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Biomedical subjects

S Sakisaka

Publications and source records attributed to S Sakisaka.

70 records · Page 4Linked to original sources
PubMed1993

Biliary copper excretion in acutely and chronically copper-loaded rats.

Biliary copper excretion was examined in rats with acute, continuous and chronic copper loads. Copper was excreted into bile, and the concentration peaked 40 min after a venous injection of copper sulfate (127 ng/gm body weight). The excretion was significantly inhibited by colchicine. Therefore some copper may be transported in hepatocytes by a vesicular pathway and excreted into bile. Biliary copper output increased over time and reached a plateau 180 min after a continuous venous infusion of copper sulfate (318 ng/gm body weight/hr) had started, when the concentration of copper in bile was much higher than that in plasma; the bile/plasma ratio of copper concentrations was 4.32 +/- 0.46. These data support the idea that copper transport involves a specific uptake and transport system. In chronically copper-loaded rats, hepatic copper content was significantly increased compared with controls, and reaction products for copper were observed in hepatocyte granules by light microscopic examination with p-dimethylaminobenzylidene rhodanine stain. The number of lysosomes in hepatocytes increased and the shape changed. In chronically copper-loaded rats the number of tubular lysosomes was very high. However, other organelles appeared to be normal. In these rats biliary excretion of not only copper but also acid phosphatase, a lysosomal enzyme, was significantly greater than the control. Therefore hepatocyte lysosomes may play an important role in biliary copper excretion. Furthermore, when biliary lysosomal excretion increases, the tubular lysosomes actively participate in this excretion.

Acid Phosphatase↗
PubMed1992

Comparative study of magnetic resonance imaging, computed tomography and histology in the assessment of liver iron overload.

Magnetic resonance imaging, computed tomography, and liver biopsy findings were compared in ten patients with serum ferritin levels over 500 ng/ml. The liver was observed as a low-intensity area on magnetic resonance imaging in all four patients with serum ferritin levels above 2,000 ng/ml, while no abnormalities were detected in four of the six patients with a serum ferritin level below 2,000 ng/ml. Computed tomography revealed the liver to be a high density area in five of the seven patients tested. However, it demonstrated no abnormality in a patient with steatosis despite a high serum ferritin concentration. Liver biopsy demonstrated iron deposits in nine of the ten patients. These findings indicate that liver biopsy remains the most accurate mean of detection of liver iron overload. Both magnetic resonance imaging and computed tomography could be used to be monitor the progress of a patient with liver iron overload treated by phlebotomy.

Adult↗
PubMed1992

Ultrastructure of intracellular membranous system and intracellular transport of asialoglycoproteins in rat hepatocytes.

The ultrastructure of the intracellular membranous system in rat hepatocytes was observed three dimensionally with a scanning electron microscope using the aldehyde prefix osmium-dimethyl sulfoxide-osmium method. Intracellular organelles were clearly observed in three dimensions, and direct connection of tubular structures with the bile canalicular membrane was clearly seen. The transcellular pathway of asialoglycoproteins in isolated cultured rat hepatocytes was also investigated, by affinity cytochemistry, using gold-conjugated asialofetuin, under a transmission electron microscope. Gold particles were clearly seen not only in vesicles, endosomes and lysosomes, but also in the tubular structures. These results suggest that the tubular structures in rat hepatocytes directly participate in the transcellular transport of macromolecules. In addition, the frequent connections of tubular structures with the bile canalicular membrane indicate that these structures around the bile canaliculus may supply membrane components to the bile canalicular membrane.

Animals↗
PubMed1991

Effect of UDCA on intracellular and biliary pH in isolated rat hepatocyte couplets and perfused livers.

