Department of Gastroenterology, Hepatology and Infectious Diseases, Otto von Guericke University of Magdeburg, Magdeburg, Germany.
Dig Dis. 2010;28(2):373-8. doi: 10.1159/000319417. Epub 2010 Sep 1.
In human acute pancreatitis (AP) the local anaesthetic procainhydrochloride (procain-HCl) is given intravenously for pain treatment. Procain has been shown to inhibit catalytic activity of pancreatic (group I) phospholipase A2 (PLA2) and non-pancreatic (group II) PLA2. Both enzymes are important mediators for the local and systemic inflammatory process in AP. To determine the effect of procain, we examined serum and tissue levels of both types of PLA2 activity in the experimental rodent taurocholate model of AP.
In 60 rats, severe pancreatitis was induced by taurocholate. Forty rats were treated with procain-HCl intravenously at a dosage of 2 mg/kg body weight/h either at or 1 h after induction of pancreatitis. Twenty rats served as controls. We measured catalytic activities of group I and group II PLA2 in serum and tissue samples of lung and pancreas.
Serum group II PLA2 catalytic activity was significantly reduced 3 and 6 h after AP induction in rats treated with procain-HCl (p < 0.001) in both treatment groups. In pancreatic and lung tissue, group II PLA2 catalytic activity was significantly reduced compared with normal values (p < 0.001).
Procain-HCl given intravenously either at or 1 h after induction of necrotizing pancreatitis significantly inhibits group II PLA2 catalytic activity in serum and tissues.
在人类急性胰腺炎(AP)中,静脉内给予局部麻醉药盐酸普鲁卡因(procain-HCl)以治疗疼痛。普鲁卡因已被证明能抑制胰腺(I 组)磷脂酶 A2(PLA2)和非胰腺(II 组)PLA2 的催化活性。这两种酶都是 AP 局部和全身炎症过程中的重要介质。为了确定普鲁卡因的作用,我们在实验性胆盐诱导的啮齿动物 AP 模型中检查了血清和组织中这两种 PLA2 活性的水平。
在 60 只大鼠中,通过胆盐诱导严重胰腺炎。40 只大鼠在胰腺炎诱导后或 1 小时后以 2mg/kg 体重/小时的剂量静脉内给予普鲁卡因-HCl 治疗。20 只大鼠作为对照。我们测量了血清和肺、胰腺组织样本中 I 组和 II 组 PLA2 的催化活性。
在接受普鲁卡因-HCl 治疗的大鼠中,AP 诱导后 3 小时和 6 小时,血清 II 组 PLA2 催化活性显著降低(p<0.001),两组治疗均如此。在胰腺和肺组织中,与正常值相比,II 组 PLA2 催化活性显著降低(p<0.001)。
在坏死性胰腺炎诱导后或 1 小时静脉内给予普鲁卡因-HCl 可显著抑制血清和组织中 II 组 PLA2 的催化活性。