Pancreatic polypeptide: a review of its involvement in neuro-endocrine reflexes, islet-acinar interactions and ethanol-evoked physiopatologic pancreatic gland changes.

prevents, in pancreocytes, the evolving of a "supramaximalecbolic-stimulation" process. The PP involvement as a modulating agent of pancreon's reactivity is reflected by the progressive increment of its plasma values in the first week of an evolving AP episode. In the AP associated to a large meal, an overpowering of the pancreon's brake might have a pivotal role. In experimental and clinical chronic alcoholism, a vagal neuropathy of the Pavlov inhibitory fibers that, as a consequence, impairs the pancreon's brake through a depression of PP secretion is at the basis of an enhanced reactivity of the duodeno-pancreatic reflexes. The latter leads to intrapancreatic cholinergic hypertonus and to Vater papilla's dysfunction. These changes, plus an enhanced pancreocyte's response to CCK, are at the core of acinar cell "supramaximal stimulation" with the organelle disruption that process implies. The intrapancreatic cholinergic hypertonus, the enhanced exocrine cell reactivity to CCK stimulation, and the augmented resistance to the pancreatic secretion flow at Oddi sphincter, explain the aggravating influence of chronic alcoholism on an episode of acute biliary pancreatitis. As the PP secretion, normally elicited by secretin, CCK, food and insulin hypoglycemia, is depressed in the presence of an augmented number of PP cells, as it is in the cases of chronic alcoholics, cystic fibrosis patients and, also, in dogs with pancreatic fibrosis (ductal ligation), it has been inferred, besides our postulated impairment of the Pavlov inhibitory fibers in the vagus nerves, that the defect of PP release is localized to the common final pathway of the above stimuli, probably in or near the PP cell itself This review was prompted by the unexpected experimental finding in canines that Tissucol-induced pancreatic ductal blockade elicits Pancreatic Polypeptide (PP) release and seems to be at the basis of the beneficial effects on taurocho- late-induced acute pancreatitis (AP). In the release mechanism of this regulatory peptide secreted by PP cells located in the periphery of Langerhans islets and scattered in the ductal epithelium, two neuroendocrine reflexes (NER) are involved. The "short" NER is evoked from the duodenum by an unknown component of bile-pancreatic secretion. The "long" NER is triggered by a vagovagal reflex. PP induces a depression of the intrapancreatic cholinergic tone. On the one hand suppressing, hormonally, nervous impulses discharge from the vagal nuclear complex in the brainstem. On the other, interfering paracrinically on the cholinergic transmission by acting, presynaptically, on post-ganglionic cholinergic neurons. The resulting PP-evoked fall of the intrapancreatic cholinergic tone depresses the hormone induced (secretin, CCK) pancreons secretory response. PP, with other agents, contributes to the "fail-safe" system or pancreon's brake that

Streptozotocin-induced diabetes, bile-pancreatic secretion and insulo-pancreon-axis interaction.

The present tests were undertaken in order to analyze in male Wistar rats the changes in the exocrine and endocrine pancreas and on the interactions that normally evolve in the insulo-pancreon-axis. To evaluate this by a single i.p. Boots secretin injection, glycemia (G), amylasemia (A) and lipasemia (L) were determined. In bile-pancreatic secretion, we analyzed, pre and post-secretin, the following parameters: volume (V), bicarbonate output (BO), amylase output (AO) and lipase output (LO). Three groups of tests were done: a) control (C); b) streptozotocin-treated non-diabetic-rats (St-ND) and c) streptozotocin-treated diabetic animals (St-D) which showed morning glycemia values higher than 16.0 mmol/l. Four months later, under Tiopental i.p anesthesia, a bile-pancreatic fistula was done. Following a 30 min basal period, Boots secretin (20 CU/kg) was i.p injected. Bile-pancreatic secretion put in evidence a significant fall of BO in both St-ND and St-D series. In controls, AO revealed a post-secretin increase of 160%, while in the St-D rats showed a depression of 41%. The behavior of L was different, being augmented (+27%) in the C, while in the St-D rats the response was significantly higher (+95%). In bile-pancreatic-secretion, the fall of BO and AO in the St-ND and St-D series in respect to the C, are probably consequence of the diminishing potentiating effects exerted normally by insulin on the secretin-induced water and bicarbonate secretion of the pancreon units. In contrast, the rising of LO in the St-D, an expression of an enhancing pancreocyte's synthesis and secretion of lipase. The blood changes of A (depression) and of L (increase) in respect to the C values, although without reaching significant level, mirror those observed in bile-pancreatic secretion.

