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Masayuki Imamura - One of the best experts on this subject based on the ideXlab platform.

  • Involvement of thromboxane A2-thromboxane A2 receptor system of the Hepatic Sinusoid in pathogenesis of cold preservation/reperfusion injury in the rat liver graft.
    Transplantation, 1995
    Co-Authors: Satoshi Ishiguro, Shigeki Arii, Kazunobu Monden, Shin Ichi Fujita, Toshio Nakamura, Mototaka Niwano, Tomika Harada, Fijmitaka Ushikubi, Shuh Narumiya, Masayuki Imamura
    Abstract:

    This study was designed to investigate the possible involvement of the thromboxane A2 (TXA2)-TXA2 receptor (TXA2R) system of the Hepatic Sinusoid in cold preservation/reperfusion injury in liver grafts. Rat livers were preserved in cold University of Wisconsin solution for either 6 or 24 hr. The number of TXARs in Sinusoidal endothelial cells isolated from 0-, 6-, and 24-hr preserved liver specimens was 22.50±1.80×10 3 / cell 12.66±1.00×10 3 /cell, and 4.17±0.65×10 3 /cell, respectively. Kd and Bmax at 0 hr, 6 hr, and 24 hr of preservation were 8.54±1.26 nM and 37.34±3.01 fmol/ 10 6 cells, 7.08±1.14 nM and 12.66±1.00 fmol/10 6 cells, and 1.91±0.10 nM and 3.88±0.59 fmol/10 6 cells, respectively. The administration of OKY-046 (inhibitor of TXA2 synthesis) to the University of Wisconsin solution suppressed this reduction in TXA2R number. Furthermore, the concentration of TXA2 in Hepatic Sinusoid was decreased by OKY-046. In a reperfusion experiment, liver tissue preserved for 24 hr exhibited a higher reperfusion pressure, and effluent levels of both aspartate aminotransferase and lactate dehydrogenase were markedly elevated. The addition of OKY-046 to the preservation solution, however, prevented the rise in reperfusion pressure almost completely and the increase in effluent enzyme levels. This study showed that the TXA2Rs in Sinusoidal endothelial cells were internalized through binding with TXA2 during cold preservation, causing activation of the TXA2-TXA2R system. This activation apparently induces an increase in reperfusion pressure, possibly due to Sinusoidal contraction, resulting in microcirculatory disturbances. Thus, the TXA2-TXA2R system in the Hepatic Sinusoid may be one of the major mechanisms of cold preservation/reperfusion injury in the liver graft

  • involvement of thromboxane a2 thromboxane a2 receptor system of the Hepatic Sinusoid in pathogenesis of cold preservation reperfusion injury in the rat liver graft
    Transplantation, 1995
    Co-Authors: Satoshi Ishiguro, Shigeki Arii, Kazunobu Monden, Shin Ichi Fujita, Toshio Nakamura, Mototaka Niwano, Tomika Harada, Fijmitaka Ushikubi, Shuh Narumiya, Masayuki Imamura
    Abstract:

    This study was designed to investigate the possible involvement of the thromboxane A2 (TXA2)-TXA2 receptor (TXA2R) system of the Hepatic Sinusoid in cold preservation/reperfusion injury in liver grafts. Rat livers were preserved in cold University of Wisconsin solution for either 6 or 24 hr. The number of TXARs in Sinusoidal endothelial cells isolated from 0-, 6-, and 24-hr preserved liver specimens was 22.50±1.80×10 3 / cell 12.66±1.00×10 3 /cell, and 4.17±0.65×10 3 /cell, respectively. Kd and Bmax at 0 hr, 6 hr, and 24 hr of preservation were 8.54±1.26 nM and 37.34±3.01 fmol/ 10 6 cells, 7.08±1.14 nM and 12.66±1.00 fmol/10 6 cells, and 1.91±0.10 nM and 3.88±0.59 fmol/10 6 cells, respectively. The administration of OKY-046 (inhibitor of TXA2 synthesis) to the University of Wisconsin solution suppressed this reduction in TXA2R number. Furthermore, the concentration of TXA2 in Hepatic Sinusoid was decreased by OKY-046. In a reperfusion experiment, liver tissue preserved for 24 hr exhibited a higher reperfusion pressure, and effluent levels of both aspartate aminotransferase and lactate dehydrogenase were markedly elevated. The addition of OKY-046 to the preservation solution, however, prevented the rise in reperfusion pressure almost completely and the increase in effluent enzyme levels. This study showed that the TXA2Rs in Sinusoidal endothelial cells were internalized through binding with TXA2 during cold preservation, causing activation of the TXA2-TXA2R system. This activation apparently induces an increase in reperfusion pressure, possibly due to Sinusoidal contraction, resulting in microcirculatory disturbances. Thus, the TXA2-TXA2R system in the Hepatic Sinusoid may be one of the major mechanisms of cold preservation/reperfusion injury in the liver graft

