The Pyloric Sphincteric Cylinder in Health and Disease

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Chapter 9 (page 36)

Somatostatin is considered to be a potent vasoconstrictor of the intestinal circulation, and some of the inhibitory effects in the gastrointestinal tract may be the result of diminished mesenteric blood flow (Konturek et al. l978). It also suppresses motility of the intestine and contractions of the gall bladder and it possesses neurotrophic effects. The findings suggest that somatostatin not only serves as a hypophysiotrophic hormone, but also as a neurotransmitter (Vale et al. l977).

Somatostatinomas of the pancreas have been documented; patients had hypoglucagonaemia, hypoinsulinaemia and mild diabetes, with remission of hyperglycaemia after removal of the tumor (Ganda et al. l977; Larsson et al. l977).

Holle et al. (l985) determined the number of somatostatin-secreting D cells in the "antrum", pre- and post-operatively, in 20 patients with duodenal and 8 with gastric ulceration. In patients with a normal population of gastrin-immunoreactive G cells, the D cells were within the normal range. High G cell values were accompanied by high D cell values and low G cell values by low D cell values. The G cell to D cell ratio was 8:1 in duodenal, and 6.6:1 in gastric ulceration. Morphologic coupling of the gastrin- somatostatin system in the "antrum" was assumed; this was constant in ulcer disease both before and after vagotomy.

According to Holle et al. (l985) the almost exclusively inhibitory function of somatostatin, combined with the proximity to glucagon A and insulin B cells in the pancreas, as well as to parietal and gastrin G cells in the stomach, raises the question of a paracrine-like mechanism. However, in addition to the direct interaction of somatostatin D cells with neighbouring cells, adrenergic and cholinergic pathways also appear to exist.

Vasoactive Intestinal Peptide (VIP)

Said and Mutt (l970) isolated a polypeptide with strong vascular effects from porcine small intestine. Termed vasoactive intestinal peptide (VIP), it was subsequently purified by Said and Mutt (l972). For some time VIP was considered to be a solely gastrointestinal hormone; later studies, however, demonstrated VIP in central and peripheral neurons, suggesting a neurotransmitter function (Larsson et al. l976). It is now known that VIP nerves have an ubiquitous occurrence in the body, being particularly numerous in the gastrointestinal, genito-urinary and respiratory tracts (Alumets et al. l978). In the peripheral autonomic system these nerves were shown to occur in various regions, including the superior and inferior mesenteric ganglia, and the submucous (Meissner's) and myenteric (Auerbach's) plexuses of the intestinal wall (Said l978).

Structures believed to exert a sphincteric function receive a particularly rich supply of VIP nerves, more so than the smooth muscle of adjacent regions. Among these are the oesophago-gastric junction, the pyloric "sphincter", sphincter of Oddi, internal anal sphincter, and the openings of the ureters and urethra into the trigonum of the bladder. The very rich supply of VIP nerves is a consistent finding in the smooth muscle of all recognized sphincters; it is thought that an evaluation of the density of VIP innervation may assist in anatomically defining a sphincter (Alumets et al. l978) (Chap. 2).

Using immuno-fluorescent techniques, Polak et al (l974) determined the cellular distribution of VIP in the mammalian (dog, pig and baboon) gastrointestinal tract, mucosal samples being taken from the gastric fornix, pyloric "antrum", duodenum, jejunum, ileum and colon. The distribution of cells was found to be wide; they were present in all regions examined, the highest number occurring in the colon in all three species. According to Bloom and Polak (l978) the highest concentration of VIP cells, more than 31 per mm², occurred in the colon. There were 11 to 30 cells per mm² in the duodenum, and in the stomach, including the pyloric mucosal zone, the concentration was 1 to 10 cells per mm². The relative numerical frequency of these cells in the different gastric mucosal zones was not determined in detail. Small numbers of cells occurred in the pancreas.

Walsh (l983) pointed out that while VIP was originally thought to be located in gastrointestinal endocrine-type cells, later data were consistent with a purely neural localization in the gut; VIP was also distributed throughout the brain and in peripheral nerves outside the gastrointestinal tract. In the stomach Ferri et al. (l984) found a dense VIP-containing nerve supply around oxyntic and pyloric mucosal glands. In the duodenum VIP (and substance P) were present in striking nerve networks in the villi and muscularis mucosae and around blood vessels. VIP was also immunostained in nerve bundles and neuronal perikarya between the lobules of Brunner's glands, while very few fibres reached the proximity of the acinar cells of these glands (Chap. 4).

The biological actions of VIP are numerous and include vasodilatation, lowered blood pressure, increased cardiac output, glycogenolysis and relaxation of smooth muscle (Piper et al. l970). VIP release from the gut was demonstrated upon electric stimulation of the vagus in pigs; significant inhibition of gastric secretion was associated with enhanced VIP release (Said l978). The physiological role of VIP, however, was uncertain (Said l978), but it appeared to be implicated in the following actions: it might serve as a neurotransmitter in the central nervous as well as the peripheral autonomic systems; its wide distribution in many tissues and the relatively constant plasma values suggested that it probably acted as a neurotransmitter in a paracrine, rather than in an endocrine, way (Modlin et al. l978). The VIP neurons have been shown to be under dual (both vagal and splanchnic) control of the autonomic system; release of VIP into venous effluent has been correlated with specific physiological mechanisms known to be mediated via non-cholinergic and non-adrenergic nerve fibres, and elicited by electrical stimulation of the vagus nerves (Fahrenkrug et al. l977). Vagal stimulation caused a frequency-dependent increase in the release of VIP; splanchnic stimulation caused a decrease in the release of VIP, an action which was annulled by alpha-adrenergic blockade. The inhibitory effect of splanchnic stimulation significantly diminished vagally induced VIP release.

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