Acta hepato-gastroenterologica最新文献

The release of histamine from isolated gastric mucosa of the rat was studied by a superfusion model. Pentagastrin increased the basal efflux of histamine in a dose dependent manner. Secretin failed to influence the release of histamine under similar conditions. The results are compatible with the view that in gastric mucosa pentagastrin releases histamine which then may react with the receptors of the parietal cell thus serving as mediator in the acid secretory process.

Gastric basal secretion was studied at rest, in the course of one hour's exertion and one hour's restitution in 10 patients with chronic duodenal ulcer, aged 21-52. The subject performed exercise on a Monark ergometer under a load that gave constant pulse rate acceleration equal to 50% of the age-related maximum. Gastric juice samples were collected with the subjects sitting, in three successive phase of rest, exercise, and restitution. It was found that during exercise there was an increase in the gastric juice volume, HCl levels in it, basal secretion volume, and overall sodium, potassium, chloride, calcium, and magnesium content, their concentration in the juice having remained constant. In the course of restitution the above values did not differ in any significant way from those obtained at rest.

Thirteen patients with essential hyperlipoproteinaemia were treated over periods of 2--29 months with hydrophilic colloid made from Psyllium. Reduction of the increased serum cholesterol levels averaged 16.9 per cent, and the corresponding figure for the increased triglyceride levels was 52.0 per cent. The reduction of cholesterol and triglyceride was statistically significant (p less than 0.0025 and p less than 0.0005 respectively). No significant change in normal blood lipid levels was observed on administration of the Psyllium colloid.

Radio gel and affin chromatography were used to study big gastrin interaction with blood proteins of man and animals. The experiments showed that big gastrin interacts with serum proteins in vitro. The gastrin-blood protein complex is labile and readily dissociates (T 1/2 = 8--14 min). A more stable complex is found in acidic medium. Ceruloplasmin is one of the blood serum proteins able to interact with big gastrin. The stability of hormone-protein complex, formed by gastrin and ceruloplasmin, is dependent upon hormone concentration. With the addition of C-terminal penta--and octapeptides to labelled hormone, binding increased. It is speculated that formation of labile gastrin-blood protein complexes is necessary for selective gastrin transport from hormone-producing cells to target cells.

The disappearance rate of bromsulphthalein (BSP) has been studied in 43 patients before and during vaginal hysterectomy under three kinds of anesthesia: Halothane anesthesia, neuroleptanalgesia, and peridural anesthesia. Furthermore, serum enzymes were measured before and after surgery. The half-life of BSP in the elimination phase is significantly prolonged during general anesthesia but not during the peridural anesthesia in the same procedure. There were slight increases of gamma-glutamyltranspeptidase in the later postoperative days with no changes of transaminases and alkaline phosphatase. It can be concluded that the known post-operative transient liver dysfunction, detected only by the BSP-test, occurs during the performance of surgery and is caused by the influence of the general anesthesia on the intrahepatic cell metabolism and not by the operative procedure itself.

The effect of intraarterial glucagon injection on the glycogen content of the intestinal mucosa of the dog and the rat has been investigated. In both species significant glucagon-induced reduction of mucosal glycogen contents was revealed.

Immunoreactive serum gastrin from portal and peripheral veins was determined in five controls and in five cirrhotic patients with indwelling portal catheters in basal conditions, during and after 30 min arginine infusion, in order to assess whether the human liver is involved in gastrin metabolism. A significant difference was found between portal and peripheral gastrin concentrations in controls at 0, 60 and 90 min; no significant differences were found in cirrhotics. Our findings support the hypothesis of an at least partial breakdown of endogenous gastrin in the human liver.

The role of alpha-fetoprotein (AFP)-suppressing factor(s) in the increased production of AFP in liver injury was investigated with carbon tetrachloride and ethionine-treated rats. Elevated concentrations of serum AFP induced by these treatments decreased upon administration of prednisolone. However, injections of methionine and adenosine 5'-triphosphate (ATP), which significantly accelerated the rapid fall of serum AFP levels after birth, produced no such effects on increased AFP levels in hepatic injury. This ineffectiveness of methionine and ATP may suggests that their metabolisms are impaired in the injured liver.

Plasma secretin, plasma gastrin and pancreatic bicarbonate output were measured in three healthy youths before and after a 10 min period of duodenal infusion of 50, 75 and 100 ml 100 mmol/1 HCl. Plasma secretin rose to a shortlived peak within 10 min, whereas plasma gastrin fell gradually to values significantly below the basal level 60 min after the start of duodenal acidification. Pancreatic bicarbonate output showed a more sustained increase following duodenal acidification. Significant positive correlations were obtained between plasma secretin and infused dose of HCl, between pancreatic bicarbonate output and infused dose of HCl and between plasma secretin and pancreatic bicarbonate output. The calculated maximal pancreatic bicarbonate output (Vmax) of 30.6 mEq/h and the calculated dose of secretin to elicit half maximal pancreatic bicarbonate output (S50) of 0.2 CU/kg-h following duodenal acidification were comparable to that seen after intravenous infusion of secretin. No significant correlation was found between plasma secretin and plasma gastrin. It is suggested that the pancreatic stimulation subsequent to duodenal acidification is mainly effected by release of secretin, and that the fall in plasma gastrin may be caused by a HCl-induced inhibition of gastrin release from the duodenum.