Ruud T E, Aasen A O, Pillgram-Larsen J, Stadaas J, Aune S
Adv Exp Med Biol. 1986;198 Pt B:413-21. doi: 10.1007/978-1-4757-0154-8_53.
Acute pancreatitis was induced in pigs by manual retrograde injection of Na-Taurocholate into the pancreatic duct. Using chromogenic peptide substrate assays, increased plasma kallikrein activity (KK), paralleled by a reduction in functional plasma kallikrein inhibition values (KKI) were found in the peritoneal exudate in untreated animals. Several of the untreated animals experienced an increased trypsin activity (TRY) in the same exudate. Five out of eight animals died during a 6 hour observation period. Pretreatment with either Cl-INH or aprotinin given intravenously, resulted in a significantly increase in KKI capacity paralleled by unchanged KK and TRY activities in the peritoneal exudate. Furthermore, inhibitor pretreatment significantly improved hemodynamic performances (AP and CO) and the survival rate. The study underlines the pathophysiological importance of trypsin and the plasma kallikrein-kinin system during acute, severe pancreatitis.
通过向猪胰管手动逆行注射牛磺胆酸钠诱导急性胰腺炎。使用发色肽底物测定法,在未经治疗的动物的腹腔渗出液中发现血浆激肽释放酶活性(KK)增加,同时功能性血浆激肽释放酶抑制值(KKI)降低。几只未经治疗的动物在同一渗出液中的胰蛋白酶活性(TRY)增加。在6小时的观察期内,8只动物中有5只死亡。静脉注射Cl-INH或抑肽酶进行预处理,导致KKI能力显著增加,同时腹腔渗出液中的KK和TRY活性不变。此外,抑制剂预处理显著改善了血流动力学性能(平均动脉压和心输出量)和存活率。该研究强调了胰蛋白酶和血浆激肽释放酶-激肽系统在急性重症胰腺炎中的病理生理重要性。