ANALIZAN LA INFLUENCIA DE LA OXITOCINA SOBRE EL TRACTO GASTROINTESTINAL





ANALIZAN LA INFLUENCIA DE LA OXITOCINA SOBRE EL TRACTO GASTROINTESTINAL

(especial para SIIC © Derechos reservados)
La oxitocina es liberada en los sujetos sanos en respuesta a la ingesta grasa y está presente a lo largo del tracto gastrointestinal. Los pacientes con diabetes mellitus y paresia gástrica tienen una secreción insuficiente de oxitocina posprandial y la administración de antagonistas de los receptores de oxitocina junto con una comida retrasa el vaciado gástrico. Debido a ello el papel de la oxitocina en la regulación fisiológica del vaciado gástrico y su impacto en la paresia gástrica merece nuevas investigaciones.
ohlsson9.jpg Autor:
Bodil Ohlsson
Columnista Experto de SIIC

Institución:
Department of Clinical Sciences, Division of Gastroenterology, Malmö University Hospital, Lund University


Artículos publicados por Bodil Ohlsson
Recepción del artículo
29 de Noviembre, 2008
Aprobación
28 de Abril, 2009
Primera edición
2 de Noviembre, 2009
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
La observación clínica de la mejoría en la constipación crónica durante la lactancia materna dio lugar a la hipótesis de que la oxitocina podría estar involucrada en la fisiología y la fisiopatología gastrointestinal. En primer lugar se evaluó la concentración de oxitocina en plasma mediante radioinmunoensayo, antes y después de una ingesta. Se examinó la presencia de oxitocina y su receptor en el tracto gastrointestinal mediante PCR e inmunofluorescencia. La tasa de vaciado gástrico se evaluó mediante ultrasonografía, y el peristaltismo del colon, con un método barostático. Se realizó una evaluación a doble ciego para examinar el papel de la oxitocina en la constipación crónica refractaria. Los resultados mostraron una liberación de oxitocina en respuesta a la ingesta de grasa en sujetos saludables de ambos sexos. Por el contrario, los pacientes que presentaban paresia gástrica no tenían liberación posprandial de oxitocina. Además, si a los sujetos sanos se les administraba un antagonista de los receptores de oxitocina junto con la comida la tasa de vaciado gástrico se prolongaba. Si bien el ARNm tanto de la oxitocina como de su receptor estaba presente a lo largo del tracto gastrointestinal, sólo la oxitocina se traducía en una proteína totalmente expresada en el sistema nervioso entérico. La administración intravenosa de oxitocina aumentó el peristaltismo en mujeres sanas. Cuando se lo hizo por inhalación nasal no se observó ningún efecto sobre la constipación crónica, pero el dolor abdominal se redujo y se experimentó un incremento en el bienestar psicológico.

Palabras clave
peristaltismo del colon, vaciado gástrico, oxitocina, receptores de oxitocina


Artículo completo

(castellano)
Extensión:  +/-9.77 páginas impresas en papel A4
Exclusivo para suscriptores/assinantes

Abstract
The clinical observation of improvement of chronic constipation during breast feeding raised the hypothesis that oxytocin may be involved in gastrointestinal physiology and pathophysiology. Firstly, the concentration of oxytocin in plasma before and after a meal was assessed by radioimmunoassay. Then, the presence of oxytocin and its receptor in the gastrointestinal tract was examined by PCR and immunofluorescence. The gastric emptying rate was evaluated by ultrasonography and the colonic peristalsis by a barostat method. A double-blind, placebo-control trial was performed to evaluate the role of oxytocin on chronic, refractory constipation. The results showed that oxytocin was released in response to a fatty meal in both sexes in healthy subjects. By contrast, patients suffering from gastro paresis had no postprandial release of oxytocin. Further, if an oxytocin receptor antagonist was administered together with the meal in healthy subjects, the gastric emptying rate was prolonged. Although mRNA for both oxytocin and its receptor was present throughout the gastrointestinal tract, only oxytocin is translated into a fully expressed protein, and was present in the enteric nervous system. Pharmacological administration of intravenous oxytocin led to increased peristalsis in healthy women. When administered by nasal inhalation, no effect was observed on chronic constipation, but abdominal pain decreased and an increased psychological well-being was experienced.

