Influence of shock on development of infection during acute pancreatitis in the rat

• Published in: Digestive diseases and sciences 1992-09, Vol.37 (9), p.1418-1425
• Main Authors: RUNKEL, N. S. F, SMITH, G. S, RODRIGUEZ, L. F, LAROCCO, M. T, MOODY, F. G, MILLER, T. A
• Format: Article
• Language: English
• Subjects: Acute Disease; Animals; Bacteria - isolation & purification; Bacterial Infections - complications; Biological and medical sciences; Gastroenterology. Liver. Pancreas. Abdomen; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Male; Medical sciences; Other diseases. Semiology; Pancreas - pathology; Pancreatitis - complications; Pancreatitis - microbiology; Pancreatitis - pathology; Rats; Rats, Inbred Strains; Shock - complications
• ISSN: 0163-2116; 1573-2568
• DOI: 10.1007/bf01296013

This study tested the hypothesis that hypovolemic shock elicits or promotes the development of infection during acute pancreatitis. Pancreatitis was induced in rats by ligation of the common biliopancreatic duct; nonlaparotomized animals served as controls. After 24 hr, the animals were subjected to either sham-shock (instrumented only) or to shock by withdrawal of blood through a femoral artery line by maintaining the mean arterial blood pressure at 30 mm Hg for 1 or 2 hr. After completion of the shock period, the shed blood was returned to the animal. All animals were sacrificed 24 hr later and specimens obtained from portal and systemic blood, liver, spleen, pancreas, and mesenteric lymph nodes for bacteriologic culture using standard techniques. The pancreas was also analyzed by morphometric techniques. The histologic changes of pancreatitis induced by biliopancreatic obstruction were characterized by marked edema with accompanying mild inflammation, hemorrhage, and necrosis. Concomitant with these morphologic findings was an associated translocation of enteric organisms to the mesenteric lymph nodes without spread to distant organs. Shock by itself induced only a mild edema in the pancreas and did not cause bacterial translocation. Furthermore, shock failed to aggravate the morphologic alterations of acute pancreatitis and did not promote bacterial spread to mesenteric nodes over that observed with pancreatitis alone. Thus, we conclude that periods of severe shock lasting up to 2 hr do not play a major role in the pathogenesis of infection in our model of pancreatitis.