Teyssen S, Tarnarzewski M, Haurand C, Bretschneider S, Singer M V
Abteilung für Gastroenterologie, Universitätsklinikum Essen.
Z Gastroenterol. 1990 Jul;28(7):343-7.
A changed exocrine pancreatic secretion could be a pathogenetic factor of an acute pancreatitis after administration of angiotensin-converting enzyme (ace) inhibitors. In six conscious dogs with gastric and duodenal Thomas fistulas we studied the effect of an intravenous (iv.) bolus injection of 10 mg enalaprilat, an intraduodenal (id.) bolus injection of 20 and 40 mg enalapril (e.), and 0.15 M NaCl (20 ml iv., resp., id.) on pancreatic bicarbonate- and protein output in response to secretin (20.5 pmol/kg bw/h and caerulein (29.6 pmol/kg bw/h). Arterial blood pressure and heart rate we also measured. The iv. and id. injection of enalapril(at) significantly increased heart rate by 28% after 10 mg of e. iv. [peak 101 +/- 11 beats/min, N = 6, X +/- SEM] and by 13 resp. 37% after 20 resp. 40 mg e. id. [peak 89 +/- 4, resp., 108 +/- 7 beats/min] as compared to control [peak 79 +/- 5 beats/min]. Systolic blood pressure was significantly decreased by 6% after 10 mg e. iv. [lowest value 121 +/- 2 mm Hg] and by 8% and 9% after 20 and 40 mg e. id., respectively, [lowest value 119 +/- 2, resp., 118 +/- 1 mm Hg] as compared to control [lowest value 129 +/- 1 mm Hg]. The applied enalapril(at) doses had no significant effect on hormonal stimulated pancreatic bicarbonate- and protein output. The results confirmed the well known effects of enalapril(at) on heart rate and on arterial blood pressure. Beyond that the results exposed that therapeutical doses of enalapril(at) had no significant effect on exocrine pancreatic secretion. Conclusion of this study is that a pathogenetic role of pancreatic exocrine secretion in the ace-inhibitors and the acute pancreatitis induced by ace-inhibitors is unlikely.
血管紧张素转换酶（ACE）抑制剂给药后，外分泌性胰腺分泌改变可能是急性胰腺炎的发病因素。在6只清醒的患有胃和十二指肠托马斯瘘管的犬中，我们研究了静脉推注10mg依那普利拉、十二指肠推注20mg和40mg依那普利以及0.15M氯化钠（分别静脉推注和十二指肠推注20ml）对胰泌素（20.5pmol/kg体重/小时）和蛙皮素（29.6pmol/kg体重/小时）刺激的胰腺碳酸氢盐和蛋白质分泌量的影响。我们还测量了动脉血压和心率。静脉推注和十二指肠推注依那普利（拉）后，与对照组相比，静脉推注10mg依那普利后心率显著增加28%[峰值101±11次/分钟，N = 6，X±SEM]，十二指肠推注20mg和40mg依那普利后心率分别增加13%和37%[峰值分别为89±4次/分钟和108±7次/分钟]，对照组心率峰值为79±5次/分钟。静脉推注10mg依那普利后收缩压显著降低6%[最低值121±2mmHg]，十二指肠推注20mg和40mg依那普利后收缩压分别降低8%和9%[最低值分别为119±2mmHg和118±1mmHg]，对照组最低值为129±1mmHg。所应用的依那普利（拉）剂量对激素刺激的胰腺碳酸氢盐和蛋白质分泌量无显著影响。结果证实了依那普利（拉）对心率和动脉血压的已知作用。除此之外，结果表明治疗剂量的依那普利（拉）对外分泌性胰腺分泌无显著影响。本研究的结论是，胰腺外分泌在ACE抑制剂及ACE抑制剂诱导的急性胰腺炎中的发病作用不太可能存在。
