Portacaval shunting attenuates portal hypertension and systemic hypotension in rat anaphylactic shock.

Anaphylactic shock in rats is characterized by antigen-induced hepatic venoconstriction and the resultant portal hypertension. We determined the role of portal hypertension in anaphylactic hypotension by using the side-to-side portacaval shunt- and sham-operated rats sensitized with ovalbumin (1 mg). We measured the mean arterial blood pressure (MAP), portal venous pressure (PVP), and central venous pressure (CVP) under pentobarbital anesthesia and spontaneous breathing. Anaphylactic hypotension was induced by an intravenous injection of ovalbumin (0.6 mg). In sham rats, the antigen caused not only an increase in PVP from 11.3 cmH(2)O to the peak of 27.9 cmH(2)O but also a decrease in MAP from 103 mmHg to the lowest value of 41 mmHg. CVP also decreased significantly after the antigen. In the portacaval shunt rats, in response to the antigen, PVP increased slightly, but significantly, to the peak of 17.5 cmH(2)O, CVP did not decrease, and MAP decreased to a lesser degree with the lowest value being 60 mmHg. These results suggest that the portacaval shunt attenuated anaphylactic portal hypertension and venous return decrease, partially preventing anaphylactic hypotension. In conclusion, portal hypertension is involved in rat anaphylactic hypotension presumably via splanchnic congestion resulting in decreased venous return and thus systemic arterial hypotension.

Small multicentric pancreatic carcinoma usefully diagnosed by positron emission tomography.

Pancreatic carcinoma has a poor prognosis, and early detection is essential for potentially curative resection. Despite a wide array of diagnostic tools, pre-operative detection of small pancreatic carcinomas is difficult. We report a case of pancreatic carcinoma that was bicentric and small. The head mass was diagnosed by computed tomography (CT), while the tail mass, which was suspected but indeterminate on CT, was diagnosed by positron emission tomography (PET). Thus, total pancreatectomy was performed. The PET results prevented our patient from undergoing tail mass biopsy, multiple surgeries and non-curative operation.

Psoas abscess and bacterial peritonitis caused by urinary tract infection in a patient of liver cirrhosis and diabetes mellitus.

Prognosis of patients with diabetes mellitus or liver cirrhosis can be worsened by the development of a variety of infectious diseases. We describe a case of psoas abscess and bacterial peritonitis in a 58-year-old woman with type C liver cirrhosis and diabetes mellitus hospitalized after having an elevated temperature caused by urinary tract infection for 2 months. The cirrhosis had not been treated and daily self-administration of insulin had been discontinued for the previous 5 months. On day 2 of hospitalization, vomiting and decreased blood pressure developed. Abdominal computed tomography scan revealed ascites, pneumoperitoneum, and psoas abscess. Laparotomy revealed psoas abscess and bacterial peritonitis without gastrointestinal perforation and psoas abscess perforation. Surgical drainage of the abscess and peritoneal cavity was performed. Immediately after the operation, upper gastrointestinal bleeding, shock, hypoglycemia, and metabolic acidosis developed, followed by hepatic failure, renal insufficiency, and cerebral dysfunction. Death occurred on postoperative day 19. Upon autopsy, bacterial peritonitis residue of psoas abscess, and urinary tract infection were confirmed. We surmise that untreated liver cirrhosis and diabetes mellitus is a risk for urinary tract infection that may spread in iliopsoas and free peritoneal space.

Increased sinusoidal resistance is responsible for the basal state and endothelin-induced venoconstriction in perfused cirrhotic rat liver.

The localization of increased intrahepatic vascular resistance and the segmental vascular responsiveness to endothelin-1 are not well known in liver cirrhosis. We determined the segmental vascular resistances and their response to endothelin-1 of isolated portally perfused bile duct ligation (BDL)-induced cirrhotic rat livers. The portal occlusion pressure (Ppo) and the hepatic venous occlusion pressure (Phvo) were obtained by analyzing the profiles of the portal (Ppv) and hepatic venous (Phv) pressures during the double occlusion maneuver of simultaneous occlusions of the inflow and outflow perfusion lines. From the pressure gradients among Ppv, Ppo, Phvo, and Phv, the portal-hepatic venous resistance was assigned to three segments of the portal [Rpv = (Ppv - Ppo)/blood flow (Q)], sinusoidal [Rsinus = (Ppo - Phvo)/Q] and hepatic venous [Rhv = (Phvo - Phv)/Q] resistances. Rsinus, but not Rpv or Rhv, was significantly greater in BDL livers than in sham livers. Endothelin-1 (0.1-1 nM) increased Rpv and Rsinus to a similar magnitude, but not Rhv, in both sham and BDL. At 3 nM, the responsiveness of Rpv was smaller in BDL than in sham, but that of Rsinus were similar between in BDL and sham. In conclusion, increased sinusoidal resistance accounts for increased intrahepatic resistance of BDL-induced liver cirrhosis. Endothelin-1 contracts portal veins and sinusoids, but not hepatic veins, in both sham and cirrhotic livers. Sinusoidal contractility to endothelin-1 is not impaired in cirrhotic livers.

