Effect Of Pancreatic Enzymes Research Articles

Octreotide does not prevent bacterial translocation in an infant piglet model of intestinal ischemia-reperfusion

The process of bacterial translocation (BT) after ischemia/reperfusion ( I R ) injury is reported to be mediated by local mucosal factors, the effects of pancreatic enzymes, epithelial disruption, and by dysfunctional intestinal motility. Octreotide (OCT), a somatostatin analog, has been postulated to protect against BT by influencing one or more of these factors. Twenty-two formula-fed piglets (weight, 3.5 ± 0.5 kg; age, 20 ± 5 days) were divided into four groups: control (no drug given; no I R ; n = 6), I R (no drug given; n = 5), I R plus low-dose OCT (LD OCT, 0.08 μg/kg; n = 6), and I R plus high-dose OCT (HD OCT, 8 μg/kg; n = 5). All experimental subjects had nonocclusive mesenteric ischemia induced by reversible pericardial tamponade with mesenteric flow decreased to 25 ± 5% of baseline for 5 hours followed by 15 ± 5 hours of reperfusion. Mesenteric lymph nodes (MLN), liver, spleen, blood, and peritoneum were harvested for blind microbial analysis. None of the animals in the control group experienced translocation to the tissues tested. All of the animals in the I R group experienced BT to the MLN. The subjects in the LD OCT and HD OCT groups experienced BT to the MLN 66% and 80% of the time, respectively. Despite the reported clinical evidence that OCT can protect the intestinal mucosa from injury and increase the clearance of bacteria from the gastrointestinal tract, in this study in which variables other than I R known to promote bacterial translocation were eliminated, OCT failed to modify or prevent the occurrence of translocation to the MLN after I R injury.

Effect of Pancreatic Enzymes in Non-Ulcer Dyspepsia

The symptomatic effect of pancreatic enzymes was examined in 37 patients with non-ulcer dyspepsia (NUD) recruited from general practice by means of a 24-day multicrossover model (MCOM) including six treatment periods and five regular interchanges between pancreatic enzymes and placebo. The evaluation was based on a comparison of the enzyme- and placebo-associated symptoms and on the number of times pancreatic enzymes were associated with less symptoms than the preceding or following placebo period in individual patients. No evidence of a short-term effect of pancreatic enzymes in NUD was found.

Effects of pancreatic enzymes on precursor of intestinal sucrase-α-dextrinase

Effects of pancreatic enzymes on precursor of intestinal sucrase-α-dextrinase

PANCREATIC ENZYMES PARTICIPATE IN THE DEGRADATION OF INTESTINAL SUCRASE-ISOMALTASE

The pancreatic ducts were by-passed with a catheter placed within the common bile duct in order to prevent the entry of pancreatic enzymes into the duodenum without interrupting bile flow. For eight days, rats were fed a diet (peptones, sucrose, coconut oil, vitamins and minerals) that could be digested without pancreatic enzymes. Control animals were sham operated and pair fed with the same diet. Relative rates of synthesis and degradation were estimated by pulse labelling and double labelling respectively, for sucrase and for total protein, in total intestinal mucosa and along the gradient of cells collected from the tip of the villus to the bottom of the crypt. The rate of degradation of sucrase was 1.7 times higher than that of total protein in controls, whereas in experimental animals it was equal to that of total protein. This change in rate of degradation produced a proportional increase of sucrase activity in experimental animals. The effect of pancreatic enzymes on sucrase was apparent along the entire length of the villus but not in the crypt. These data support the hypothesis that pancreatic proteases release sucrase-isomaltase from the brush-border membrane, resulting in the observed increase of the rate of degradation. Electrophoretic separation of immunoprecipitated sucrase-isomaltase showed that the intact pro-sucrase-isomaltase observed in operated animals is split into two subunits (sucrase and isomaltase) by the action of pancreatic proteases in control animals. Supported in part by grant # 1 T32 HD 07266-01 NIH

Effect of pancreatic enzymes on protruding ileostomy stomas.

The effects of dry air, saline, and ileostomy fluid containing trypsin were independently measured on two types of ileostomies in 16 dogs for two weeks. In all instances, the everting type of ileostomy retained its original length, pliability, and patency. The ileostomies with exposed serosa underwent up to 92% shortening with stenosis and rigidity when exposed to fluid containing pancreatic enzymes. The proteolytic activity of ileostomy fluid was found to liberate from 0.128 to 0.396 millimol of tyrosine per liter per minute with the Anson-Mirsky method. Air exposure or constant saline moisture resulted in lesser shortenings, 37% and 40% respectively, in ileostomies with serosa exposed.

Mechanism of canine gastric hypersecretion after complete pancreatic ductal obstruction.

The effect of pancreatic enzymes (Viokase) on the gastric hypersecretion induced by pancreatic ductal ligation was studied in seven dogs with Heidenhain pouches. The pancreatic ducts were completely ligated after base-line determinations of the daily output of acid and secretory response of the pouches to histamine and tests of hepatic function. The influence on these tests of the preligation control diet and the following experimental diets was studied after the pancreatic duct ligation in varying sequence for 5–47 days: 1) control diet incubated with Viokase; 2) control diet mixed but not incubated with Viokase; 3) control diet incubated with heat-inactivated Viokase. Complete ligation of the pancreatic ducts was followed by marked gastric hypersecretion while the dogs were fed the control diet. Both the diet incubated with Viokase and the diet mixed with Viokase and then allowed to stand for 1–3 hr before feeding caused significant reduction of such hypersecretion. Evidence of hepatocellular damage was found after pancreatic ductal obstruction when active pancreatic enzymes were not added to the control diet.