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The influence of a bowel-trophic neurotensin (NT) treatment (13 days, 300 micrograms/kg/every 12 hrs.) on neurotensin-like immunopositive structures (neurons, fibres and epithelial-N-cells) and the neurotensin receptors (NTr) in the residual bowel after resection (90% small bowel or 75% colon) in the rat was studied using histochemical methods. Somatostatin-like (ST) immunopositive structures (neurons, fibres and epithelial-D-cells) and somatostatin receptors (STr) were also studied, comparatively. The results displayed a general increase of N-cells (11-17%) but not of D-cells, and a higher degree of variability section-to-section in the NT and ST immunopositive nervous structures (without increased density) after both resections, both with or without NT treatment. Receptors did not change after the small bowel resection but the colon resection and/or the NT treatment produced variations in the NT binding (from -24.3 to +16.85) in different intestinal regions. In a general sense, the variations among 1) the controls, 2) the resected animals, and 3) the resected and NT-treated animals, were of less extent (< or = 24%) than previously supposed for explaining the trophic effect of NT. Our results: a) confirm the autonomy, injury-resistance and tendency to maintain the physiological features of the bowel in very diverse situations; b) open new questions on both, the neurotensinergic changes after bowel resection and the mechanisms of the trophic effect of NT treatment, and c) suggest that, when neurotensin was applied as a trophic treatment in the cases of the need of a bowel resection, no important neurotensinergic or somatostatinergic side effects should be expected in the remaining bowel. However, the higher degree of variability section-to-section after surgery in the nervous structures was not modified by the NT treatment. This fact, and the different response of various intestinal regions to the NT treatment, suggest that functional problems in the remaining bowel could be maintained despite the growth of the mucosa induced by the NT treatment.
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
June 1987,
Cell and tissue research,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
January 1987,
Peptides,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
May 1990,
Scandinavian journal of gastroenterology,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
January 1986,
Peptides,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
December 1978,
Cell and tissue research,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
May 1988,
Cell and tissue research,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
January 1987,
Histochemistry,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
January 1979,
Advances in experimental medicine and biology,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
July 1983,
The Journal of comparative neurology,
A Toledano, and
J J Rodríguez-Arellano, and
I A Gómez de Segura, and
E De Miguel, and
R Martínez-Rodríguez
October 1989,
Endocrinologia japonica,