To study how ursodeoxycholic acid (UDCA) increases biliary HCO3- concentration and alkalinizes bile, intracellular pH (pHi) and canalicular pH (pHc) were measured microfluorimetrically in isolated rat hepatocyte couplets (IRHC). Isolated perfused rat livers (IPRL) were also used to assess the roles of Cl-, HCO3-, and zone III hepatocytes. In IRHC, UDCA diminished pHi only when HCO3- was omitted. pHi recovery was inhibited by amiloride. UDCA did not affect pHi recovery from an acid load (NH4Cl) nor modify pHc (+HCO3-). In IPRL, biliary HCO3- concentration increased following UDCA despite removal of Cl- (to inhibit Cl(-)-HCO3- exchanger) or destruction of zone III hepatocytes with digitonin. Moreover, when HCO3- was omitted from the perfusate, biliary pH rose following UDCA even though the hypercholeresis was abolished. Thus 1) hepatic UDCA uptake represents an acid load that is counteracted by Na(+)-H+ exchange when HCO3- is absent; 2) UDCA does not alkalinize pHc; and 3) alkalinization of biliary pH in IPRL is not HCO3- dependent, does not involve Cl(-)-HCO3- exchange, or zonal differences in UDCA metabolism or excretion. UDCA appears to alkalinize bile by protonation within the bile duct lumen. UDCAH may then cross the biliary epithelium.

Animals↗
PubMed1988

Tubulovesicular transcytotic pathway in isolated rat hepatocyte couplets in culture. Effect of colchicine and taurocholate.

Isolated rat hepatocyte couplets in short-term culture (6 h) were labeled for 3 min with horseradish peroxidase (HRP) to characterize the transcytotic vesicle transport pathway in this cell culture system that retained an "apical" canalicular membrane polarity. Microtubules were identified with monoclonal antibodies to beta-tubulin and fluorescein iso-thiocyanate-labeled goat-antimouse antibody and were concentrated in the apical domain, a structural polarity that was eliminated by pretreatment with colchicine. In control cells, HRP immediately labeled vesicles and tubules in the submembrane regions of the periphery of the cell. Within 10 min tubules and vesicles were prominently labeled in pericanalicular regions, a process blocked by colchicine but not by lumicolchine or taurocholate administration. A quantitative morphometric analysis utilizing a Zeiss Videoplan-2 image analyzer established that (a) HRP-containing structures increased in density, area, length, and diameter in the pericanalicular region by 10 min; (b) colchicine, but not lumicolchicine, pretreatment diminished their density, area, and length; and (c) taurocholate (50 microM), a choleretic and biliary lipid-stimulating bile acid, had no effect on HRP density or percentage of area in the pericanalicular region, but decreased the diameter of the pericanalicular HRP-containing structures and increased the percentage of tubules containing HRP from 29% to 40%. Tubules were particularly prominent in thick sections (400 nm) in both peripheral and pericanalicular regions and were viewed as continuous anastomosing linear arrays in stereo-paired micrographs. These studies established that isolated rat hepatocyte couplets maintain a highly polarized tubulovesicular transcytotic pathway in short-term culture that is micro-tubule-dependent. Taurocholate stimulates the transformation of tubules from vesicles in this isolated rat hepatocyte couplet system.

Animals↗
PubMed1986

Demonstration of a transcellular vesicle pathway for biliary excretion of inulin in rat liver.

We tested the hypothesis that the blood to bile transport of hydrophilic inert nonelectrolytes such as inulin is mediated in part by a transcellular pathway involving endosomelike vesicles (transcytosis). Forty minutes after intravenous injection of [3H]methoxyinulin into renal pedicle ligated rats, 0.8% of the radioactivity was recovered in liver homogenate and 85% +/- 3.6% of this radioactivity was associated with membrane bound vesicles. Subcellular fractionation studies and electron microscopy confirmed this association. If rats were treated with taurochenodeoxycholic acid, 5 mumol/100 g body wt, the hepatocellular uptake of [3H]methoxyinulin increased approximately twofold and [3H]methoxyinulin was again recovered in small subcellular vesicles. Furthermore, taurochenodeoxycholic acid also stimulated the biliary excretion of [3H]methoxyinulin, which peaked in bile at 20 min. Taurochenodeoxycholic acid had similar effects on the biliary excretion of horseradish peroxidase, a protein known to be transported from blood to bile by membrane vesicles. Thus under the conditions of these experiments, the dihydroxy bile acid taurochenodeoxycholic acid can stimulate the rate of vesicle-dependent transcellular transport into bile. If inulin clearance represents a maximal estimate of this process, only 6%-8% of total bile production in the rat under basal conditions would be mediated by vesicle-mediated transcytosis.

