secretin/edema

Large pharmacological doses of ceruletide administered to conscious dogs by intravenous (i.v.) infusion uniformly induce a severe acute necrotizing pancreatitis within 4 h. High-dose i.v. secretin administered for a period of 24 h after cessation of ceruletide infusion resulted in a significant

Inhibition of pancreatic secretion is a widely accepted therapeutical principle of acute pancreatitis. However, stimulation of water and bicarbonate secretion may be beneficial by washing out the ductular system in pancreatitis. Secretin (2 and 16 CU/kg body weight) or saline were given to rats at

Pharmacological doses of ceruletide administered intravenously to unconscious rats uniformly induces acute pancreatitis (AP) as well as a striking reduction in pure pancreatic juice (PPJ) and protein output. High-dose intravenous secretin administered to rats with ceruletide-induced AP effects a

BACKGROUND Chronic pancreatitis in its early stages may defy diagnosis despite existing diagnostic modalities. Endoscopic retrograde pancreatography (ERCP), secretin test, and conventional ultrasound are insensitive in detecting the early stages of chronic pancreatitis. The aim of this study was to

OBJECTIVE Pituitary adenylate cyclase activating-peptide (PACAP) is a late member of the secretin/glucagon/vasoactive intestinal peptide (VIP) family of brain-gut peptides. It is unknown whether PACAP takes part in the development of acute pancreatitis and whether PACAP or its antagonists can be

In a variety of animal models of acute pancreatitis, cholecystokinin-receptor antagonists have ameliorated the injury response. These results suggest that cholecystokinin may play a primary role in the pathogenesis of pancreatitis initiated by multiple stimuli. In an effort to test this theory, a

Blood components have been implicated as factors which modulate organ injury in acute pancreatitis. To isolate these effects we compared a standardized isolated, blood-perfused, canine pancreas model as described by Herman-Taylor and modified by Cameron with a model using fluosol, a fluorocarbon, as

A vascular pathogenesis of pancreatitis has been postulated in diabetics, the aged, Ortner's Syndrome, and various low-flow states. This report studies canine pancreatic secretion in a preparation of hypovolemic shock produced by controlled hemorrhage maintained for varying durations. Pancreatic

Severe pancreatitis and a pseudocyst occurred in a patient following accidental ingestion of an anticholinesterase insecticide, a substance not previously known to produce pancreatitis. Experiments were done to elucidate the mechanism. In one group of dogs the pancreatic duct was perfused and

To determine whether hepatic artery blood flow is essential in maintaining the function and structure of bile ductules/ducts, the acute effects of hepatic artery ligation on bile secretion and hepatic ultrastructure were examined in anesthetized, bile duct-cannulated guinea pigs. Sixty minutes after

In studies on the pathogenesis of ischemic cell injury and of other pancreatic diseases the knowledge of the actual pancreatic energy state is an important factor. Therefore, it would be advantageous to have a simple and inexpensive method to determine this parameter and its alterations in the

Enterokinase is a glycoprotein and is now designated enteropeptidase (E.C.3.4.4.8.). It is present in the duodenal and jejunal mucosa. Pancreatic proteolytic enzymes are secreted as proenzymes. Enterokinase converts trypsinogen to trypsin in the duodenal lumen. Duodenopancreatic reflux of duodenal

Intracellular Ca(2+)-changes not only participate in important signaling pathways but have also been implicated in a number of disease states including acute pancreatitis. To investigate the underlying mechanisms in an experimental model mimicking human gallstone-induced pancreatitis, we ligated the

In a previous report from this laboratory, 1 h of hypovolemia induced a significant decrease in pancreatic flow, bicarbonate and enzyme secretion. These parameters recover after restoration of blood volume, but never return to pre-shock levels. Furthermore, increasing the period of hypovolemia

The current study was done to evaluate the effects of short term (60 minutes) pancreatic biliary duct obstruction (PBDO) with intraductal hypertension (IDH) stimulated by secretin (0.2 clinical unit per kilogram per hour) and caerulein (0.2 microgram per kilogram per hour) plus 30 minutes of