Anotioxidant Effect of Calcium Channel Blocker on Acute Necrotizing Pancreatitis in Rats

Kim, In Ho; Roe, Im Hwan; Park, Sang Hyun; Yang, Mi Ra; Lim, Chang Young; Lee, Myung In; Oh, Hyng Tae; Cho, Jeong Hee; Kim, Suk Bae; Huh, Jae Hyung

Abstract

BACKGROUND/AIMS: Cellular calcium, a key physiological signaling element in cell function and also a crucial pathological intracellular messenger in cell injury, appears to be involved in the initiation and development of acute pancreatitis. The aim of this study was to evaluate the role of cellular calcium and the effect of a calcium channel blocker (nicardipine) as an antioxidant in acute necrotizing pancreatitis in rats.
METHODS
In male Sprague-Dawley rats, pancreatitis was induced by intraductal infusion of 3% sodium taurocholate. Then, nicardipine was administrated 1 hour before and after induction of pancreatitis. The level of serum-amylase, glutathione (GSH) and malondialde-hyde (MDA) in the pancreatic tissue, and the histologic damage were examined 6 hours after inducing pancreatitis.
RESULTS
Nicardipine administration reduced the amount of serum-amylase Moreover, pre- or post- ztreatment with nicardipine had a significant protective effect on free radical induced injury. Pre-treatment with nicardipine was better than the post-treatment. In addition, nicardipine treatment minimized pancreatic necrosis and hemorrhage.
CONCLUSIONS
The oxygen free radicals and the intracellular calcium are major factors in the pathogenesis of acute necrotizing pancreatitis, and the administration of calcium channel blocker ameliorates pancreatic injury and exerts an antioxidant effect.