Animals↗
PubMedDate not supplied

Budd-Chiari syndrome complicated by hepatocellular carcinoma with no evidence of infection with hepatitis virus: a case report.

Hepatocellular carcinoma occurs in patients with Budd-Chiari syndrome. However, the etiology of hepatocellular carcinoma accompanied with Budd-Chiari syndrome has not been elucidated. We report a case of Budd-Chiari syndrome with membranous obstruction of the inferior vena cava complicated by hepatocellular carcinoma in an 80 year-old man. There was no evidence of co-infection with hepatitis A, B, C, D, E, and G virus. Histologically, the non-cancerous liver tissue showed chronic venous congestion with no evidence of hepatitis virus-associated liver cirrhosis. This case suggests that chronic venous congestion of the liver may be one of the pathologic conditions that occurs in hepatocellular carcinoma.

Aged↗
PubMedDate not supplied

Successful treatment for bronchial bleeding from invasive pulmonary metastasis of hepatocellular carcinoma: a case report.

Pulmonary metastasis is frequently seen in patients with advanced hepatocellular carcinoma. However, information is limited concerning life-threatening complications and effective treatment of pulmonary metastasis because of the poor prognosis of patients with advanced hepatocellular carcinoma. Recent remarkable progress in detection and treatment of hepatocellular carcinoma has improved prognosis, making management of pulmonary metastasis an important clinical issue. We describe a 68-year-old man with pulmonary metastasis of hepatocellular carcinoma and sudden onset of hemoptysis from bronchial invasion. Transcatheter embolization was performed successfully via the bronchial artery with disappearance of bloody sputum. Peribronchial pulmonary metastasis of hepatocellular carcinoma can cause life-threatening hemoptysis. Transcatheter arterial embolization may be one of therapeutics for hemoptysis from invasive pulmonary metastasis of hepatocellular carcinoma.

Aged↗
PubMedDate not supplied

Biliary secretion of endotoxin and pathogenesis of primary biliary cirrhosis.

Previous studies suggested endotoxin, derived from the intestine through the portal blood to the liver, was predominantly metabolized by Kupffer cells. In the present study, fluorescent-labeled endotoxin injected into the rat portal vein was demonstrated not only in Kupffer cells but also in hepatocytes. Furthermore a great amount of labeled endotoxin was recovered in bile. In the livers of patients with primary biliary cirrhosis (PBC), immunohistochemistry demonstrated significant retention of endotoxin in the biliary epithelial cells, and treatment with ursodeoxycholic acid significantly reduced the retention in those cells. The study for detection of apoptosis demonstrated increased rates of apoptosis in hepatocytes and biliary epithelial cells in PBC liver, and the rate of apoptosis in biliary epithelial cells was significantly reduced after treatment with ursodeoxycholic acid. Immunohistochemistry in PBC liver demonstrated significant reduction of fluorescence intensity for a 7H6 antigen in biliary epithelial cells, indicating the increased paracellular permeability of bile ducts, because cellular immunolocalization of that antigen has been shown to be inversely correlated with the paracellular permeability of the tight junction. These results suggest that, in biliary epithelial cells, retention of endotoxin, increased apoptosis, and increased permeability of tight junctions may be involved in the pathogenesis of PBC.

Animals↗