Jae Ho Byun - One of the best experts on this subject based on the ideXlab platform.

  • Three-Dimensional Imaging of Hepatic Sinusoids in Mice Using Synchrotron Radiation Micro-Computed Tomography
    2016
    Co-Authors: Yae Jin Yoon, Soeun Chang, Bo-kyeong Kang, Jae Ho Byun, Jaesung Park, Oh Youn Kim, Jae-hong Lim, Yun Huang, Yoon-keun Kim, Yong Song Gho
    Abstract:

    Hepatic Sinusoid, the smallest vessel in the liver, plays important roles in Hepatic microcirculation. Although the structure of the Hepatic Sinusoids affects diverse functions of the liver, little is known about morphological alterations in the Sinusoids under pathological conditions. In this study, we show that the structure of Hepatic Sinusoids can be identified three-dimensionally in normal and carbon tetrachloride-injured mouse liver, using the absorption mode of synchrotron radiation micro-computed tomography. We observed that the Hepatic Sinusoidal structure on tomographic slice images was similar to that on histological images of normal and acutely injured mice. Moreover, centrilobular necrosis and structural alterations of the Sinusoids in the necrotic region were detectable on tomographic slice and volume-rendered images of the acutely injured mice. Furthermore, quantitative analyses on 3D volume-rendered images of the injured Sinusoid revealed decrease in the volume of the Sinusoid and connectivity of the Sinusoidal network. Our results suggest that the use of synchrotron radiation micro-computed tomography may improve our understanding of the pathogenesis of Hepatic diseases by detecting the Hepatic Sinusoids and thei

  • Three-dimensional imaging of Hepatic Sinusoids in mice using synchrotron radiation micro-computed tomography.
    PLOS ONE, 2013
    Co-Authors: Yae Jin Yoon, Soeun Chang, Bo-kyeong Kang, Jung Yun Huang, Jaesung Park, Jae Ho Byun
    Abstract:

    Hepatic Sinusoid, the smallest vessel in the liver, plays important roles in Hepatic microcirculation. Although the structure of the Hepatic Sinusoids affects diverse functions of the liver, little is known about morphological alterations in the Sinusoids under pathological conditions. In this study, we show that the structure of Hepatic Sinusoids can be identified three-dimensionally in normal and carbon tetrachloride-injured mouse liver, using the absorption mode of synchrotron radiation micro-computed tomography. We observed that the Hepatic Sinusoidal structure on tomographic slice images was similar to that on histological images of normal and acutely injured mice. Moreover, centrilobular necrosis and structural alterations of the Sinusoids in the necrotic region were detectable on tomographic slice and volume-rendered images of the acutely injured mice. Furthermore, quantitative analyses on 3D volume-rendered images of the injured Sinusoid revealed decrease in the volume of the Sinusoid and connectivity of the Sinusoidal network. Our results suggest that the use of synchrotron radiation micro-computed tomography may improve our understanding of the pathogenesis of Hepatic diseases by detecting the Hepatic Sinusoids and their alterations in three-dimensional structures of the damaged liver.

Hirokazu Yokoyama - One of the best experts on this subject based on the ideXlab platform.

