Tanikawa M, Hayakawa T, Kondo T, Shibata T, Kitagawa M, Kodaira T, Hamaoka T
2nd Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Arzneimittelforschung. 1993 Jan;43(1):35-9.
Inhibitory effect of loxiglumide (D,L-4-(3, 4-dichlorobenzoylamino)-5-(N-3-methoxypropyl-pentylamino)-5- oxo-pentanoic acid, CAS 107097-80-3) on exocrine pancreatic secretion was compared between intraduodenal and intravenous administration. Doubling doses of intravenous cholecystokinin octapeptide (CCK-8) resulted in a dose-dependent increase of pancreatic secretion from 50 to 400 ng/kg/h. Both intraduodenal and intravenous loxiglumide of 5 and 10 mg/kg/h produced a dose-dependent inhibition of the pancreatic protein secretion to all doses of CCK-8. Cumulative increment of pancreatic protein output was inhibited by 79% and 77% at 10 mg/kg/h of intraduodenal and intravenous loxiglumide, respectively. Extents of the inhibition were similar to each other between the two routes of loxiglumide infusion. However, plasma levels of loxiglumide after intraduodenal administration were about half of those observed after intravenous administration of the corresponding dose, although plasma CCK levels were not different. Intraduodenal loxiglumide is as effective as intravenous loxiglumide in inhibitory potency on pancreatic secretion. Therefore, possible therapeutic indications of oral loxiglumide could be expected.
比较了洛西谷胺（D,L-4-(3,4-二氯苯甲酰氨基)-5-(N-3-甲氧基丙基-戊基氨基)-5-氧代-戊酸，CAS 107097-80-3）十二指肠内给药和静脉给药对外分泌性胰腺分泌的抑制作用。静脉注射胆囊收缩素八肽（CCK-8）剂量加倍会导致胰腺分泌量从50 ng/kg/h剂量依赖性增加至400 ng/kg/h。十二指肠内和静脉注射5和10 mg/kg/h的洛西谷胺均对所有剂量的CCK-8引起的胰腺蛋白质分泌产生剂量依赖性抑制。十二指肠内和静脉注射10 mg/kg/h洛西谷胺时，胰腺蛋白质输出的累积增量分别被抑制79%和77%。两种洛西谷胺输注途径的抑制程度相似。然而，尽管血浆CCK水平无差异，但十二指肠内给药后洛西谷胺的血浆水平约为静脉注射相应剂量后观察到的血浆水平的一半。十二指肠内洛西谷胺在抑制胰腺分泌方面的效力与静脉注射洛西谷胺相同。因此，可以预期口服洛西谷胺可能的治疗适应症。
