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Biomedical subjects

D R Guarita

Publications and source records attributed to D R Guarita.

At least 19 recordsLinked to original sources
PubMed2001

PYY potently inhibits pancreatic exocrine secretion mediated through CCK-secretin-stimulated pathways but not 2-DG-stimulated pathways in awake rats.

Peptide YY (PYY) is an important modulator of stimulated pancreatic exocrine secretion. PYY acts proximal to the acinar cell but the exact site and mechanism of action are unknown. The aim of the present study is to determine the pathway through which PYY exerts its effect on the exocrine pancreas in awake rats under physiological condition. When pancreatic secretion was stimulated by graded doses of cholecystokinin (CCK) (14, 28, 58 pmol/kg/hr) with secretin (1.25, 2.5, 5.0 pmol/kg/hr) or CCK alone at 28 pmol/kg/hr, PYY1-36 dose-dependently inhibited pancreatic secretory responses. Moreover, PYY1-36 at 50 pmol/kg/hr almost completely blocked the stimulation by CCK (P < 0.01). Although background infusion of PYY1-36 or PYY3-36 at 12.5 pmol/kg/hr inhibited basal pancreatic fluid and protein secretion, but both of them only partly inhibited the subsequent 2-DG stimulated pancreatic fluid and protein secretion. Furthermore, PYY1-36 at 50 pmol/kg/hr failed to inhibit 2-DG-stimulated pancreatic secretion. These results confirm that PYY1-36 inhibits CCK-stimulated pancreatic secretion under all experimental conditions. However, in the awake, surgically recovered rat, PYY1-36 at both low and high doses failed to fully inhibit 2-DG-stimulated pancreatic secretion. Therefore, the site of PYY's inhibitory action on pancreatic secretion appears to be primarily on the CCK-stimulated pathway at a site proximal to the convergence of the CCK and 2-DG pathways.

Animals↗
PubMed2001

Area postrema lesion alters the effects of peptide YY on 2-DG-stimulated pancreatic exocrine secretion.

Previously we demonstrated that circulating peptide YY (PYY), which inhibits pancreatic exocrine secretion, binds to specific receptors in the area postrema (AP); therefore we have tested the hypothesis that the removal of the AP (APX) will alter the effects of PYY on pancreatic secretion in awake rats. One-month after AP lesion or sham lesion, rats were implanted with pancreatic, biliary, duodenal, and intravenous catheters. After recovery from the surgery, unanesthetized rats were infused with vehicle or PYY (30 pmol/kg/hr or 100 pmol/kg/hr) under basal or 2-deoxy-D-glucose (2-DG) stimulated (75 mg/kg, intravenous bolus) conditions. PYY at 30 pmol/kg/hr inhibited basal pancreatic fluid secretion in sham-operated rats, but not APX rats. PYY at 100 pmol/kg/hr stimulated basal pancreatic protein secretion in sham-operated rats, and this effect was also lost in APX rats. PYY at 30 and 100 pmol/kg/hr inhibited peak 2-DG stimulated protein secretion to a greater extent in APX rats as compared to sham-operated rats (P < 0.05). Since PYY inhibition of basal pancreatic secretion is AP dependent and inhibition of 2-DG stimulated pancreatic secretion is AP independent, we conclude that the 2-DG pathway of pancreatic secretion differs from the pathway responsible for basal secretion, and that APX potentiates the inhibitory effect of PYY on the 2-DG pathway.

Animals↗
PubMed2001

PYY inhibits CCK-stimulated pancreatic secretion through the area postrema in unanesthetized rats.

