Takako Mizuno

MR imaging of peripheral cholangiocarcinoma

A prospective study was performed to compare MR spin-echo (SE) sequences [repetition time/echo time (TR/TE) 2,000/80, 500/44 ms], unenhanced CT, and rapid intravenous contrast enhanced CT in eight consecutive patients with peripheral cholangiocarcinoma. All the tumors (ranging from 5 to 9.6 cm in size) were detected with all four techniques. Tumor contrast, however, was qualitatively greatest on long TR/TE SE images. With long TR/TE SE images, tumors were demonstrated as well-demarcated homogeneous regions of high signal intensity, and the anatomic relations between tumors and intrahepatic blood vessels were easily perceived. Detection of small intrahepatic metastatic foci was best on long TR/TE images. Tumor invasion of the portal veins branches was also best seen on long TR/TE SE images. These results indicate that long TR/TE SE sequence is the most effective initial screening method in demonstrating the presence and determining resectability of peripheral cholangiocarcinoma.

Role of endogenous platelet-activating factor in caerulein-induced acute pancreatitis in rats: Protective effects of a PAF-antagonist

The role of endogenous platelet‐activating factor (PAF) in the pathogenesis of acute pancreatitis was investigated by determining whether CV‐6209, a selective PAF‐antagonist, confers protection against caerulein‐induced acute pancreatitis in rats. Continuous intravenous infusion of caerulein (5 μg/kg x h) induced time‐dependent increase in serum pancreatic enzymes, pancreatic weight, and protein content of the pancreas, and produced histologic evidence of acute pancreatitis. Pretreatment with CV‐6209 (1 mg/kg) significantly inhibited the elevation of serum pancreatic enzymes, pancreatic weight, and protein content of the pancreas. Caerulein‐induced tissue oedema and recruitment of leucocytic cells were markedly ameliorated with CV‐6209. Platelet‐activating factor may be released endogenously and may play a role during acute pancreatitis.

Role of Endogenous Endothelin in Gastric Mucosal Injury Induced by Hemorrhagic Shock in Rats

We examined the role of endogenous endothelin in the pathogenesis of hemorrhagic shock-induced gastric mucosal injury in rats. Animals were bled to induce hypotension (20-30 mm Hg) for 20 min and the shed blood was retransfused. Rats were sacrificed at the end of hypotension, 20 min, and 60 min after retransfusion, respectively. Gastric erosions were induced with this experimental protocol. The total area of erosions was minimal only at the end of hypotension, and increased time-dependently after blood retransfusion. Plasma endothelin concentration significantly increased at the end of hypotension and persistently increased after retransfusion, whereas in gastric endothelin concentration a significant increase was observed at 60 min after retransfusion. The gastric mucosal hemodynamics as assessed by continuous measurement with reflectance spectrophotometry showed ischemia associated with congestion after retransfusion. Treatment with a monoclonal antibody against endothelin (0.2 mg/100 g BW/h) prevented these hemodynamic disturbances, rendering a significant decrease in the total area of erosions at 20 and 60 min after retransfusion. These results strongly suggest an important role of circulating endothelin in the pathogenesis of hemorrhagic shock-induced gastric mucosal injury through mucosal microcirculatory perturbation.

Cell proliferation kinetics in acetic acid-induced gastric ulcer evaluated by immunohistochemical staining of proliferating cell nuclear antigen.

A monoclonal antibody to proliferating cell nuclear antigen (PCNA) has been previously shown to be capable of identifying proliferating cells. We investigated proliferative activity in the healing process of acetic acid-induced gastric ulcer by immunohistochemical staining of PCNA and 5-bromo-2-deoxyuridine (BrdU), and the two methods were compared. Cell proliferative activity of regenerated mucosa around ulcers showed continuous acceleration for 42 days, and PCNA-labeled cells had stained nuclei as clearly discernible as those of BrdU-labeled cells. In addition, immunohistochemical staining of PCNA provided reproducible and quantifiable results without the requirement of pretreatment. We conclude that immunohistochemical staining of PCNA may represent a useful technique for analysis of proliferative activity during healing of gastric ulcers.

Anatomical variation of pancreatobiliary ducts in biliary stone diseases

Endoscopic retrograde cholangiopancreatography examinations were prospectively analyzed to determine whether anatomical variations of ductal systems have a role in the pathogenesis of cholecystolithiasis and choledocholithiasis. Included were 140 normal examinations (control group), 102 patients with cholecystolithiasis, and 68 patients with choledocholithiasis (primary stones in the common bile duct). Low entry of the cystic duct was observed frequently in patients with cholecystolithiasis (15.7% vs. 2.1% in control, p < 0.01). No preferential type of course of the cystic duct was observed in patients with cholecystolithiasis and choledocholithiasis. Separate openings of the bile and pancreatic ducts were significantly prevalent in patients with choledocholithiasis (53.5% vs. 30.6% in control, p < 0.01). Common channel was significantly short in patients with cholecystolithiasis. Incidence of juxtapapillary duodenal diverticula was significant in patients with choledocholithiasis. These observations suggest that some of the pancreatobiliary ductal anatomy may be closely implicated in the development of gallstone diseases.