  • Superoxide anion release into the Hepatic Sinusoid after an acute ethanol challenge and its attenuation by Kupffer cell depletion.
    Alcoholism clinical and experimental research, 1999
    Co-Authors: Hirokazu Yokoyama, Takeshi Mizukami, Yoshitaka Kamegaya, Masahiko Fukuda, Yukishige Okamura, Shinzo Kato, Hideki Ohgo, Hiromasa Ishii
    Abstract:

    Superoxide anion release into the Hepatic Sinusoids and subsequent damage to the endothelial cells of the Hepatic Sinusoids after ethanol challenge was examined. A 250 mg/kg body weight/hr dose of ethanol was given to rats for 3 hr, and superoxide anion release into the Hepatic Sinusoids was examined in a liver perfusion model using the cytochrome c method. Ethanol treatment resulted in superoxide anion release into the Hepatic Sinusoids (0.20 ± 0.01 vs. 0.12 ± 0.02 o.d., p < 0.05) and an increase in the purine nucleoside phosphorylase/alanine aminotransferase ratio in the liver perfusate, a marker of damage to the endothelial cells of the Hepatic Sinusoids (0.003 ± 0.002 vs. 0.008 ± 0.002; p < 0.05). Tumor necrosis factor-alpha was not detectable in either group, and there were no significant differences in the population of Hepatic macrophages, leukocytes, or Kupffer cells between the two groups. To clarify the role of Kupffer cells in the mechanism, 10 mg/kg of body weight of gadolinium chloride was given to rats twice, 24 hr apart, resulting in depletion of ED2-positive cells from the Hepatic lobules. The superoxide anion release after the ethanol challenge was significantly attenuated in the Kupffer cell-depleted rats, compared with the controls (0.14 ± 0.02;p < 0.05, compared with ethanol alone). The change was associated with a significant decrease in the purine nucleoside phosphorylase/alanine aminotransferase ratio in the liver perfusate (0.004 ± 0.002; p < 0.05, compared with ethanol alone). Ethanol causes superoxide anion release into the Hepatic Sinusoid and subsequent damage to the Sinusoidal endothelial cells. These changes were reduced by Kupffer cell depletion. This supports the view that Kupffer cell depletion has a protective effect on ethanol-induced liver injury.

  • Formation of superoxide anion in the Hepatic Sinusoid after lipopolysaccharide challenge
    Alcoholism clinical and experimental research, 1998
    Co-Authors: Hirokazu Yokoyama, Takeshi Mizukami, Yoshitaka Kamegaya, Masahiko Fukuda, Yukishige Okamura, Michinaga Matsumoto, Shinzo Kato, Hiromasa Ishii
    Abstract:

    Using the cytochrome c method, superoxide anion that is released into the Hepatic Sinusoid was measured after a lipopolysaccharide challenge in a liver perfusion system. Moreover, damages of epithelial cells of the Hepatic Sinusoid were estimated with scanning electron microscopic analysis and levels of purine nucleoside phosphorylase/GPT ratio. Lipopclysacchadde administration increased the conversion of oxidized cytochrome c into reduced cytochrome c in the perfusate, indicating that superoxide anion was formed in the Hepatic Sinusoid. This change was associated with increase in levels of portal tumor necrosis factor-a and attenuated by the simultaneous administration of superoxide dismutase. Scanning electron microscope analysis revealed that diameters of Sinusoidal fenestrae increased in rats treated with lipopolysaccharide, compared with controls. Moreover, levels of purine nucleoside phosphorylase/GPT ratio was significantly increased in the liver perfusate in lipopolysaccharide-treated rats, compared with controls. Superoxide anion in Hepatic Sinusoid may be one of the pathogenic factors behind damages of epithelial cells of the Hepatic Sinusoid caused by lipopolysaccharide.

  • Effect of chronic ethanol feeding on endotoxin-induced Hepatic injury: role of adhesion molecules on leukocytes and Hepatic Sinusoid
    Alcoholism clinical and experimental research, 1998
    Co-Authors: Eiji Ohki, Takeshi Mizukami, Masahiko Fukuda, Yukishige Okamura, Michinaga Matsumoto, Shinzo Kato, Hideki Ohgo, Hironao Tamai, Hidekazu Suzuki, Hirokazu Yokoyama
    Abstract:

