pituitrin and Peritonitis

Portal hypertension is one of the main consequences of cirrhosis. It results from a combination of increased intrahepatic vascular resistance and increased blood flow through the portal venous system. The condition leads to the formation of portosystemic collateral veins. Esophagogastric varices have the greatest clinical impact, with a risk of bleeding as high as 30% within 2 years of medium or large varices developing. Ascites, another important complication of advanced cirrhosis and severe portal hypertension, is sometimes refractory to treatment and is complicated by spontaneous bacterial peritonitis and hepatorenal syndrome. We describe the pathophysiology of portal hypertension and the current management of its complications, with emphasis on the prophylaxis and treatment of variceal bleeding and ascites.

Topics: Algorithms; Anti-Bacterial Agents; Ascites; Collateral Circulation; Diuretics; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hepatorenal Syndrome; Hormones; Hypertension, Portal; Liver Cirrhosis; Lypressin; Peritonitis; Portasystemic Shunt, Transjugular Intrahepatic; Sclerotherapy; Secondary Prevention; Somatostatin; Spironolactone; Terlipressin; Vascular Resistance; Vasoconstrictor Agents; Vasodilation; Vasopressins

Topics: Adrenergic beta-Antagonists; Ascites; Carcinoma, Hepatocellular; Catheterization; Diuretics; Hemorrhage; Hepatic Encephalopathy; Humans; Hypertension, Portal; Liver Cirrhosis; Liver Neoplasms; Nitroglycerin; Peritonitis; Somatostatin; Vasopressins

A systemic inflammatory response to infection characterizes sepsis which associated to refractory hypotension, turns into severe sepsis. Our aim was to evaluate hormonal and cardiovascular alterations after experimental sepsis induced by cecal ligation and puncture (CLP). Male Wistar rats (200-250 g) were submitted to CLP or sham operation. The animals were decapitated at 0, 2, 4, 6 and 8 h after surgery for collection of blood samples for plasma osmolality, sodium and vasopressin (AVP) measurements. The mean arterial pressure (MAP) and heart rate (HR) were recorded 1 h before and to each 1 h during 5hs after surgery. The spontaneous baroreflex sensitivity and spectral analysis of HR and MAP variability were analyzed after recording. The plasma osmolality and sodium did not show any alterations compared to the sham group. MAP decreased from 3 h (85 vs.103 mm Hg, P<0.05) to 5 h in the CLP group (76 vs.106 mm Hg, P<0.05). This was accompanied by an increase in HR. The AVP plasma level was elevated at 4 h (6.0+/-1.1 vs. 1.1+/-0.2 pg/mL, P<0.05) and returned to basal levels at 8 h after CLP (2.3+/-0.5 vs. 1.9+/-0.2 pg/mL, P>0.05). A reduction in baroreflex sensitivity occurred 1 h after injury. The CLP group showed a reduction in overall variability, low-frequency power, and low/high-frequency ratio of HR and low-frequency power of MAP. The data suggest an impairment of autonomic control of the heart and vessels during polymicrobial sepsis. This reduction in autonomic nervous system activity causes the impairment of baroreflex that in turn may contribute to the reduction of vasopressin plasma levels in the late phase of severe sepsis.

Topics: Animals; Autonomic Nervous System; Autonomic Nervous System Diseases; Baroreflex; Blood Pressure; Cecum; Disease Models, Animal; Heart Rate; Hypotension; Ligation; Male; Osmolar Concentration; Peritonitis; Rats; Rats, Wistar; Sepsis; Shock, Septic; Sodium; Time Factors; Up-Regulation; Vasopressins

Two patients developed spontaneous bacterial peritonitis after infusions of vasopressin into the superior mesenteric or gastroduodenal arteries for upper gastrointestinal hemorrhage. The peritonitis in these patients differed from the typical picture in which a single aerobic organism is responsible, by the presence of multiple organisms, some of which were anaerobic. These findings suggest that the arterial vasoconstriction decreased the integrity of the intestinal mucosal barrier and permitted the transmural migration of enteric organisms from the lumen of the bowel into the ascites-filled peritoneal cavity.

Topics: Anaerobiosis; Arteries; Ascitic Fluid; Bacterial Infections; Duodenum; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Infusions, Parenteral; Intestines; Male; Mesenteric Arteries; Middle Aged; Peritonitis; Stomach; Stomach Ulcer; Vasopressins