Lower density of antral somatostatin-immunoreactive cells in the digestive form of chronic Chagas' disease

Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P>0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (l6.4 (6.9-54.4) vs 59.3 (29.6-113.8), P<0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.

Effect of chlorpromazine and biliary drainage on portal blood flow and mitochondrial function during extrahepatic cholestasis

The present study examines the effect of chlorpromazine and biliary drainage in cholestatic rats. The time course of portal blood flow was studied 24,48, and 72 h and seven days after bile duct ligation. Portal blood flow decreased after 72 h. Chlorpromazine reduced biliary hydrostatic pressure in sham-operated control rats, but 24-h obstruction was sufficient to prevent this effect in cholestatic rats. The drug ameliorated the mitochondrial and cell membrane function of cholestatic rats before and after drainage. The data present further support for the role of ischemia in cholestasis