Key words
colonic peristalsis, gastric emptying, gastrointestinal tract, oxytocin, oxytocin receptor


Full text
(english)
para suscriptores/ assinantes

Clasificación en siicsalud
Artículos originales > Expertos del Mundo >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Gastroenterología
Relacionadas: Anatomía Patológica, Bioquímica, Endocrinología y Metabolismo, Farmacología, Medicina Interna, Obstetricia y Ginecología



Comprar este artículo
Extensión: 9.77 páginas impresas en papel A4

file05.gif (1491 bytes) Artículos seleccionados para su compra



Enviar correspondencia a:
Bodil Ohlsson, Department of Medicine, Malmö University Hospital, Entrance 35, S-205 02, Malmö, Suecia
Patrocinio y reconocimiento:
Estas investigaciones recibieron becas de Knut y Alice Wallenberg's Foundation, Åke Wibergs Foundation, Tore Nilsson Foundation, Magnus Bergwall Foundation, Ernold Lundström Foundation, Malmö Diabetes Association, Swedish Medical Association, de las compañías farmacéuticas Novo Nordic y Tika Pharmacy y de la Development Foundation de la región de Skåne.
Bibliografía del artículo

1. Ohlsson B, Forsling ML, Rehfeld JF, Sjölund K. Cholecystokinin leads to increased oxytocin secretion in healthy women. Eur J Surg 168:114-118, 2002.
2. Balment RJ, Brimble MJ, Forsling ML, Musabayane CT. The influence of neurophysial homones on renal function in acutely hypophysectomized rat. J Physiol 381:439-452, 1986.
3. Rehfeld JF, Accurate measurement of cholecystokinin in plasma. Clin Chem 44:991-1001, 1998.
4. Verbalis JG, McCann MJ, McHale CM, Stricker EM. Oxytocin secretion in response to cholecystokinin and food: Differentiation of nausea from satiety. Science 232:1417-1419, 1986.
5. Verbalis JG, Stricker EM, Robinson AG, Hoffman GE. Cholecystokinin activates c-fos expression in hypothalamic oxytocin and corticotropin-releasing hormone neurons. J Neuroendocrinology 3:205-214, 1991.
6. Monstein H-J, Grahn N, Truedsson M, Ohlsson B. Oxytocin and oxytocin receptor mRNA expression in the human gastrointestinal tract: A polymerase chain reaction study. Regul Pept 119:39-44, 2004.
7. Ohlsson B, Rehfeld JF, Forsling ML. Oxytocin and cholecystokinin secretion in patients with colectomy. BMC Gastroenterology 4:25 (on-line paper), 2004.
8. Petring OU. The effect of oxytocin on basal and pethidine-induced delayed gastric emptying. Br J Clin Pharmacol 28:329-332, 1989.
9. Hashmonai M, Torem S, Argov S, Barzilai A, Schramek A. Prolonged post-vagotomy gastric atony treated by oxytocin. Br J Surg 66:550-551, 1979.
10. Stocks S, Uvnäs-Moberg K. Increased plasma levels of oxytocin in response to afferent electrical stimulation of the sciatic and vagal nerves and in response to touch and pinch in anaesthetised rats. Acta Physiol 132:29-34, 1988.
11. Ohlsson B, Ringström G, Abrahamsson H, Simrén M, Björnsson ES. Oxytocin stimulates colonic motor activity in healthy women. Neurogastroenterol Mot 16:233-240, 2004.
12. Jankovic S, Beleslin D. Relaxant effects of oxytocin and 8-l-lysine-vasopressin on guinea pig and human gallbladder strips in vitro contracted by histamine. Digestion 48:18-24, 1991.
13. Wierup N, Svensson H, Mulder H, Sundler F. The ghrelin cell: a novel developmentally regulated islet cell in the human pancreas. Regul Pept 107:63-69, 2002.
14. Ohlsson B, Truedsson M, Djerf P, Sundler F. Oxytocin is present throughout the human gastrointestinal tract. Regul Pept, in press.
15. Kimura T, Ito Y, Einspanier A. Expression and immunolocalization of the oxytocin receptor in human lactating and non-lactating mammary glands. Human Reproduction 13:2645-2653, 1998.
16. Thibonnier M, Conarty DM, Preston JA, Plesnicher CL, Dweik RA, Erzurum SC. Human vascular endothelial cells express oxytocin receptors. Endocrinology 140:1301-1309, 1999.
17. Ermrich A, Barth T, Ruhle HJ, Skopkova J, Hrbas P, Landgraf R. On the blood-brain barrier to peptides: accumulation of labelled vasopressin, DesGlyNH2 vasopressin and oxytocin by brain regions. Endocrinol Exp 19:29-37, 1985.
18. McCann NJ, Rogers RC. Oxytocin excites gastric-related neurones in rat dorsal vagal complex. J Physiol 428:95-108, 1990.
