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Biomedical subjects

S Rosell

Publications and source records attributed to S Rosell.

At least 73 records · Page 4Linked to original sources
PubMed1980

Report on a patient with watery diarrhoea syndrome caused by a pancreatic tumour containing neurotensin, enkephalin and calcitonin.

A patient with water diarrhoea syndrome (WDS) is described. A pancreatic tumour was found containing many cells with immunoreactivity to enkephalin and neurotensin, a few with immunoreactivity to calcitonin but none to vasoactive intestinal peptide (VIP). High levels of calcitonin, neurotensin, VIP and pancreatic polypeptide (PP) were present in plasma as measured by radioimmunoassay. After removal of the tumour, the plasma levels of the first three peptides returned to normal and the WDS disappeared. On the other hand, plasma PP did not change. No specific symptoms could be attributed to the new spectrum of peptides found in the tumour. This is the first report of a pancreatic tumour containing high levels of neurotensin.

Aged↗
PubMed1980

Plasma concentration of neurotensin-like immunoreactivity (NTLI) and lower esophageal sphincter (LES) pressure in man following infusion of (Gln4)-neurotensin.

(Gln4)-neurotensin was infused i.v. for 5 to 70 min at 3 different infusion rates (6, 12 and 18 pmol X kg-1 X min-1, respectively) in 19 male volunteers, aged 26-47. The plasma concentration of neurotensin-like immunoreactivity (NTLI), the lower esophageal sphincter (LES) pressure, blood pressure, heart rate. ECG and blood glucose concentration were measured. The volunteers did not report any subjective effects during the infusion. Following infusion periods of 30 min or more the volunteers often reported bowel movements starting 5 min or more after cessation of the infusion. Neither blood pressure nor heart rate changed significantly. No changes were noted in the continuous ECG or in the blood glucose concentration. Apparent steady state levels of about 300 pM NTLI were reached at about 40 min during infusion of 12 pmol X kg-1 X min-1 (Gln4)-neurotensin. In all volunteers the LES pressure was significantly reduced within 5 min of starting the infusion. In 6 volunteers 12 pmol X kg-1 X min-1 (Gln4)-neurotensin was infused i.v. for 5 min. The LES pressure decreased significantly (P less than 0.01) from 13.7 +/- 1.3 mmHg to 5.3 +/- 0.8 mmHg. The decrease in the LES pressure occurred at plasma NTLI concentrations of approximately 50 pM, i.e. at levels below those obtained in man after a meal or the ingestion of fat. The present data further support the hypothesis that in man plasma neurotensin, or a neurotensin metabolite is an endocrine hormone involved in the postprandial regulation of the motor functions of the gastrointestinal tract.

Adult↗
PubMed1980

Inhibition of acid secretion from vagally innervated and denervated gastric pouches by (Gln4)-neurotensin.

In dogs with innervated fundic pouches an intravenous infusion of (Gln4)-neurotensin, 60 pmol X kg-1 X min-1, reduced the pentagastrin-stimulated acid secretion to 40% of the control secretory rate. After vagal denervation of the fundic pouches the same dose of (Gln4)-neurotensin did not significantly change the secretion. These findings suggest that (Gln4)-neurotensin does not act directly on parietal cells but inhibits acid secretion at a presynaptic level.

Animals↗
PubMed1980

Substance P and neurotensin in the control of gastrointestinal function.

Our experimental data show that neurotensin or a metabolite satisfies the rigid physiological criteria that should be met before a substance is classified as a true hormone with endocrine function. The gastrointestinal actions are produced by very small concentrations; the release into the blood is produced by a physiological stimulus (ingestion of food, especially fat); and the plasma concentrations of NTLI following the ingestion of food are comparable to those obtained by giving exogenous neurotensin at doses which produce effects in the gastrointestinal tract.

Animals↗
PubMed1979

The effect of ingestion of amino acids, glucose and fat on circulating neurotensin-like immunoreactivity (NTLI) in man.

The effect of ingestion of amino acids (Vamin N), glucose, and fat (Intralipid) on the concentration of neurotensin-like immunoreactivity (NTLI) in plasma was determined in 6 healthy male volunteers. After ingestion of Intralipid (55 ml, 200 mgxml-1) there was a significant increase in the plasma concentration of NTLI. The calculated integrated total NTLI response (6.7 +/- 2.5 nM over 180 min) was statistically significant. Although isocaloric amounts of Vamin and glucose also increased the plasma concentration of NTLI, these increases were not statistically significant. The data indicate that fat is an important stimulus for the release of NTLI from the small intestine. It is suggested that neurotensin, or a metabolite, in blood may be a hormone involved in the postprandial inhibition of gastric motility and gastric acid secretion elicited from the small intestine.

Administration, Oral↗
PubMed1979

Synthesis of substance P analogs and agonistic and antagonistic activities.

Fourteen analogs of substances P (SP), six previously synthesized by a solution method and eight newly synthesized by a solid-phase technique, have been tested for agonistic and antagonistic activities utilizing the isolated guinea pig ileum. The primary objective is to achieve effective inhibitors of SP. These analogs had agonistic activities ranging from negligible to that equivalent to SP. Six of the fourteen analogs had some degree of antagonistic activity [D-Leu8, D-Phe9]-SP is an analog which constitutes a lead to new substitutions, because it had antagonistic activity, but only negligible agonistic activity. One concept for effective antagonistic activity requires negligible or no agonistic activity.

Animals↗
PubMed1978

Indirect vascular actions of (Gln4)-neurotensin in canine adipose tissue.

The vasoconstrictor action of the tridecapeptide (Gln4)-neurotensin has been studied in subcutaneous adipose tissue in the inquinal region of anesthetized dogs. Close intra-arterial infusion of (Gln4)-neurotensin, 30--120 pmol X kg-1 b.wt. X min-1, elicited similar vasoconstrictions in the adipose tissue on the infusion side and on the contralateral side. This suggests that (Gln4)-neurotensin must enter the general circulation before it can elicit vasoconstriction. Removal of parts of the gastrointestinal tract did not change the vasoconstrictor response. Thus, there is no indication of release of vasoactive substances from the gastrointestinal tract by (Gln4)-neurotensin. Infusion into the portal vein elicited the same vasoconstriction in adipose tissue as the same dose administered i.v. It is suggested that the vasoconstrictor action in adipose tissue is not caused by (Gln4)-neurotensin per se. Instead, vasoactive substance(s) may be formed from (Gln4)-neurotensin.

Adipose Tissue↗