Peptide YY (PYY) inhibits CCK-8-secretin-stimulated pancreatic secretion in vivo. To investigate whether CCK-8-secretin-stimulated pancreatic secretion is mediated through a vago-vagal pathway and whether PYY inhibits this pathway through the area postrema (AP), chronic pancreatic, biliary, and duodenal catheters were implanted in AP-lesioned (APX) or sham-operated rats. The effects of APX on pancreatic secretion stimulated by bethanechol, pancreatic juice diversion (PJD), or CCK-8-secretin, were tested, with and without background PYY infusion, in unanesthetized rats. APX reduced basal pancreatic secretion by 15-20% (P < 0.01). APX had no effect on bethanechol-stimulated secretion and potentiated protein secretion stimulated by PJD (396 vs. 284%) and exogenous CCK-8-secretin. In sham-operated rats, background PYY potently inhibited CCK-8-secretin-stimulated pancreatic fluid (1.8 vs. 48.2%) and protein secretion (3.7 vs. 45.8%) but potentiated fluid (52.9 vs. 43.1%) and protein (132.9 vs. 68.9%) secretion in APX rats. Our findings demonstrate that PYY inhibits CCK-8-secretin-stimulated pancreatic secretion through an AP-dependent mechanism in sham-operated rats. The AP also contributes to basal pancreatic secretion.

Animals↗
PubMed2000

PYY regulates pancreatic exocrine secretion through multiple receptors in the awake rat.

Peptide YY (PYY) is one of several regulatory peptides reported to modulate pancreatic secretion. PYY circulates in two forms, PYY1-36 and PYY3-36, and binds to multiple receptor subtypes. We sought to determine if PYY1-36 or PYY3-36 regulates neurally mediated pancreatic secretion through the Y1, Y2, and/or Y5 receptor subtypes. Experiments were conducted in awake, surgically recovered rats. In order to determine the effects of the PYYs on basal pancreatic secretion, either PYY1-36, [Pro34] PYY1-36 (a Y1/Y5 agonist), or PYY3-36 (a Y2/Y5 agonist) were infused for 40 min at doses of 0, 12.5, 25, or 50 pmol/kg/hr while measuring pancreatic juice volume and protein. PYY1-36 increased pancreatic protein secretion at 25 and 50 pmol/kg/hr (P < 0.05) in a dose-dependent manner (P < 0.001, R2 = 0.990). The Y2/Y5 receptor agonist PYY3-36 significantly inhibited pancreatic juice volume and protein at 12.5 and 25 pmol/kg/hr, but stimulated protein secretion at higher doses (P < 0.001, R2 = 0.995). The Y1/Y5 agonist, [Pro34] PYY1-36, had no significant effect on basal pancreatic exocrine secretion. Therefore, PYY1-36, PYY3-36 and [Pro34] PYY1-36 produced different, dose-dependent changes on basal pancreatic exocrine secretion. Inhibition of pancreatic secretion by circulating PYY1-36 and PYY3-36 are primarily mediated by the Y2 receptor. Since [Pro34] PYY1-36 did not change pancreatic secretion, it can be concluded that circulating PYY1-36 or PYY3-36 does not modulate pancreatic secretion through the Y1 or Y5 receptors. Since the stimulatory effects of PYY1-36 on pancreatic secretion could not be explained by the actions of PYY3-36 or [Pro34] PYY1-36 on Y1 or Y2 receptors, and since PYY1-36 fails to bind to Y3 or Y4 receptors, we also conclude that PYY1-36 may stimulate pancreatic secretion in a dose-dependent mechanism through a PYY receptor subtype different from Y1, Y2, Y3, Y4 or Y5.

Animals↗
PubMed1990

Epidemiology and etiology of chronic pancreatitis in Brazil: a tale of two cities.

We observed 797 consecutive cases of chronic pancreatitis from 1963 to 1987 in the cities of Belo Horizonte and São Paulo. Alcoholism was the main etiological agent, responsible for 714 cases (89.6%). Chronic calcifying pancreatitis from different etiologies, alcohol, idiopathic, nutritional, and familial, was the most important form of chronic pancreatitis, with 786 cases (98.6%). Only three cases of chronic obstructive pancreatitis were diagnosed. Eight cases of chronic pancreatitis, anatomicopathologically studied, have not showed the typical pancreatic changes of either chronic calcifying pancreatitis or of obstructive pancreatitis and were impossible to classify according to the 1984 Marseilles' classification.

Alcoholism↗
PubMedDate not supplied

[Gastro-entero-pancreatic hormones in patients with chronic Chagas' disease].

