The effects of calcium channel blocker and thyrotropin releasing hormone on acute necrotizing pancreatitis in rats

Abstract

The main purpose of this study was to investigate the influence of nimodipine, a calcium channel blocker (CCB) and thyroid-releasing hormone (TRH) on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats. CCB decreased blood pressure in rats in the control and pancreatitis groups. TRH corrected this decrease. CCB alone had no effect on PO2 serum amylase activity, calcium concentration, liver transaminases, lactate dehydrogenase or the degree of pancreatic damage, except for the serum concentration of creatinine. CCB+TRH reduced the concentrations of serum urea and creatinine, the degree of pancreatic damage, and increased PO2 and serum calcium concentration. CCB and CCB+TRH had no effect on pancreatic myeloperoxidase activity. CCB alone had no effect on the course of ANP, but CCB+TRH had beneficial effects on the course of the ANP and various systems.

Thyrotropin-Releasing Hormone (TRH) a Small Molecule in Pancreas Promotes Insulin Producing Cell Proliferation

“…Evaluation of R1 function by receptor affinity found various kDa values in ß -cells [23]. ß -cell intracellular calcium concentration was significantly increased by L-PHP and removal of extracellular calcium does not change this effect [24]. Our group work has shown R1 expression in rat-derived β-cell lines as well as whole pancreas that included nonislet tissue [25].…”