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Biomedical subjects

V P Dinoso

Publications and source records attributed to V P Dinoso.

At least 19 recordsLinked to original sources

Neurohormonal mechanisms of cigarette smoke-induced duodenal mucosal bicarbonate secretion in the rat.

The effect of cigarette smoke and nicotine on duodenal mucosal bicarbonate secretion (DMBS) was studied in rats. Cigarette smoke but not intravenous nicotine administered acutely to anesthetized rats via a tracheostomy tube stimulated DMBS by 47 +/- 6%. The increase was neurally mediated via atropine-sensitive postganglionic cholinergic neurons. Introduction of cigarette smoke after the infusion of vasoactive intestinal peptide and porcine histidine isoleucine (PHI) also caused a delayed increase in DMBS. However, the magnitude of this increase was similar to that seen in control non-peptide-infused rats. The increase in bicarbonate secretion predominantly involved Brunner's glands. Rats exposed to cigarette smoke for 4 and 8 days before direct instillation of smoke via tracheostomy tube did not show any increase in their DMBS. These studies indicate that in the rat, cigarette smoke increases DMBS, most likely secreted by the Brunner's glands. The increase is neurally mediated via atropine-sensitive postganglionic cholinergic neurons. Gastroenteric neuropeptides do not exert any influence on cigarette smoke-mediated DMBS secretion in the rat. Unlike acute exposure to cigarette smoke, chronic exposure (4 and 8 days) of rats to cigarette smoke abolishes increase in DMBS induced by subsequent exposure to cigarette smoke. This last observation may, in part, may explain the tendency of chronic smokers who have duodenal bulb ulcers to show greater propensity to higher rate of recurrence and protracted healing.

Animals↗

Bile acid and pancreatic trypsin outputs are parallel during intraduodenal infusion of essential amino acids.

There is disagreement as to whether contraction of the gallbladder occurs simultaneously with secretion of pancreatic enzymes during food ingestion. One study that employed exogenous cholecystokinin (CCK) alone showed dissociation of total bile acids (TBA) and trypsin outputs, while another study that employed exogenous CCK plus secretin showed parallel outputs of TBA and trypsin. Since previous studies have suggested that intraduodenal infusion of essential amino acids (EAA) evokes pancreaticobiliary secretion similar to that observed with food ingestion, we infused increasing doses of EAA intraduodenally in 10 subjects with intact gallbladder and in 10 subjects with previous cholecystectomy and measured total bile acids and trypsin outputs serially. In subjects with intact gallbladder, increasing molar doses of EAA induced parallel increases of TBA and trypsin outputs. In subjects with previous cholecystectomy trypsin outputs during infusion of EAA were similar to subjects with intact gallbladder, but their TBA outputs remained constant during the entire infusion period. Serial concentrations of plasma secretin did not change during intraduodenal infusion of EAA. These observations suggest that the gallbladder empties bile in concert with secretion of pancreatic enzymes following food ingestion.

Amino Acids, Essential↗

Basal motor activity of the distal colon: a reappraisal.

The significance of recent motor data on the distal colon in irritable bowel syndrome is obscured by methodological questions such as bowel preparation, variability and reproducibility of motor activity and segmental differences. Thirty subjects were studied after prior bowel cleansing with a water enema on two separate occasions 1 wk apart (10 with one bowel movement per day, 10 with two to three per week, and 10 with three to 12 per day). Two additional studies were performed in 10 of the subjects, one with and one without prior cleansing. The motility indices of the cleansed and unwashed colon were dissimilar. The motility index per 3 min varied markedly over 3 h, and the indices between the paired studies were rarely identical. Marked segmental differences were noted. The mean motility index per 3 min of the constipated and the diarrhea groups was significantly greater than that of normals only in the 15-cm segment. In view of these variables, caution should be exercised in the interpretation of basal motor activity of the distal colon.

Colon↗

Gastric and pancreatic function in patients with end-stage renal disease.

