Surgical gastroenterology最新文献

The isoamylase profile in 24 patients undergoing ERCP were prospectively studied. Serum samples were obtained prior to and 4 hours following ERCP. All patients had the bile duct successfully visualized and in all but one patient the pancreatic duct was seen. Twenty-two of the 24 patients had a rise in the total serum amylase following ERCP. Most often this was from pancreatic sources, but two patients had a substantial rise in the salivary isoamylase. No patient developed clinical signs of acute pancreatitis. The patients in whom ductal pathology was found had a significant rise in pancreatic isoamylase following ERCP. Patients with normal pancreatic ducts did not show a significant rise in the pancreatic isoamylase. Patients who were hyperamylasemic prior to ERCP had a statistically significant post-ERCP rise in pancreatic isoamylase. In contrast, those who were normoamylasemic had no significant change in their pancreatic isoamylase level following the procedure. Development of hyperamylasemia is an expected sequela of ERCP, most often is due to pancreatic sources, and is rarely of clinical significance.

Pharmacological attempts to alter the course of experimental pancreatitis in the opossum were made using synthetic 16, 16-dimethyl prostaglandin E2 (16, 16-dm PGE2). Anatomically, the opossum has an elongated ampulla resulting in a supraduodenal pancreatic duct-common bile duct junction allowing for bile reflux pancreatitis to be produced by ligating the distal common bile duct. Preliminary evaluation demonstrated that at 72 hours common bile duct ligation distal to the pancreatic duct orifice produced pancreatitis comparable in severity to that produced by a Pfeffer loop. When the oppossum distal common bile duct was ligated, serum amylase concentrations progressively increased from control values of 182 +/- 43 to 742 +/- 62 Somogyi units/dl at 5 hours. Administration of 0.2 microgram-kg-1-min-1 16, 16-dm PGE2 significantly decreased the hyperamylasemia associated with bile reflux pancreatitis and, in addition, decreased the pancreatic gland weights when compared to control values. Subsequent evaluation of the administration of 75 micrograms-kg-1 16, 16-dm PGE2 every 12 hours for 72 hours to opossums with distal common bile duct ligation demonstrated no significant differences in serum amylase concentrations when compared to control values. Histologic evaluation of the pancreas glands at 72 hours demonstrated increased glandular integrity when the pancreas glands from the opossums receiving 16,16-dm PGE2 were compared to the glands subjected to distal common bile duct ligation alone. This report identifies several favorable characteristics in the course of experimental pancreatitis associated with the administration of a synthesis PGE analog at the onset of the inflammatory process.(ABSTRACT TRUNCATED AT 250 WORDS)

Three patients with postoperative external biliary fistula are described. In each, radionuclide 99Tcm HIDA was used to define the anatomy of the fistula. The extent of the fistula and the presence of distal obstruction to bile flow could also be determined. This information was used to predict the likelihood of spontaneous fistula closure. HIDA scanning is a useful noninvasive alternative to other investigations, such as fistulography and cholangiography, which do not always provide useful information. The results of HIDA scanning can aid the clinical decision on the need for surgical intervention to correct an external biliary fistula.

Unlabelled: The demonstration of gastrointestinal ctyoprotection by PGF2 alpha (a supposed vasoconstrictor) has been cited as evidence against alteration of mucosal blood flow as a mechanism for the cytoprotection phenomenon. However, cytoprotection by PGF2 alpha has never been demonstrated in a model having concomitant documentation of gastrointestinal blood flow. This experiment was designed to accomplish two objectives. First, the effect of intravenous PGF2 alpha (0.1, 1.0, 10.0 mcg/kg/minute) on blood flow throughout the gastrointestinal tract was documented in a chloralose anesthetized miniature swine model (n = 7). Second, the effect of intravenous PGF2 alpha (1.0 mcg/kg/minute) on both gastric mucosal blood flow and stress ulceration was assessed during a 3-hour period of hemorrhagic shock in the same model (six controls, six PGF2 alpha). The radiolabeled microsphere technique of blood flow determination was employed.

Results: Intravenous PGF2 alpha significantly decreased myocardial blood flow at all doses employed. Although blood flow in the gastrointestinal tract tended to decrease with the largest dose of PGF2 alpha, this did not reach statistical significance. During shock PGF2 alpha had no effect on gastrointestinal blood flow. Furthermore, there was no evidence of gastric mucosal cytoprotection compared to controls. These results suggest that PGF2 alpha is neither vasoconstrictive nor cytoprotective when sub maximal doses are used. Dismissal of mucosal blood flow as a possible mechanism of prostaglandin-mediated cytoprotection is premature.