Somatostatin-28-(1-12)-like immunoreactivity (S28(1-12)LI) in brains of
Eck fistula dogs, prepared as an experimental model of
hepatic encephalopathy, was measured. Significant reductions of S28(1-12)LI were observed in all cortical regions of
Eck fistula dogs. The reductions of S28(1-12)LI were significantly correlated with decreases in somatostatin-14-like immunoreactivity (S14LI) in the cortical region. The ratios of S28(1-12)LI to S14LI in all cortical regions were not different between
Eck fistula and normal dogs. Additionally, no difference in gel chromatographic profiles of S28(1-12)LI and S14LI was observed between
Eck fistula and normal dogs. These results imply that reduced
somatostatin immunoreactivity in
hepatic encephalopathy may be caused not by altered degradation but by reduced production of
prosomatostatin. Our S28(1-12)LI assay system could detect prosomatostatin(1-76) and S28(1-12) and the S14LI system
prosomatostatin, S28 and S14. S28(1-12)LI/S14LI ratios in cortex were 0.64-0.83 and these were significantly different from those (1.02-1.36) in thalamus, midbrain and medulla. Relative proportions of
prosomatostatin (20%) and S28 (23-24%) in cortex were larger than those (6-7% and 5-7%, respectively) in thalamus, midbrain and medulla. The differential distribution of these molecular forms suggests that processing of
prosomatostatin in cortex may be different from that in thalamus, midbrain and medulla.