Streptozotocin-induced diabetes, bile-pancreatic secretion and insulo-pancreon-axis interaction / Streptozotocin-induced diabetes, bile-pancreatic secretion and insulo-pancreon-axis interaction.

The present tests were undertaken in order to analyze in male Wistar rats the changes in the exocrine and endocrine pancreas and on the interactions that normally evolve in the insulo-pancreon-axis. To evaluate this by a single i.p. Boots secretin injection, glycemia (G), amylasemia (A) and lipasemia (L) were determined. In bile-pancreatic secretion, we analyzed, pre and post-secretin, the following parameters: volume (V), bicarbonate output (BO), amylase output (AO) and lipase output (LO). Three groups of tests were done: a) control (C); b) streptozotocin-treated non-diabetic-rats (St-ND) and c) streptozotocin-treated diabetic animals (St-D) which showed morning glycemia values higher than 16.0 mmol/l. Four months later, under Tiopental i.p anesthesia, a bile-pancreatic fistula was done. Following a 30 min basal period, Boots secretin (20 CU/kg) was i.p injected. Bile-pancreatic secretion put in evidence a significant fall of BO in both St-ND and St-D series. In controls, AO revealed a post-secretin increase of 160

, while in the St-D rats showed a depression of 41

. The behavior of L was different, being augmented (+27

) in the C, while in the St-D rats the response was significantly higher (+95

). In bile-pancreatic-secretion, the fall of BO and AO in the St-ND and St-D series in respect to the C, are probably consequence of the diminishing potentiating effects exerted normally by insulin on the secretin-induced water and bicarbonate secretion of the pancreon units. In contrast, the rising of LO in the St-D, an expression of an enhancing pancreocyte’s synthesis and secretion of lipase. The blood changes of A (depression) and of L (increase) in respect to the C values, although without reaching significant level, mirror those observed in bile-pancreatic secretion.

Lipasa: una enzima singular por sus interacciones neuro-hormonales. (Revisión y análisis experimental y clínico) / Lipase: a particular enzyme because of its neuro-hormonal interactions

Un objetivo de esta presentación es el de analizar las peculiaridades distintivas de la enzima lipasa proveniente de diferentes fuentes: gástrica (LG), intestinal (LI)hepática (LH), lipoproteica (LLP), pero, en especial, aquella de la pancreática (LP), sobre todo en lo relativo a sus interacciones neuro-hormonales.

Lipoma de válvula ileocecal / Ileum cecal valve lipoma

Se presenta un paciente con lipoma de la válvula ileocecal, efectuándose una revisión bibliográfica y discutiéndose metodología diagnóstica y táctica quirúrgica.

Pancreatitis aguda experimental en la rata: acción de la lidocaína (xylocaína) instilada en el plexo solar / Acute experimental pancreatitis in rats: effect of injected lydocaine (xylocaine) in the solar plexus

Mediante el método de Pfeffer "modificado" por los autores se indujo pancreatitis aguda en 38 ratas. En 17 animales se instiló lidocaína en las proximidades del plexo solar simutáneamente con la provocación de la enfermedad, a la dosis de 0,2 ml al 2%, una vez por día. La sobrevida en el grupo experimental fue mayor y estadísticamente significativa. El grupo 1 (control) sobrevivió 43,5% hs y el 2 (tratado) 114 hs. Las lesiones en el grupo 1 fueron más intensas a nivel pancreático, gástrico, pulmonar, hepático y renal. Las conclusiones apoyan la hipótesis de un mecanismo de excitación simpática en la producción de la pancreatitis aguda y dan una base racional al uso de la lidocaína en el tratamiento de la pancreatitis aguda en el humano

Pseudoobstrucción aguda del colon / Pseudo-obstruction acute of the colon

El síndrome de pseudooclusión colónica fue diagnósticado en 11 pacientes. Los factores asociados fueron: operaciones cesáreas en 6, pancreatitis aguda en 2 y en los restantes vaciamiento de cuello, colocación de marcapaso y puente arterial iliofemoral. En el grupo de pacientes postcesárea, en 5 se efectuó cecostomía y en 1 tratamiento médico. La mortalidad fue nula. En el grupo con factores asociados diversos fallecieron 3

Ulcera péptica antral postsección y reanastomosis antrofundica en la rata: puesta de manifiesto de un probable centro neuroendócrino antrofúndico / Post-seccional antral peptic ulcer and antrofundic re-anastomosis in rats: manifestation of a probable antrofundic neuroendocrine enter

