Effect of suppression of endocrine or exocrine pancreatic function in hemorrhagic shock.
Somatostatin did not influence the pathologic consequences of hemorrhagic shock, but pancreatic duct ligation prevented the post-oligemic decline of arterial pressure and formation of toxic factors. These results indicate that pancreatic acinar cells release myocardial depressant factor and are important in the pathophysiology of shock.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002403:Cathepsins / Q000097:blood; D002415:Cats; D007515:Islets of Langerhans / Q000503:physiopathology; D008026:Ligation; D008297:Male; D009201:Myocardial Depressant Factor / Q000502:physiology; D010179:Pancreas / Q000503:physiopathology*; D010183:Pancreatic Ducts / Q000503:physiopathology; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D012965:Sodium Chloride / Q000494:pharmacology; D013004:Somatostatin / Q000494:pharmacology*
D009201:Myocardial Depressant Factor; D012965:Sodium Chloride; D013004:Somatostatin; D002403:Cathepsins