    Endotoxin is postulated to be an important aggravating factor for alcoholic liver disease. We have previously reported that rats fed ethanol are more vulnerable to endotoxin-induced liver damage, and Hepatic microcirculatory disturbance plays an important role for this liver damage by observation with an intravital microscopy. In this study, we have investigated the role of adhesion molecules in endotoxin-induced microcirculatory disturbance in chronic ethanol-fed rats. Male Wistar rats were pair-fed with ethanol liquid diet (ethanol group) or an isocaloric control diet (control group) for 6 weeks. Leukocyte adherence to the Hepatic Sinusoid by stimulation with lipopolysaccharides (1 mg/kg of body weight) was observed by an inverted fluorescence microscopy equipped with a silicon-intensified target camera and was found to be enhanced in ethanol-fed rats. Tumor necrosis factor-α and GRO/CINC-1 (rat counterpart of interleukin-8) was increased in the blood in these animals. Subsequent expression of adhesion molecules, LFA-1 β-chain on leukocytes were demonstrated by flow cytometry, which suggests a possible involvement of leukocyte adherence to the Hepatic damage in ethanol-fed animals. Preadministration of anti-rat LFA-1 β-chain monoclonal antibody effectively suppressed leukocyte adherence to the Hepatic Sinusoid. These results suggest that the enhanced sequestration of neutrophils to the liver with these adhesion molecules may play a significant role in the pathogenesis of alcoholic liver disease.

  • Induction of NADPH Cytochrome P-450 Reductase in Kupffer Cells After Chronic Ethanol Consumption Associated with Increase of Superoxide Anion Formation
    Oxygen Homeostasis and Its Dynamics, 1998
    Co-Authors: Hirokazu Yokoyama, Takeshi Mizukami, Masahiko Fukuda, Yukishige Okamura, Michinaga Matsumoto, Hidekazu Suzuki, Yasutada Akiba, Hiromasa Ishii
    Abstract:

    Using native polyacrylamide gel electrophoresis (PAGE) and diaphorase staining, NADPH cytochrome c P-450 reductase was examined in the Kupffer cells of rats fed ethanol chronically as well as in controls. Formation of superoxide anion released from Kupffer cells into the Hepatic Sinusoid was estimated using the cytochrome c method, which was applied to a liver perfusion model in both groups after an additional acute ethanol challenge. Kupffer cells were found to carry NADPH cytochrome c P-450 reductase, and chronic ethanol consumption resulted in its induction being doubled. This change was associated with increase of superoxide anion release from Kupffer cells into the Hepatic Sinusoid after an acute ethanol challenge (0.020 ± 0.03 O.D./g liver versus 0.012 ± 0.002 O.D./g liver; P < .05). In conclusion, release of superoxide anion from Kupffer cells into the Hepatic Sinusoid increases in rats chronically fed ethanol. Induction of NADPH reductase in Kupffer cells caused by chronic ethanol consumption may, at least in part, be involved in this mechanism.

Hiromasa Ishii - One of the best experts on this subject based on the ideXlab platform.

  • Superoxide anion release into the Hepatic Sinusoid after an acute ethanol challenge and its attenuation by Kupffer cell depletion.
    Alcoholism clinical and experimental research, 1999
    Co-Authors: Hirokazu Yokoyama, Takeshi Mizukami, Yoshitaka Kamegaya, Masahiko Fukuda, Yukishige Okamura, Shinzo Kato, Hideki Ohgo, Hiromasa Ishii
    Abstract:

    Superoxide anion release into the Hepatic Sinusoids and subsequent damage to the endothelial cells of the Hepatic Sinusoids after ethanol challenge was examined. A 250 mg/kg body weight/hr dose of ethanol was given to rats for 3 hr, and superoxide anion release into the Hepatic Sinusoids was examined in a liver perfusion model using the cytochrome c method. Ethanol treatment resulted in superoxide anion release into the Hepatic Sinusoids (0.20 ± 0.01 vs. 0.12 ± 0.02 o.d., p < 0.05) and an increase in the purine nucleoside phosphorylase/alanine aminotransferase ratio in the liver perfusate, a marker of damage to the endothelial cells of the Hepatic Sinusoids (0.003 ± 0.002 vs. 0.008 ± 0.002; p < 0.05). Tumor necrosis factor-alpha was not detectable in either group, and there were no significant differences in the population of Hepatic macrophages, leukocytes, or Kupffer cells between the two groups. To clarify the role of Kupffer cells in the mechanism, 10 mg/kg of body weight of gadolinium chloride was given to rats twice, 24 hr apart, resulting in depletion of ED2-positive cells from the Hepatic lobules. The superoxide anion release after the ethanol challenge was significantly attenuated in the Kupffer cell-depleted rats, compared with the controls (0.14 ± 0.02;p < 0.05, compared with ethanol alone). The change was associated with a significant decrease in the purine nucleoside phosphorylase/alanine aminotransferase ratio in the liver perfusate (0.004 ± 0.002; p < 0.05, compared with ethanol alone). Ethanol causes superoxide anion release into the Hepatic Sinusoid and subsequent damage to the Sinusoidal endothelial cells. These changes were reduced by Kupffer cell depletion. This supports the view that Kupffer cell depletion has a protective effect on ethanol-induced liver injury.

