Dietary fiber supplementation: effect on exocrine pancreatic secretion in man.

The effect of a dietary fiber supplementation program (20 g/d) on exocrine pancreatic gland secretion was evaluated in six healthy male subjects who underwent quantitative assessment of pancreatic enzyme secretion both before and after 4 wk of dietary fiber supplementation. A duodenal perfusion technique was used to quantify the concentrations and output of pancreatic enzymes after ingestion of a standard test meal. Samples were aspirated from the ligament of Trietz and analyzed for pH, total protein, amylase, trypsin, and lipase activity. No significant changes were observed in duodenal flow rate pH, total protein, amylase, or trypsin concentrations and outputs after fiber supplementation. A marked increase in mean (+/- SEM) lipase concentration (U/mL) and output (kU/min) in both the resting and postprandial states was seen, reaching statistical significance (p less than 0.05) at 120 min postprandial. These data suggest that in man, a 4-wk dietary fiber supplementation program can modulate pancreatic lipase secretion.

Functional and structural changes in parotid glands of alcoholic cirrhotic patients.

The parotid gland function and structure was studied in 30 patients with biopsy-proven alcoholic cirrhosis and in 43 age- and sex-matched alcoholic and nonalcoholic control subjects. Mean simulated parotid saliva flow rate was significantly (p less than 0.05) lower in patients with alcoholic cirrhosis as compared with alcoholic and nonalcoholic control subjects. A similar reduction was observed in mean basal parotid saliva flow rate in patients with alcoholic cirrhosis that reached statistical significance (p less than 0.05) in comparison with nonalcoholic control subjects. In addition, the concentration of sodium, bicarbonate, and total proteins in stimulated parotid saliva was significantly (p less than 0.005) lower in patients with alcoholic cirrhosis as compared with the two groups of control subjects. Sialograms in 6 patients with alcoholic cirrhosis did not reveal any obstructive lesion in the primary parotid duct or its branches. Histology of salivary tissue revealed an increase in the interstromal fatty infiltration, edema, and fibrosis without evidence of inflammatory reaction in 5 patients as compared with the control subjects. These data provide evidence for marked parotid gland dysfunction in patients with alcoholic cirrhosis presumably due to metabolic derangement and altered parotid gland structure.

Interactions of bombesin and substance P at the feline lower esophageal sphincter.

The purpose of this study was to determine the interactions between bombesin and substance P at the feline lower esophageal sphincter (LES). Intraluminal pressures were recorded using a fixed, perfused catheter assembly. Myoelectrical activity was recorded using bipolar Ag-AgCl serosal electrodes. Bombesin, i.v., gave a dose-dependent increase in LES pressure and electronically counted spike activity. The threshold dose was 10(-7) g/kg, while the maximal dose, 10(-5) g/kg, increased LES pressure by 65.5 +/- 14.8 mmHg. The neuroantagonist, tetrodotoxin, decreased the LES response to bombesin by 74.1% +/- 7.9% (P less than 0.05), but had no significant effect on the LES response to substance P. The sphincteric response to bombesin was not inhibited by bilateral cervical vagotomy, atropine, propranolol, or phentolamine (P less than 0.10). Bombesin tachyphylaxis abolished the LES response to bombesin but had no effect on the response to substance P. Conversely, substance P tachyphylaxis completely abolished the LES response to bombesin (P less than 0.001). The substance P antagonist [D-Pro2, D-Trp7,9]substance P also significantly inhibited the LES response to bombesin (P less than 0.05). Acidification of the distal esophagus with 2.0 ml of 0.1 N HCl increased LES pressure by 32.5 +/- 5.2 mmHg (P less than 0.02). The LES response to acid was inhibited by bombesin tachyphylaxis (maximal pressure response, 4.7 +/- 2.1 mmHg, P less than 0.01 compared with control acid response). The tachyphylaxis techniques were specific for the peptides giving no effect on the LES responses to phenylephrine, bethanechol, or pentagastrin. We drew the following conclusions: (a) bombesin increased feline LES pressure via nonvagal neural pathways that were insensitive to adrenergic or cholinergic antagonists; (b) bombesin may be involved in the enteric pathways that mediate the feline LES response to distal esophageal acidification; and (c) substance P mediates the effect of bombesin at the LES and is a neurotransmitter in the LES response to acidification.