Somatostatinoma: collision with neurofibroma and ultrastructural features.

The clinical presentation, histopathology and immunoelectron microscopic features of two cases of duodenal somatostatinoma are described, one of which is a hitherto unreported example of a collision tumour with a neurofibroma. Ultrastructural morphometric immunoelectron microscopy studies revealed the presence of four types of cells in both tumours, but there was no difference in the proportions of these cells between the collision tumour and the non-collision tumour. Neurosecretory granules ranging in size from 255-815 nm were generally larger than those previously reported for somatostatinomas and somatostatin was identified in granules of all sizes across this range. Neither tumour was associated with the somatostatinoma syndrome comprising associated diabetes mellitis, steatorrhoea and cholelithiasis.

Myocardial vasoactive intestinal peptide and fibrosis induced by nitric oxide synthase inhibition in the rat.

AIMS: In both normotensive and hypertensive rats, the degree of myocardial fibrosis is inversely correlated with the concentration of vasoactive intestinal peptide (VIP) in the myocardium. Treatment with nitric oxide (NO) synthase inhibitors also causes myocardial fibrosis. In this study, we sought to determine whether the myocardial fibrosis induced by treatment with the NO synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME) was also associated with depletion of VIP in the myocardium. METHODS: Male Wistar Kyoto (WKY) and spontaneous hypertensive rats (SHR) rats treated with l-NAME were randomized to low, intermediate or high salt content diets. After 4 weeks, the hearts were harvested, the degree of fibrosis quantified and VIP concentration measured. RESULTS: In WKY, systolic blood pressure increased with increasing dietary sodium (P < 0.05). Myocardial fibrosis also increased with increasing dietary sodium (P < 0.005). Myocardial VIP concentration decreased with increasing dietary sodium (P < 0.025). In contrast, in the SHR treated with l-NAME, systolic blood pressure increased but the increase was not affected by sodium intake. Further, myocardial fibrosis and myocardial VIP were unchanged by increased dietary sodium. Higher doses of l-NAME in the SHR did not increase the systolic blood pressure, increase the degree of myocardial fibrosis or decrease the myocardial concentration of VIP. These differences in myocardial VIP concentration may reflect differing effects of l-NAME on VIP metabolism, as l-NAME increased VIP metabolism in the WKY (P < 0.05) but did not change VIP metabolism in the SHR. CONCLUSIONS: We conclude that depletion of VIP in the myocardium is associated with increasing myocardial fibrosis in l-NAME treated WKY. As VIP depletion occurs in other models of myocardial fibrosis, it appears to be a common mechanism. Myocardial VIP depletion may therefore be a new and important factor in the pathogenesis of cardiac fibrosis.