  • Formation of superoxide anion in the Hepatic Sinusoid after lipopolysaccharide challenge
    Alcoholism clinical and experimental research, 1998
    Co-Authors: Hirokazu Yokoyama, Takeshi Mizukami, Yoshitaka Kamegaya, Masahiko Fukuda, Yukishige Okamura, Michinaga Matsumoto, Shinzo Kato, Hiromasa Ishii
    Abstract:

    Using the cytochrome c method, superoxide anion that is released into the Hepatic Sinusoid was measured after a lipopolysaccharide challenge in a liver perfusion system. Moreover, damages of epithelial cells of the Hepatic Sinusoid were estimated with scanning electron microscopic analysis and levels of purine nucleoside phosphorylase/GPT ratio. Lipopclysacchadde administration increased the conversion of oxidized cytochrome c into reduced cytochrome c in the perfusate, indicating that superoxide anion was formed in the Hepatic Sinusoid. This change was associated with increase in levels of portal tumor necrosis factor-a and attenuated by the simultaneous administration of superoxide dismutase. Scanning electron microscope analysis revealed that diameters of Sinusoidal fenestrae increased in rats treated with lipopolysaccharide, compared with controls. Moreover, levels of purine nucleoside phosphorylase/GPT ratio was significantly increased in the liver perfusate in lipopolysaccharide-treated rats, compared with controls. Superoxide anion in Hepatic Sinusoid may be one of the pathogenic factors behind damages of epithelial cells of the Hepatic Sinusoid caused by lipopolysaccharide.

  • Induction of NADPH Cytochrome P-450 Reductase in Kupffer Cells After Chronic Ethanol Consumption Associated with Increase of Superoxide Anion Formation
    Oxygen Homeostasis and Its Dynamics, 1998
    Co-Authors: Hirokazu Yokoyama, Takeshi Mizukami, Masahiko Fukuda, Yukishige Okamura, Michinaga Matsumoto, Hidekazu Suzuki, Yasutada Akiba, Hiromasa Ishii
    Abstract:

    Using native polyacrylamide gel electrophoresis (PAGE) and diaphorase staining, NADPH cytochrome c P-450 reductase was examined in the Kupffer cells of rats fed ethanol chronically as well as in controls. Formation of superoxide anion released from Kupffer cells into the Hepatic Sinusoid was estimated using the cytochrome c method, which was applied to a liver perfusion model in both groups after an additional acute ethanol challenge. Kupffer cells were found to carry NADPH cytochrome c P-450 reductase, and chronic ethanol consumption resulted in its induction being doubled. This change was associated with increase of superoxide anion release from Kupffer cells into the Hepatic Sinusoid after an acute ethanol challenge (0.020 ± 0.03 O.D./g liver versus 0.012 ± 0.002 O.D./g liver; P < .05). In conclusion, release of superoxide anion from Kupffer cells into the Hepatic Sinusoid increases in rats chronically fed ethanol. Induction of NADPH reductase in Kupffer cells caused by chronic ethanol consumption may, at least in part, be involved in this mechanism.

Satoshi Ishiguro - One of the best experts on this subject based on the ideXlab platform.

