Brain-gut peptides in sauna-induced hyperthermia.

The release of brain-gut peptides during sauna bathing was studied in seven women. All women underwent a 20 min sauna bath. Their sublingual temperature rose from 36.9 +/- 0.1 degrees C to 38.6 +/- 0.2 degrees C (mean +/- SEM). A significant increase in circulating plasma vasoactive intestinal polypeptide (VIP) was observed during heat exposure, whereas plasma pancreatic polypeptide (PP), motilin and blood glucose rose and stayed significantly elevated first during the ensuing 60 min (P less than 0.05 in all cases). A similar increase in plasma insulin failed to reach statistical significance, whereas the plasma levels of somatostatin and cholecystokinin (CCK) remained unchanged. It is suggested that the plasma VIP levels are related to compensatory mechanisms during heat exposure with vasodilatation and heat loss.

Gastrointestinal peptides in serum and synovial fluid from patients with inflammatory joint disease.

The concentrations of immunoreactive vasoactive intestinal polypeptide (ir-VIP), immunoreactive pancreatic polypeptide (ir-PP), ir-somatostatin, and ir-secretin were measured in serum and synovial fluid from patients suffering from various inflammatory joint diseases. One group of patients were not taking any medication, while another group received anti-inflammatory treatment at the time of sampling. High levels of ir-VIP in the synovial fluid were observed in the untreated group of patients, and the concentration of ir-VIP in the synovial fluid was significantly higher than in parallel serum samples. On the other hand, no significant differences in the concentrations of the other peptides were observed either between serum and synovial fluid or between the two groups of patients. It is suggested that VIP is released locally at the inflammatory site and that VIP may be of significance in inflammatory disorders.

Smoking, alcohol, coffee, and familial factors: any associations with peptic ulcer disease? A clinically and radiologically prospective study.

In the period between 1980 and 1983 smoking habits, alcohol consumption, coffee drinking, and familial occurrences of peptic ulcers were studied in patients with gastric or duodenal ulcer in North Norway. The results were compared with those in two control groups matched for sex and age but without anamnestically known previous peptic ulcer disease. Statistically significant increased familial occurrences of peptic ulcer were found in relatives of patients both with gastric and with duodenal ulcer, compared with the control group. Furthermore, significantly more smokers were found in the two groups of patients than in the control groups. Patients with duodenal ulcers smoked more than those with gastric ulcer. Both the consumption of coffee and that of alcohol, however, were significantly reduced in the ulcer patients compared with their controls. Therefore, both familial factors and smoking habits appear to have some relationship or even play etiologic roles in the development of peptic ulcer disease, at least in the northern part of Norway. Coffee drinking and intake of alcohol seem to be of no importance. Both tobacco smoking and familial accumulation of peptic ulcers increased the relative risks of getting both gastric and duodenal ulcer as compared with 'non-exposed' persons. Furthermore, a positive correlation was found in men between the quantity of smoking and the risk of developing duodenal ulcer.

Release of gastrointestinal regulatory peptides after a soap enema.

A 1-l soap enema given to nine healthy volunteers elicited significantly elevated plasma levels of vasoactive intestinal polypeptide (VIP) and cholecystokinin (CCK), together with a transient somatostatin peak. These rises coincided with significant rises both in systolic and diastolic blood pressure, whereas plasma levels of motilin and pancreatic polypeptide remained unchanged. It is suggested that the peptide releases are of colonic origin and that VIP and CCK may play mediatory roles in the enema-induced defecation.

Somatostatin release and plasma molecular somatostatin components in man.

The present paper describes a sensitive, precise and specific radioimmunoassay method for measurements of plasma somatostatin; significant rises in plasma somatostatin following a test meal, intraduodenal infusion of fat and HCl, and intravenous injection of insulin; and separation of immunoreactive plasma somatostatin into two components probably representing bound and free molecular forms of somatostatin both in fasting and postprandial human plasmas.

Release of plasma pancreatic polypeptide in achlorhydric patients after intravenous infusion of gastric inhibitory polypeptide.

In order to evaluate whether gastric inhibitory polypeptide (GIP) could be responsible for the postprandial fall in serum gastrin previously observed in patients with achlorhydria, 7 achlorhydric patients were given 100 ml Lipomul (66 g triglycerides) on one occasion, and 5 of these patients were later given a 30-min intravenous infusion of porcine GIP in a dose of 1 microgram/kg. Following the Lipomul ingestion, serum gastrin fell significantly, whereas no effect on serum gastrin was seen during the intravenous GIP infusion. A small, but significant release of serum insulin was seen shortly after starting the GIP infusion, together with a significant and more sustained release of plasma pancreatic polypeptide (PP). It is concluded that GIP does not lower the serum gastrin levels in achlorhydric patients, but that GIP might participate in the intestinal phase of the PP release.

Iodination with Iodo-gen and radioimmunoassay of cholecystokinin (CCK) in acidified plasma, CCK release, and molecular CCK components in man.

The preparation of a stable fully immunoreactive 125I-labeled CCK39 using a modified Iodo-gen method with high specific radioactivity; the production of an avid and specific cholecystokinin (CCK) antiserum, and a sensitive, precise and specific radioimmunoassay method allowing measurements of fasting plasma CCK in the low picomole per liter range together with the significant rises in plasma CCK following a test meal and duodenal infusion of fat are described. Apparent immunoreactive fasting plasma CCK was eluted from a Sephadex G-50 Fine column in one peak probably representing plasma CCK bound to plasma proteins and nonspecific plasma effects. Apparent immunoreactive postprandial plasma CCK was eluted from a Sephadex G-50 Fine column in four peaks. The first peak probably represents plasma CCK bound to plasma proteins and nonspecific plasma effects; the second peak probably represents component I with a molecular weight between some 5,000 and 30,000; the third peak probably represents component II or CCK33, and the fourth peak probably represents component IV or CCK8.