Investigators induced acute pancreatitis in rats that also received either the NO synthase substrate L-arginine, the NO donor sodium nitroprusside, or the NO synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME). After six hours, pancreatic injury (edema, leukocyte content, ectopic trypsinogen activation) was analyzed, and pancreatic oxygenation and perfusion were determined. A direct effect of NO on amylase secretion and trypsinogen activation was studied separately in vitro.
Both NO donors reduced the degree of inflammation. NO protects against pancreatitis injury in the intact animal but has no discernible effect on isolated acini, the scientists conclude. It is likely that NO acts indirectly in pancreatitis via microcirculatory changes, including inhibition of leukocyte activation and maintenance of capillary perfusion, they added.
On the protective mechanisms of nitric oxide in acute pancreatitis
Found at Alkohol adé (German)