  • Involvement of thromboxane A2-thromboxane A2 receptor system of the Hepatic Sinusoid in pathogenesis of cold preservation/reperfusion injury in the rat liver graft.
    Transplantation, 1995
    Co-Authors: Satoshi Ishiguro, Shigeki Arii, Kazunobu Monden, Shin Ichi Fujita, Toshio Nakamura, Mototaka Niwano, Tomika Harada, Fijmitaka Ushikubi, Shuh Narumiya, Masayuki Imamura
    Abstract:

    This study was designed to investigate the possible involvement of the thromboxane A2 (TXA2)-TXA2 receptor (TXA2R) system of the Hepatic Sinusoid in cold preservation/reperfusion injury in liver grafts. Rat livers were preserved in cold University of Wisconsin solution for either 6 or 24 hr. The number of TXARs in Sinusoidal endothelial cells isolated from 0-, 6-, and 24-hr preserved liver specimens was 22.50±1.80×10 3 / cell 12.66±1.00×10 3 /cell, and 4.17±0.65×10 3 /cell, respectively. Kd and Bmax at 0 hr, 6 hr, and 24 hr of preservation were 8.54±1.26 nM and 37.34±3.01 fmol/ 10 6 cells, 7.08±1.14 nM and 12.66±1.00 fmol/10 6 cells, and 1.91±0.10 nM and 3.88±0.59 fmol/10 6 cells, respectively. The administration of OKY-046 (inhibitor of TXA2 synthesis) to the University of Wisconsin solution suppressed this reduction in TXA2R number. Furthermore, the concentration of TXA2 in Hepatic Sinusoid was decreased by OKY-046. In a reperfusion experiment, liver tissue preserved for 24 hr exhibited a higher reperfusion pressure, and effluent levels of both aspartate aminotransferase and lactate dehydrogenase were markedly elevated. The addition of OKY-046 to the preservation solution, however, prevented the rise in reperfusion pressure almost completely and the increase in effluent enzyme levels. This study showed that the TXA2Rs in Sinusoidal endothelial cells were internalized through binding with TXA2 during cold preservation, causing activation of the TXA2-TXA2R system. This activation apparently induces an increase in reperfusion pressure, possibly due to Sinusoidal contraction, resulting in microcirculatory disturbances. Thus, the TXA2-TXA2R system in the Hepatic Sinusoid may be one of the major mechanisms of cold preservation/reperfusion injury in the liver graft

  • involvement of thromboxane a2 thromboxane a2 receptor system of the Hepatic Sinusoid in pathogenesis of cold preservation reperfusion injury in the rat liver graft
    Transplantation, 1995
    Co-Authors: Satoshi Ishiguro, Shigeki Arii, Kazunobu Monden, Shin Ichi Fujita, Toshio Nakamura, Mototaka Niwano, Tomika Harada, Fijmitaka Ushikubi, Shuh Narumiya, Masayuki Imamura
    Abstract:

    This study was designed to investigate the possible involvement of the thromboxane A2 (TXA2)-TXA2 receptor (TXA2R) system of the Hepatic Sinusoid in cold preservation/reperfusion injury in liver grafts. Rat livers were preserved in cold University of Wisconsin solution for either 6 or 24 hr. The number of TXARs in Sinusoidal endothelial cells isolated from 0-, 6-, and 24-hr preserved liver specimens was 22.50±1.80×10 3 / cell 12.66±1.00×10 3 /cell, and 4.17±0.65×10 3 /cell, respectively. Kd and Bmax at 0 hr, 6 hr, and 24 hr of preservation were 8.54±1.26 nM and 37.34±3.01 fmol/ 10 6 cells, 7.08±1.14 nM and 12.66±1.00 fmol/10 6 cells, and 1.91±0.10 nM and 3.88±0.59 fmol/10 6 cells, respectively. The administration of OKY-046 (inhibitor of TXA2 synthesis) to the University of Wisconsin solution suppressed this reduction in TXA2R number. Furthermore, the concentration of TXA2 in Hepatic Sinusoid was decreased by OKY-046. In a reperfusion experiment, liver tissue preserved for 24 hr exhibited a higher reperfusion pressure, and effluent levels of both aspartate aminotransferase and lactate dehydrogenase were markedly elevated. The addition of OKY-046 to the preservation solution, however, prevented the rise in reperfusion pressure almost completely and the increase in effluent enzyme levels. This study showed that the TXA2Rs in Sinusoidal endothelial cells were internalized through binding with TXA2 during cold preservation, causing activation of the TXA2-TXA2R system. This activation apparently induces an increase in reperfusion pressure, possibly due to Sinusoidal contraction, resulting in microcirculatory disturbances. Thus, the TXA2-TXA2R system in the Hepatic Sinusoid may be one of the major mechanisms of cold preservation/reperfusion injury in the liver graft