Gastroduodenal disease such as peptic ulcer and duodenitis is increased in patients with end-stage renal disease. Gastric hypersecretion of acid proposed as the underlying mechanism has been disputed because peptic ulcer has occurred even in those with normal or low gastric acid secretion. We studied the pancreatic exocrine secretion of bicarbonate (HCO3) and the concentration of plasma pepsinogens in addition to gastric acid secretion in 15 patients on chronic hemodialysis, 10 patients wih previous renal transplantation and compared them with 10 subjects without gastrointestinal or renal disease. We confirmed hypersecretion of gastric acid in renal disease. We confirmed hypersecretion of gastric acid in renal patients on chronic hemodialysis but not in transplant patients. In addition, we found basal but hyposecretion of HCO3 and hyperpepsinogenemia in both renal groups. These observations suggest that the high incidence of gastroduodenal disease in end-stage renal disease might, in part, be due to the simultaneous occurrence of gastric acid hypersecretion, basal hyposecretion of HCO3 by the pancreas, and hyperpepsinogenemia.

Adult↗

Effect of pH, substrate, and temperature on tryptic activity of duodenal samples.

Many tests of pancreatic exocrine function are based on the estimation of tryptic activity in duodenal juice. However, tryptic activity may be influenced by substrate, pH, and temperature. We studied the effect of substrate, pH, and temperature on tryptic activity of duodenal juice in vitro and in vivo. TAME yielded higher tryptic activity in vitro (11.25 times) and in vivo (4.54 times) compared to BAEE and BAME. Our in vitro studies also indicated that trypsin was denatured slowly between pH 6 and 4.25 and rapidly between 4.25 and 3.75. The rate of denaturation was faster at room temperature and slower in ice over a broad range of pHs. In our in vivo studies, hypersecretors showed tryptic activities consistently lower than normosecretors. The duodenal pHs of the hypersecretors were consistently lower than those of normosecretors, suggesting that the low tryptic activities were secondary to denaturation by acid. These studies indicate that the activity of trypsin in duodenal juice varies significantly with substrate, pH, and temperature. These factors must, therefore, be considered in the analysis and interpretation of trypsin.

Duodenum↗

Serial pH changes in the duodenal bulb during smoking.

The effect of smoking on the pH of the duodenal bulb was studied in 10 normosecretors and 10 hypersecretors using a Beckman pH electrode. The pH was monitored during three study periods, basal, smoking, and postsmoking, of 1 hr each. The pH remained below 3.5 significantly longer during the smoking period compared to the basal period for both groups. The bulbar pH remained under 3.5 during the smoking period longer in the hypersecretor group compared to the normosecretor group (60 versus 20%). Hypersecretors who were smokers exhibited acidic bulbar pH values longer and more consistently than hypersecretor-nonsmokers during smoking. In 5 hypersecretors with data for both bulbar pH and bicarbonate output, inhibition of bicarbonate output during smoking was generally associated with acidic pH values in the bulb. These observations suggest that the association between cigarette smoking and peptic ulcer disease may be attributable to, in part, the persistently acidic pH values in the duodenal bulb during smoking. This study further suggests that the degree and the duration of acidification of the duodenal bulb during smoking are influenced by the secretory and the smoking status of the subject.

Adult↗

Gastrointestinal plasma protein loss during ethanol ingestion.

Plasma and "equivalent" albumin loss in the feces were quantitated before and during ingestion of 40% ethanol using 51Cr-labeled albumin. Five subjects were studied in each classification of normal gastric mucosa, superficial gastritis, and chronic atrophic gastritis. During the control period, plasma albumin loss was minimal and similar in all three groups. Exposure to ethanol resulted in a greater output of plasma albumin in the feces of all subjects. This loss was statistically significant in subjects with superficial gastritis (P less that 0.01) and chronic atrophic gastritis (P less than 0.005). Two subjects from each group underwent gastric clearance studies of 51Cr-labeled albumin. Increased gastric clearance of plasma was observed in all 6 subjects during ethanol ingestion; the increase was highly significant in subjects with atrophic gastritis (P less than 0.001). We conclude that ethanol ingestion can cause increased loss of plasma protein in the feces, which may be of clinical significance in subjects with atrophic gastritis.

Adult↗

Simultaneous measurement of basal pancreatic, gastric acid secretion, plasma gastrin, and secretin during smoking.

The effect of smoking one unfiltered cigarette every 15 min for 1 hr on basal gastric acid and pancreatic secretion was studied in 10 subjects with a history of duodenal ulcer and 10 without duodenal ulcer. Smoking induced a transient rise of basal acid output followed by a slight decrease. This effect was more pronounced in the duodenal ulcer group. Smoking markedly inhibited fluid and bicarbonate secretion during the smoking period. The bicarbonate and fluid secretion returned to control levels within 30 to 60 min in the ulcer group and in 60 to 90 min in the nonulcer group. There was no difference in the degree of inhibition of pancreatic secretion between the two groups. Immunoreactive gastrin and secretin in the peripheral venous blood did not change significantly during smoking. The degree of inhibition of basal pancreatic secretion correlated well with the plasma concentrations of nicotine. These observations indicate that smoking in the fasting state induces alterations of basal gastric and pancreatic secretions which are not related to changes in plasma gastrin and secretin concentration, but to plasma concentrations of nicotine. The implication of this study in relation to a possible causal association between cigarette smoking and peptic ulcer disease is discussed.