The seric levels of gastrin, pancreatic glucagon, pancreatic polypeptide, enteroglucagon, motilin and cholecistokinin were evaluated in ten patients with chronic Chagas' disease and compared with those observed in nine normal control subjects. The seric values of all the hormones were determined on basal stimulation, after continuous intravenous secretin infusion and infusion of stepwise increased concentrations of caerulein (direct stimulation), and after intravenous secretin administration followed by intraduodenal instilation of increased concentrations of phenylalanina (combined stimulation). All the hormones, basal and after direct stimulation, showed similar values, except gastrin that in the chagasic group presented higher levels than in control subjects. Phenylalanine and pancreatic polypeptide showed significantly higher values in the control group than in the one of patients with Chagas' disease. The hormonal response in patients with chronic Chagas' disease suggested a neural impairment of the enteropancreatic axis.

Adolescent↗
PubMedDate not supplied

[Etiology of chronic pancreatitis in São Paulo: a study of 407 cases].

The etiology of chronic pancreatitis was investigated in 407 patients: 381 (93.6%) had a history of heavy alcoholic ingestion (average = 295.3 +/- 171.3 g of ethanol) during a time of 19.2 +/- 8.0 years: five patients (1.0%) had familial background of pancreatitis, two (0.5%) had the obstructive form, and two (0.5%) presented history of malnutrition. In 18 patients (4.4%) it was not possible to determine the etiology. Patients with the alcoholic form started the alcohol abuse at the age of 19.4 +/- 6.0 years. A careful dietetic inquiry showed that patients with chronic pancreatitis lived on a diet which was significantly richer in protein than that of patients of the control group (p less than 0.01). Attention is called to the high incidence of chronic alcohol abuse in patients with chronic pancreatitis.

Adolescent↗
PubMedDate not supplied

[Chronic pancreatitis: clinical characteristics, complications and association with other diseases].

The clinical aspects, complications and association with other diseases were investigated in 407 patients with chronic pancreatitis. The most frequent symptoms were abdominal pain (93.6%), weight loss (91.6%), diabetes (37.8%) and malabsorption (31.7%). Pancreatic cysts (32.6%), ascites and/or pleural effusion (12.5%), pancreatic necrosis (11.2%), gastrointestinal bleeding (12.8%) and pancreatic abscess (7.3%) were the most frequent complications. The symptoms and complications observed are discussed and their incidences compared to those reported from other countries.

Chronic Disease↗
PubMedDate not supplied

[Spontaneous remission of pancreatic cysts in patients with chronic pancreatitis].

Thirty one alcoholic patients with pancreatic cysts were studied by ultrasonographic scanning with the purpose to observe the evolution of the cysts. The mean time of the follow-up was 15.6 +/- 9.2 months; the patients were aged 40.2 +/- 9.3 years (male = 93.5%; female = 6.4%) the average pure ethanol intake was 288.3 +/- 185.9 ml for a period of 20.8 +/- 9.3 years. In 21 of the 31 patients (67.7%) the ultrasonographic examination showed total spontaneous resolution of the cysts within a time span of less than 18 months. The majority of the parameters studied (age, time and volume of ethanol intake, pain, diabetes, calcifications and previous cyst drainage) had no relation with the evolution of the cysts. In 11 patients (52.3%) the cysts showed an initial enlargement before decreasing in size. The cysts located in the pancreatic head showed less tendency to spontaneous resolution. Complications were observed in two patients: intra-cystic haemorrhage in one and rupture into the peritoneal cavity in the other. Our observations suggest that patients with pancreatic cysts secondary to chronic alcoholic pancreatitis should be controlled with periodical ultrasonography. Surgical approach should be reserved for patients with complications.

Adult↗
PubMedDate not supplied

[Splenic vein thrombosis as cause of digestive hemorrhage: ruptured esophageal varices or hemorrhagic gastritis secondary to portal hypertension?].

The clinical evolution and treatment of two patients with alcoholic chronic pancreatitis complicated with digestive hemorrhage localized in the gastric corpus and fundus are discussed. The clinical picture and the endoscopic features suggested that the hemorrhage was due to hemorrhagic gastritis and not to rupture of varicose veins. Hemorrhagic gastritis as a consequence of segmentary portal hypertension may be responsible for the difficulty in establishing the etiology of digestive hemorrhage in such cases.

Adult↗