罗Ⅱ式胃切除患者摄入脂肪后血浆CCK升高幅度相似。