Acquired intrahepatic portal vein aneurysm

With the recent improvement in imaging procedures, repor ted cases of the intrahepatic portal vein aneurysm have been increasing (1-7). The pathogenesis of the disease, however , has not been well known. It is controversial whether the disease is congenital or acquired. Some of the reported cases have been considered to be acquired, but not conclusively proven in any of the cases. Altered portal venous hemodynamics may contribute to the development of portal vein aneurysm because of the fact that a number of cases have underlying portal hyper tension (1-4). Here we report a case of intrahepatic portal vein aneurysm that was discovered in a cirrhotic patient during his medical follow-up after the treatment of esophageal varices b y endoscopic injection sclerotherapy. Periodic close observation using various imaging procedures disclosed the etiology of the acquired portal vein aneurysm. Portal blood shunting to hepatic vein via the aneurysm was also noted.

Serum platelet-activating factor acetylhydrolase activity in rats with gastric ulcers induced by water-immersion stress.

Platelet-activating factor (PAF) acetylhydrolase is an enzyme which hydrolyzes PAF to yield inactive lysoPAF. This study focused on the influence of water-immersion stress on serum PAF acetylhydrolase activity. The enzyme activity was determined by measurement of [3H]acetate produced from 1-O-alkyl-2-[3H]acetyl-sn-glycero-3-phosphocholine upon precipitation of the complex of the radioactive substrate and albumin with trichloroacetic acid. The onset of water-immersion stress caused the development of gastric lesions associated with a significant increase in serum PAF acetylhydrolase activity. Serum PAF acetylhydrolase may leak into the blood from some tissues in rats with gastric injury induced by water-immersion stress and might control the action of PAF.

Gastric Hemodynamic Disturbance Induced by Hemorrhagic Shock in Rats: Role of Platelet-Activating Factor

The role of platelet-activating factor (PAF) in the induction of rat gastric mucosal damage by ischemia-reperfusion was examined with reference to hemodynamic characteristics. Gastric mucosal hemodynamics was measured continuously, using laser-Doppler flowmetry and reflectance spectrophotometry. Not only gastric mucosal damage but also characteristic hemodynamic change--that is, ischemia with congestion--was observed in the PAF infusion and reperfusion periods of the ischemia-reperfusion model. CV-6209, a specific PAF antagonist, significantly alleviated gastric mucosal damage and hemodynamic disturbance induced by ischemia-reperfusion. These results strongly suggest that PAF is a potent mediator of gastric mucosal damage during reperfusion in the ischemia-reperfusion model.

DIFFUSE CALCIFICATION IN GASTRIC CANCER

The progressive expansion of calcification into the wall of the stomach and peritoneal metastatic foci was observed in a 31-year-old female with Borrmann type 4 calcified advanced gastric cancer. Despite treatment with systemic lentinan, uracil tegaful and mitomycin C, together with intraperitoneal injections of mitomycin C, OK-432 and prednisolone, the patient died 27 months after first presentation. The case provided a useful means of studying the mechanism of calcification.

Hepatic parenchymal changes after the intraarterial injection of lipiodol in tumor-bearing rabbits.

RATIONALE AND OBJECTIVES.The influence of lipiodol injection on hepatic morphology and function was investigated in 119 rabbits with hepatic VX2 tumors. METHODS.The rabbits were divided into the following three groups, according to the materials injected via the proper hepatic artery: group 1 received doxorubicin (Adriamycin [ADM]); group 2 received lipiodol (LPD); and group 3 received LPD plus ADM. Groups 2 and 3 were each divided into three subgroups, according to the dose of LPD injected (0.3, 0.6, and 1.2 mL). Non-tumorous regions in the tumor-bearing lobe and the tumor-free lobe were examined histologically; low-kilovolt x-ray studies and computed tomography (CT) also were performed in 84 rabbits. Liver function tests were performed in 35 rabbits. RESULTS.Elevation of the serum aminotransferase levels was observed after the administration of LPD. Hepatocellular degeneration was marked in the tumor-free lobe, but was much more severe in the tumor-bearing lobe in groups 2 and 3. The degree of degeneration depended on the dose of LPD. Both low-kilovolt x-ray studies and CT showed the heavy accumulation of LPD in the tumor-bearing lobe. CONCLUSIONS.The current study shows that the histologic and functional adverse effects of oily chemoembolization depend on the dose of LPD administered to the liver.