La sección y reanastomosis antrofúndica (ARAF) desencadena, en ratas Wistar macho, verdaderas úlceras pépticas antrales. Se inician a los 20 días. Son de evolución progresiva, penetrando todas a las paredes gástricas. Entre los 7 y 8 meses involucran órganos vecinos (bazo, hígado, páncreas) y generan una gran reacción inflamatória de los ganglios peripancreáticos. La úlcera péptica antral se induce sea que se seccionen o no los nervios de la curvatura menor gástrica y se efectúe o no una piloroplastia concomitante. La hemisección gástrica, sea anterior o posterior, desencadena la úlcera péptica solamente en el mismo lado de la interrupción antrofúndica. En todas estas situaciones, salvo en los casos de piloroplastia concomitante, se comprueba un marcado y significativo incremento del índice gástrico (g/Kg) pero no del pancreático. En la serie de STAF con sección nerviosa en la curvatura menor y sin piloroplastia, el porcentaje de úlceras antrales pépticas es del 56%. Se postula la probable existencia, a nivel antrofúndico, de un centro neuroendócrino. Su anulación o pertubación por el procedimiento de sección y reanatomosis podría generar la úlcera antral y demás cambios histológicos (aumento de las células "G", hiperplasia de las células parietales y de las ECL y "A-like") por una o varias vías hipotéticas: 1. Acción directa, anulando la normal función bloqueadora de la somatostatina sobre las células "G" y/o célulkas parietales. 2. Pertubando o anulando el efecto de bomba motora del antro gástrico y, de esta manera, favoreciendo el reflujo duodenogástrico con todos los efectos deletéreos conocidos de la bilis en el antro, sobre todo en medio ácido. 3. Modificando en sentido inverso la sensibilidad, por un lado, de la masa de células "G" y, por el otro, de las células parietales, ECL y "A-like". La depresión de la sensibilidad fúndica induciría la hiperplasia de las células "G", la hipersecreción de gastrina y, a posteriori, todos los efectos secretorios y tróficos característicos de ésta...

Necrosis pancreática: aspectos clínicos y terapéuticos / Pancreatic necrosis: clinical and therapeutical aspects

Se analizan retrospectivamente 22 pacientes portadores de necrosis pancreática. De los exámenes complementarios por imágenes, la tomografía computada es la más útil para el diagnóstico y evaluación de la extensión de la necrosis pancreática y peripancreática. Si bien la presente serie favorecería la indicación de necrosectomía y cierre primario del abdómen abierto, el número de pacientes y la imposibilidad ética de realizar estudios "randomizados", impiden conclusiones definitivas. La mortalidad global fue del 54% y las causas más importantes, fallas multiorgánicas y sepsis. Se estima que la alta mortalidad se debe a demora en el diagnóstico, debridamiento incompleto e insuficiente apoyo nutricional.

Existe la regeneración pancreática? Certificación morfológica y funcional luego de una esplenopancreatectomía corporocaudal / There is pancreatic regeneration? Morphological and functional certification after a corporocaudal splenopancreatectomy

INTRODUCTION: The process of pancreatic regeneration, well known and accepted, is less known than the hepatic and includes different mechanisms and factors. Pancreatic regeneration is better known in acute pancreatitis. After an extensive pancreatic necrosis, the morphological and functional regeneration is assessed by dynamic computed tomography associated with normalization of glycemia and the exocrine function. Different groups identified and evaluated experimentally and clinically the actions of multiple factors involved in the process of pancreatic regeneration. Even difficult to assess, pancreatic regeneration after partial pancreatectomy is well documented and of capital importance. CASE REPORT: A 57-year-old woman with discomfort in the upper-left abdominal quadrant. CT scans showed a tumor in the body and tail of the pancreas adherent to the spleen. Preoperative CA 19-9 was normal. She was operated on and the tumor resected en bloc with the spleen. Only the head of the pancreas was preserved. Intraoperative pathological examination of the specimen showed a mucinous cistoadenoma with no malignant degeneration. Postoperative course was uneventful and discharged at p.o. day 10, with ongoing diabetes. Four month later she presented pain in the upper-left quadrant with hyperamylasemia. CT scans showed a normal body and tail with an image of pseudocyst at the top of the pancreatic tail. One year after the initial surgery she remained asymptomatic, without diabetes and with no dietary restrictions. Further CT controls showed images of the entire regeneration of the body and tail of the pancreas...