Congenital intrahepatic arteriovenous fistulae, a rare hepatic vascular anomaly, in an 8-mo-old female beagle dog was investigated. The animal showed anorexia, repeated vomiting, hemorrhagic diarrhea, and jaundice for approximately 2 wk. There was mild to severe increase of serum alkaline phosphatase, glutamic-oxalacetic transaminase, glutamic pyruvic transaminase, total cholesterol, total bilirubin, and gamma-glutamyl transpeptidase. Macroscopically, the main abdominal organs showed hemorrhagic edema together with bloody ascites. Other characteristic findings were severe hepatic atrophy (right medial, quadrate, left medial, and lateral lobes) with multiple vascular cysts and compensatory hypertrophy of the other lobes. The cystic vessels seemed to extend from the proper hepatic arteries and their branches but were indistinguishable from the portal vein. Histopathologically, the atrophied hepatic lobes were characterized by wide, fibrous septa containing severe hyperplasia and anastomosis of the arteriolae and venulae and proliferation of bile ducts.

Animals↗

PubMedDate not supplied

Mechanism of induction of prostaglandin E2 production by endothelin 1 in cultured rat mesangial cells.

The phospholipase A2 inhibitors mepacrine, ONO-RS-082, and AACOCF3 completely inhibited prostaglandin E2 production induced by endothelin 1 in cultured rat mesangial cells, suggesting that phospholipase A2 is a critical enzyme in this process. TMB-8, an inhibitor of calcium mobilization from intracellular stores, abolished its production, while neither nicardipine nor chelation of extracellular calcium by EGTA did. The protein kinase C inhibitors, H-7 and staurosporine, and downregulation of protein kinase C could not inhibit prostaglandin E2 production, while W-7, a calmodulin inhibitor, abolished it. Pertussis toxin never influenced its production. Thus, endothelin 1 evokes prostaglandin E2 production in mesangial cells mainly through the activation of phospholipase A2, dependent on intracellular calcium and calmodulin and independent of extracellular calcium, protein kinase C, and pertussis toxin sensitive guanosine 5'-triphosphate binding proteins.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