Somatostatin cells in the stomach of the rat have a characteristic shape and distribution. In the antral mucosa they occur together with gastrin cells and enterochromaffin cells at the base of the glands. In the oxyntic mucosa they are scattered along the entire glands with some predominance in the zone of parietal cells. Throughout the gastric mucosa the somatostatin cells possess long and slender processes that emerge from the base of the cell and end in club-like swellings. Such processes appear to contact a certain proportion of neighbouring gastrin cells in the antral mucosa and parietal cells in the oxyntic mucosa. Exogenous somatostatin given by intravenous infusion to conscious rats counteracted the release of gastrin stimulated by feeding, elevated antral pH or vagal excitation. Gastrin causes parietal cells to secrete HCl and endocrine cells in the oxyntic mucosa to mobilise and synthesise histamine. Somatostatin is known to block the respone of the parietal cells to gastrin. In contrast, somatostatin did not block the response of the histamine-storing endocrine cells to gastrin, perhaps because these endocrine cells lack receptors to somatostatin. Conceivably, somatostatin in the gastric mucosa has a paracrine mode of action. The observations of the present study suggest that somatostatin may affect some, but not all of the various cell types in the stomach. Under physiological conditions this selectivity may be achieved in the following ways: 1) Communication may be based on direct cell-to-cell contact. 2) Only certain cell types are supplied with somatostatin receptors.

SUMMARY1. Chronic stimulation of the antral gastrin cells by elevated antral pH was achieved by fundectomy, antrum exclusion, fundectomy plus antrum exclusion, antrocolic transposition, and vagal denervation plus pyloroplasty. For comparison we studied also the effects of pyloroplasty alone and of portacaval shunting.2. All operations that elevated the antral pH resulted in high gastrin concentrations in serum. Particularly high concentrations were observed in fundectomized rats. Vagal denervation of fundectomized or antrum excluded rats reduced the serum gastrin concentration slightly compared with the corresponding innervated animals. Portacaval shunting reduced the gastrin concentration in serum.3. The antral gastrin concentration was raised or unchanged following fundectomy and vagal denervation, and reduced following antrum exclusion, antrum exclusion plus vagotomy, fundectomy plus antrum exclusion, fundectomy plus vagotomy, antrocolic transposition and portacaval shunt. The gastrin cell density in the antral mucosa was raised following fundectomy, vagotomy, and fundectomy plus vagotomy, unchanged following fundectomy plus antrum exclusion and antrocolic transposition, and reduced following antrum exclusion and portacaval shunting.4. Ultrastructurally the gastrin (G) cells in the excluded antrum and in the antrum of fundectomized rats showed signs of secretary activity in that the granule volume density or the number of granules per unit cytoplasm was lowered. In the fundectomized rats moreover, the endoplasmic reticulum of the G cells was increased, the Golgi area enlarged and the proportion and volume density of electron dense granules greatly increased. The granule profile diameter was not affected by either antrum exclusion or fundectomy.5. The results on the excluded antrum indicate that elevated antral pH per se is not sufficient to produce gastrin cell proliferation. In the fundectomized rats, where the hrperlasia of antral gastrin cells was considerable, there is the added stimulus of ingested food. In fundectomized plus antrum excluded rats this stimulus is eliminated and no proliferation ensues. The passage of intestinal material, as in the rats subjected to antrocolic transposition, did not elicit gastrin cell proliferation which seems 0022-3751/80/6410-0155 $07.50

SUMMARY1. Following antrum exclusion the serum gastrin concentration was raised and independent of the prandial state. The antral gastrin concentration and number of gastrin cells were greatly lowered.2. The histamine content and the number of histamine-storing endocrine ('enterochromaffin-like') cells in the oxyntic mucosa was almost doubled and the mucosal histidine decarboxylase activity was greatly elevated following antrum exclusion. 3. At the ultrastructural level both types of histamine-storing endocrine cells (ECL and A-like) were found to be enlarged and to have a reduced number of granules per unit cytoplasm. These changes are compatible with an increased secretory activity. The G (gastrin) cells were not increased in size but their granule volume density was lowered.4. We propose that antrum exclusion results in uninhibited gastrin release causing profound changes in the histamine-storing endocrine cells of the oxyntic mucosa. The cells respond to the hypergastrinemia by an increase in functional activity (activation of histidine decarboxylase and reduction of granule volume density) as well as by an increase in number and size.

125 Sudanese patients suffering from vitiligo were investigated for the distribution of serum proteins (haptoglobins and transferrins), red cell enzymes (acid phosphatase, 6-phosphogluconate dehydrogenase, phosphoglucomutase and glucose-6-phosphate dehydrogenase) and hemoglobins. The results were compared with the published healthy population series investigated for the same genetic markers. There was no significant association with any of the marker systems in vitiligo except glucose-6-phosphate dehydrogenase. An excess deficiency of this enzyme was observed in vitiligo patients compared to the control series.

One hundred and seventy Sudanese patients suffering from vitiligo were investigated for the distribution of A,A,BO, MNSs, Rhesus (genotypes), Kell and Duffy blood groups. The same genetic markers were investigated in Sudanese controls, consisting of two series: a published population series and a random sample of healthy blood donors. The relative frequencies of these blood groups were examined between the vitiligo patients and either or both of the control series. There was no significant association of ABO, Ss, Rhesus, Kell and Duffy blood groups in vitiligo. However, a significant association was observed with the MN system with an excess of homozygotes and of the M gene in vitiligo.