Adult↗

Ultrastructural changes of the canine gastric mucosa after topical application of graded concentrations of ethanol.

Changes in the fine structure of the gastric mucosa following exposure to graded concentrations of ethanol were studied in dogs. 300 ml of 12.5, 20, and 40%, vol/vol, were instilled intragastrically for 30 min. Mucosa from the midbody and midantrum along the greater curvature was examined by light and electron microscopy. Ethanol produced a gradation of changes in the surface epithelial cells and in the lamina propria without affecting the parietal cells and chief cells. 12.5% ethanol produced widened and irregular intercellular spaces while 20 and 40% disrupted the apical cell membrane with concomitant exudation of mucin into the gastric lumen. These changes were more severe after 40% ethanol. The tight junction between cells remained intact following exposure to the lower concentrations of ethanol, but focal separation of cell junctions was observed in severely damaged areas. Quantitation of protein, sodium, and potassium concentrations in the gastric contents revealed marked increases following exposure to ethanol which correlated with the concentration. These studies provide additional morphological data on the relationship between structural changes and functional abnormalities induced by agents which break the gastric mucosal barrier.

Administration, Topical↗

Changes in mucosal and venous histamine concentrations during instillation of ethanol in the canine stomach.

Histamine concentrations in the gastric mucosa, gastric vein blood, and gastric contents were measured after instillation of 300 ml of 40%, 20% and 12.5%, vol/vol, ethanol intragastrically for 30 min in anesthetized dogs. The mean histamine concentration in the gastric mucosa, gastric vein blood, and gastric contents in dogs treated with 40% ethanol was significantly higher than in dogs treated with sodium chloride (NaCl). Serial studies of the gastric vein blood of the ethanol-treated dogs should significant elevation of histamine concentrations for 2 hr after instillation of 40% ethanol, but less increases at 20 and 30 min after instillation of 12.5% and 20%, respectively. No change was observed after administration of 50% glucose and 25% mannitol. Morphologically, the gastric mucosa of the ethanol-treated dogs was edematous, congested and hemorrhagic. The severity of these changes increased with the concentration used. The mucosa of the dogs treated with sodium chloride, glucose, or mannitol was normal. The factors that may underlie the increase in histamine concentrations in the gastric vein blood and the possible relation of such an increase to the morphologic alterations are discussed.

Administration, Topical↗

Upper gastrointestinal hemorrhage clinical, radiological and endoscopic correlation of 100 consecutive cases.

One hundred consecutive cases of upper gastrointestinal hemorrhage were studied clinically, radiologically and endoscopically. Erosive gastritis, duodenal and gastric ulcer, and bleeding esophageal varices accounted for 85% of the cases. The presenting sign of hematamesis or melena was of no value in localizing the bleeding site relative to the pyloric sphincter. Erosive lesions of the esophagus and stomach were suspected clinically in less than 50% of the cases and were the lesions least amenable to radiologic diagnosis and where early endoscopy was most useful. Our observations demonstrate again the frequent association between ethanol or aspirin ingestion and erosive gastritis.

Adult↗

Characterization of a hyperactive segment at the rectosigmoid junction.

During a study of intraluminal motor patterns of the colon and rectum, spontaneous wave activity of a continuous complex type was observed at the rectosigmoid junction in constipated subjects. To assess the frequency and characteristics of this hyperactive segment, 36 subjects with colonic motor disorders and 12 healthy controls were studied. Eighteen of 24 patients with constipation (75%) and 1 of 7 subjects with asymptomatic diverticulosis exhibited a persistent hyperactive segment at the rectosigmoid junction. Neither secretin nor cholecystokinin influenced the wave activity of the hyperactive segment. In contrast, atropine and glucagon inhibited markedly all wave activity and decreased the motility index of this segment significantly, suggesting overactivity of the muscarinic effector cells. It is concluded that a segmental area of overactivity exists at the rectosigmoid junction in most constipated subjects regardless of their underlying disorders.

Adult↗