19. Bisset GW, Lewis GP. A spectrum of pharmacological activity in some biologically active peptides. Brit J Pharmacol 19:168-182, 1962.
20. Flanagan LM, Olson BR, Sved AF, Verbalis JG, Stricker EM. Gastric motility in conscious rats given oxytocin and an oxytocin antagonist centrally. Brain Res 578:256-260, 1992.
21. Wu CL, Hung CR, Chang FY, Pau KY, Wang PS. Pharmacological effects of oxytocin on gastric emptying and intestinal transit of a non-nutritive liquid meal in female rats. Naunyn-Schiedeberg´s Arch Pharmacol 367:406-413, 2003.
22. Grider JR. Role of cholecystokinin in the regulation of gastrointestinal motility. J Nutr 124:1334S-1339S, 1994.
23. Abrahamsson H, Antov S, Bosaeus I. Gastrointestinal and colonic segmental transit time evaluated by a single abdominal X-ray in healthy subjects and constipated patients. Scand J Gastroenterol 23:72-80, 1988.
24. Ohlsson B, Sjölund K. Oxytocin increased stool frequency in patients with chronic constipation. A preliminary report. Int J of Surg Investig 3:287-292, 2001.
25. Ohlsson B, Truedsson M, Bengtsson M, et al. Effects of long-term treatment with oxytocin in chronic constipation; a double blind, placebo-controlled pilot trial. Neurogastroenterol Motil 17:697-704, 2005.
26. Ohlsson B. Bowel habits during pregnancy, breast feeding and after breast feeding. J Clin Gastroenterol, in press.
27. Ohlsson B, Björgell O, Ekberg O, Darwiche G. The oxytocin/vasopressin receptor antagonist atosiban delays the gastric emptying of a semisolid meal compared to saline in human. BMC Gastroenterology 6:11 (on-line paper), 2006.
28. Louvel D, Delvaux M, Felez A et al. Oxytocin increases thresholds of colonic visceral perception in patients with irritable bowel syndrome. Gut 39:741-747, 1996.
29. Uvnäs-Moberg K, Bruzelius G, Alster P, Bileviciute I, Lundeberg T. Oxytocin increases and a specific oxytocin antagonist decreases pain threshold in male rats. Acta Physiol Scand 144:487-488, 1992.
30. Petersson M, Alster P, Lundeberg T, Uvnäs-Moberg K. Oxytocin increases nociceptive thresholds in a long-term perspective in female and male rats. Neurosci Lett 212:87-90, 1996.
31. Yang Q, Wu ZZ, Li X, Li ZW, Wei JB, Hu QS. Modulation by oxytocin of ATP-activated currents in rat dorsal root ganglion neurons. Neuropharmacology 43:910-916, 2002.
32. Arletti R, Benelli A, Poggioloi R, Luppi P, Menozzi B, Bertolini A. Aged rats are still responsive to the antidepressant and memory improving effects of oxytocin. Neuropeptides 29:177-182, 1995.
33. Uvnäs-Moberg K, Bjorkstrand E, Hillegaart V, Ahlenius S. Oxytocin as a possible mediator of SSRI-induced antidepressant effects. Psychopharmacology 142:95-101, 1999.
34. Uvnäs-Moberg K. Oxytocin linked antistress effects-the relaxation and growth response. Acta Physiol Scand Suppl 640:38-42, 1997.
35. Alfven G. Plasma oxytocin in children with recurrent abdominal pain. J Pediatr Gastroenterol Nutr 38:513-517, 2004.
36. Uvnäs-Moberg K, Arn I, Theorell I, Jonson CO. Gastrin, somatostatin and oxytocin levels in the patients with functional disorders of the gastrointestinal tract and their response to feeding and interaction. J Psychosom Res 35:525-533, 1991.
37. Anderberg UM, Uvnäs-Moberg K. Plasma oxytocin levels in female fibromyalgia syndrome patients. Z Rheumatol 59:373-379, 2000.
38. Frasch A, Zetzsche T, Steiger A, Jirikowski GF. Reduction of plasma oxytocin levels in patients suffering from major depression. Adv Exp Med Biol 395:257-258, 1995.
39. Lydiard RB, Fossey MD, Marsh W, Ballenger JC. Prevalence of psychiatric disorders in patients with irritable bowel syndrome. Psychosomatics 34:229-234, 1993.
40. Sperber AD, Atzmon Y, Neumann L et al. Fibromyalgia in the irritable bowel syndrome: Studies of prevalence and clinical implications. Am J Gastroenterol 3541-3546, 1999.

 
 
 
 
 
 
 
 
 
 
 
 
Está expresamente prohibida la redistribución y la redifusión de todo o parte de los contenidos de la Sociedad Iberoamericana de Información Científica (SIIC) S.A. sin previo y expreso consentimiento de SIIC.
ua31618