Seven cases of hepatic arterioportal fistulae in young dogs (mean age 6 months) are described. All cases were presumed to be congenital in origin. The onset of clinical signs, which frequently included gastrointestinal and neurological disturbances, was usually sudden. All dogs had clinical evidence of portal hypertension in the form of ascites, and all developed multiple extrahepatic portacaval venous shunts consequential to portal hypertension. The neurological disturbances were likely the result of portacaval shunting. The arterial and venous vessels involved in the fistulae had markedly altered wall structure. Hepatic regions adjacent to the fistulae frequently evidenced marked bile duct proliferation. Hepatic parenchymal atrophy, relative collapse of distributing portal veins, dilatation of hepatic arterial branches and proliferation of hepatic arterioles were seen throughout the liver; these changes closely resembled those present with portacaval shunting in the absence of hepatic arterioportal fistulae. The importance of recognizing that hepatic arterioportal fistulae and multiple extrahepatic portacaval shunts usually coexist and separately influence the morphological appearance of the liver is stressed.

A technique for temporary hepatic vascular occlusion during partial hepatectomy for hepatic arteriovenous (AV) fistulas in the dog is presented in seven dogs, and three additional cases of hepatic AV fistulas are reviewed. Hematologic, serum biochemical, radiologic, and nuclear scintigraphic parameters before and after surgery are discussed; abnormalities included anemia, hypoproteinemia, leukocytosis, increased liver function tests, retrograde filling of the portal vein during celiac angiography, and increased arteriovenous ratios during nuclear scintigraphy. Hemodynamic and pathologic findings are presented, and portal hypertension and secondary multiple portosystemic shunts are described. Clinical improvement was observed in four dogs with follow‐up periods ranging from 5 months to 3 years.

Surface oxygen tension (PSO2) was measured in dogs during experimental manipulation of the portal vein and hepatic artery, and during surgery to correct portosystemic shunting. There was no alteration in PSO2 of liver, pancreas, duodenum, or jejunum during partial (50%) or complete reduction of hepatic artery flow. After 100% reduction in portal vein blood flow, PSO2 was lower in jejunum, duodenum, and liver. With 50% reduction in portal flow, PSO2 was significantly decreased only in jejunum. In six dogs with single extrahepatic shunts, there was a significant correlation between portal pressure and jejunal PSO2. It was concluded that measurement of visceral organ PSO2 represents an accurate noninvasive means of obtaining objective data on the effect of reduction in hepatic blood flow on perfusion of other select splanchnic organs.

Transcolonic 123I‐Iodoamphetamine is rapidly absorbed across the colonic mucosa and binds to amine receptors in the liver and lungs. During the first ten minutes following colonic administration, a simple ratio of lung counts to lung counts plus liver counts provides an accurate estimate of the fraction of portal blood that bypasses hepatic sinusoids in dogs with portosystemic shunts. Studies were performed on 24 dogs with suspect portosystemic shunt. Shunt fraction values for 18 dogs with surgically confirmed portosystemic shunt were obviously higher than published values for normal dogs, and also significantly higher than values for the other six dogs, later confirmed to lack shunts. Postoperative studies were repeated on ten dogs with single shunt vessels 1–2 days after shunt closure. Total shunt ligation resulted in normal postoperative shunt fraction, whereas partial shunt ligation resulted in persistant elevation of shunt fraction. Transcolonic iodoamphetamine scintigraphy is noninvasive, easy to perform, and provides an accurate method to diagnose dogs with portosystemic shunt.

A chromogenic Limulus amebocyte lysate assay was used to measure portal and peripheral venous endotoxin concentrations in ten medically managed dogs undergoing surgery for correction of a single extrahepatic portosystemic shunt. In all dogs, both peripheral and portal venous blood samples were obtained at the time of surgical manipulation of the anomalous vessel. In six dogs, peripheral venous samples were obtained an average of 8.0 months after surgery. Five physically normal dogs without biochemical or histologic evidence of liver disease served as controls. Data analysis failed to demonstrate significant differences in peripheral and portal venous endotoxin concentrations between the control and study groups. Postoperatively five of six dogs showed a measurable reduction in peripheral venous endotoxin concentration over intraoperatively obtained values, but the differences were not statistically significant (P = 0.06). Based on results of this study it was concluded that systemic endotoxemia was not present in dogs with a single extrahepatic portosystemic shunt that were medically stable prior to surgery. (Journal of Veterinary Internal Medicine 1991; 571-74) ENDOTOXIN is a lipopolysaccharide constituent of the cell wall of gram-negative bacteria that is freed upon death of the organism.' Under normal circumstances endotoxins from intestinal bacteria are absorbed into the portal circulation but are then cleared by the hepatic reticuloendothelial system (RES).2-4 Results of several studies indicate that in the presence of experimentally induced or naturally occurring hepatic disease, systemic endotoxemia may e~i s t .~,~-'~ Endotoxin may be detected in clinical samples by complement activation, radioimmunoassay for O-antigen, and the Limulus amebocyte lysate (LAL) assay.'2-20 Of these available methods, the LAL assay is by far the most sensitive. By using a synthetic chromogenic substrate for the Limulus enzyme the LAL assay has the capability of detecting endotoxin at picogram concentrations.