Inoue K, Tobe T, Suzuki T, Hosotani R, Kogire M, Fuchigami A, Miyashita T, Tsuda K, Seino Y
Ann Surg. 1987 Aug;206(2):148-54. doi: 10.1097/00000658-198708000-00006.
This study was conducted to elucidate plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) response after pancreatoduodenectomy and to compare response of CCK and PP in patients who had pancreatoduodenectomy with Billroth I and Billroth II type of reconstruction. Basal levels of plasma CCK were significantly lower in patients who had pancreatoduodenectomy (9.6 +/- 0.8 pmol/L) than in the control (preoperative patients: 14.6 +/- 2.0 pmol/L) probably because of the removal of the entire duodenum due to pancreatoduodenectomy, since vagotomy, which is concomitantly brought about by pancreatoduodenectomy, does not appear to interfere with release of CCK. Significant amounts of CCK (integrated CCK: 497 +/- 111 pmol-120 min/L), although less amounts than in the preoperative patients (integrated CCK: 901 +/- 167 pmol-120 min/L), were still released in response to oral fatty meal after pancreatoduodenectomy. Plasma CCK response to oral fatty meal was significantly greater in patients who had pancreatoduodenectomy with Billroth I type of reconstruction (integrated CCK: 705 +/- 153 pmol-120 min/L) than in patients who had pancreatoduodenectomy with Billroth II type of reconstruction (248 +/- 63 pmol-120 min/L). Simultaneous measurement of plasma levels of PP revealed complete abolishment of PP response by pancreatoduodenectomy. Since PP secretion can be produced by vagal stimulation, it is most likely that the decreased PP secretion is due to vagotomy rather than removal of the duodenum and pancreas. Significant amounts of CCK released after pancreatoduodenectomy, in which the main sources of release of CCK are removed, may suggest the compensatory mechanism of the remnant upper small intestine. This study also suggests the necessity of re-evaluating Billroth I type of anastomosis as a physiologic reconstruction procedure for the remnant alimentary tract after pancreatoduodenectomy.
本研究旨在阐明胰十二指肠切除术后血浆胆囊收缩素(CCK)和胰多肽(PP)的反应,并比较采用毕Ⅰ式和毕Ⅱ式重建的胰十二指肠切除术患者中CCK和PP的反应。胰十二指肠切除术患者的血浆CCK基础水平(9.6±0.8 pmol/L)显著低于对照组(术前患者:14.6±2.0 pmol/L),这可能是由于胰十二指肠切除术切除了整个十二指肠,因为胰十二指肠切除术同时进行的迷走神经切断术似乎并不干扰CCK的释放。尽管胰十二指肠切除术后对口服脂肪餐释放的CCK量(整合CCK:497±111 pmol-120分钟/L)比术前患者少(整合CCK:901±167 pmol-120分钟/L),但仍有大量CCK释放。采用毕Ⅰ式重建的胰十二指肠切除术患者对口服脂肪餐的血浆CCK反应(整合CCK:705±153 pmol-120分钟/L)显著大于采用毕Ⅱ式重建的胰十二指肠切除术患者(248±63 pmol-120分钟/L)。同时测量血浆PP水平显示,胰十二指肠切除术使PP反应完全消失。由于PP分泌可由迷走神经刺激产生,因此PP分泌减少很可能是由于迷走神经切断术而非十二指肠和胰腺的切除。在切除了CCK主要释放源的胰十二指肠切除术后仍有大量CCK释放,这可能提示残余上段小肠的代偿机制。本研究还表明,有必要重新评估毕Ⅰ式吻合术作为胰十二指肠切除术后残余消化道的生理性重建手术的必要性。