Gas embolism caused by portal vein gas: case report and literature review.

INTRODUCTION: We describe a case of pulmonary gas embolism caused by portal vein gas (PVG) observed using echocardiography. Echography revealed gas flowing through the hepatic vein, inferior vena cava, right atrium, and right ventricle, as well as pulmonary hypertension. The patient was diagnosed as having pulmonary gas embolism caused by PVG. OBJECTIVE: We consider PVG routes to pulmonary circulation, diagnosis of gas embolism caused by PVG, and treatment of gas embolism caused by PVG. METHODS: We reviewed reports of eight cases of gas embolism caused by PVG and compared these cases to cases of gas embolism without PVG. RESULTS: Mortality of gas embolism caused by PVG was 67%, positive blood culture was observed in six cases, and pulmonary edema was seen in three cases. PVG initially excites microbubble formation, which causes tissue damage in the liver and liver abscess. A large volume of PVG causes portal obstruction. As a result, portal hypertension, a portosystemic shunt or gastrointestinal congestion can occur. PVG can travel to the systemic vein through the liver or portosystemic shunt without anomaly and cause pulmonary gas embolism, followed by arterial embolism. In this environment, sepsis easily occurs. Echocardiography is useful for diagnosis of gas embolism caused by PVG, but the gas can be seen intermittently. The view of pulmonary edema is important for pulmonary gas embolism caused by PVG. CONCLUSION: It is important to treat the underlying disease, but PVG must be considered and treated as the gas embolism's source.

[A case of effective multidisciplinary treatment with hepatic resection for synchronous multiple liver metastases from rectal cancer].

A 56-year-old-man complained of abdominal pain, and was diagnosed as having advanced rectal cancer with synchronous multiple metastatic liver cancer (H 3) in July 1999. He underwent low anterior resection and hepatic partial resection (S 1, S 2+S 3, S 5, S 6, S 8) in August 1999. In addition, he underwent hepatic arterial infusion chemotherapy (HAI) 6 times at ADM 30 mg+5-FU 1,000 mg+MMC 16 mg between October 1999 and July 2000 for recurrent metastatic liver cancer. He has survived more than 6 years after the initial surgery. Multidisciplinary treatment with hepatic resection may well be a strategy for patients with multiple colorectal liver cancer, even though H 3 type of metastasis.

Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers.

We studied the effects of blood hematocrit (Hct), blood flow, or norepinephrine on segmental vascular resistances in isolated portally perfused rat livers. Total portal hepatic venous resistance (Rt) was assigned to the portal (Rpv), sinusoidal (Rsinus), and hepatic venous (Rhv) resistances using the portal occlusion (Ppo) and the hepatic venous occlusion (Phvo) pressures that were obtained during occlusion of the respective line. Four levels of Hct (30%, 20%, 10%, and 0%) were studied. Rpv comprises 44% of Rt, 37% of Rsinus, and 19% of Rhv in livers perfused at 30% Hct and portal venous pressure of 9.1 cmH2O. As Hct increased at a given blood flow, all three segmental vascular resistances of Rpv, Rsinus, and Rhv increased at flow >15 ml/min. As blood flow increased at a given Hct, only Rsinus increased without changes in Rpv or Rhv. Norepinephrine increased predominantly Rpv, and, to a smaller extent, Rsinus, but it did not affect Rhv. Finally, we estimated Ppo and Phvo from the double occlusion maneuver, which occluded simultaneously both the portal and hepatic venous lines. The regression line analysis revealed that Ppo and Phvo were identical with those measured by double occlusion. In conclusion, changes in blood Hct affect all three segmental vascular resistances, whereas changes in blood flow affect Rsinus, but not Rpv or Rhv. Norepinephrine increases mainly presinusoidal resistance. Ppo and Phvo can be obtained by the double occlusion method in isolated perfused rat livers.