Experimental studies on morphological changes of microcirculation of DMN‐induced liver cirrhosis after normothermic ischemia with charge‐coupled device microscope

Shimamoto, Tsuyoshi; Mori, Yoshio; Takagi, Hisato; Yamada, Takuya; Sakamoto, Kenichi; Matsuo, Hiroshi; Nitta, Toyoo; Mizutani, Tomohiro; Iwata, Hiroji

doi:10.1046/j.1440-1746.2003.03121.x

Cited by 4 publications

(1 citation statement)

References 30 publications

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“…Dimethyl-nitrosamine induces liver necrosis and carcinogenesis by a number of mechanisms, which include calcium activated DNA fragmentation [33] and activation of metalloproteases [34] . Microcirculatory differences have been noted in DMN-induced cirrhotic livers during ischemia–reperfusion [35] and intravascular coagulation has been shown to occur in DMN-induced liver injury [36] . Our ALT and histology data suggests that a single 10 mg/kg body weight dose of DMN results in moderate liver injury within 24 h, which begins to resolve by 48 h. This is probably expected, since only a single administration was carried out, with no additional treatments which could have sustained the injury.…”

Section: Discussionmentioning

confidence: 99%

Acute liver injury induced by low dose dimethylnitrosamine alters mediators of hepatic vascular flow

et al. 2014

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Alterations in liver vascular tone play an important role in chronic liver disease. The hepatic stellate cell (HSC) and mediators such as nitric oxide (NO) and hydrogen sulfide (H2S) have been implicated in regulation of vascular tone and intra-hepatic pressure. Though these have been studied in chronic liver damage, changes in response to acute liver injury induced by hepatotoxins such as dimethyl nitrosamine are not well understood. Liver injury was induced in mice by a single intra-peritoneal injection of dimethylnitrosamine (DMN), following which animals were sacrificed at 24, 48 and 72 h. Changes in vascular mediators such as NO and H2S as well as stellate cell activation was then examined. It was found that a single low dose of DMN in mice is sufficient to induce activation of hepatic stellate cells within 24 h, accompanied by oxidative stress, compromised metabolism of H2S and decreased levels of the von Willebrand factor (vWF) cleaving protease; a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), which functions in intravascular thrombosis. A suppression of hepatic NO levels is also initiated at this time point, which progresses further and is sustained up to 72 h, at which point the HSC activation is still present. Compromised levels of ADAMTS13 and H2S metabolism however, begin to recover by 48 h and are almost similar to control by 72 h. In conclusion, these data suggest that even moderate acute insults in the liver can have far reaching consequences on a number of mediators of vascular flow in the liver.

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Section: Discussionmentioning

confidence: 99%

Acute liver injury induced by low dose dimethylnitrosamine alters mediators of hepatic vascular flow

et al. 2014

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Progress in experimental study on inhibitory effect of traditional Chinese medicine on liver fibrosis

Zhou

Wang²

2006

J Chin Integr Med

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Cordyceps mycelia extract decreases portal hypertension in rats with dimethylnitrosamine-induced liver cirrhosis: a study on its histological basis

Wang¹

2008

J Chin Integr Med

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Experimental studies on morphological changes of microcirculation of DMN‐induced liver cirrhosis after normothermic ischemia with charge‐coupled device microscope

Abstract: SD and Vv indicate microcirculatory differences and indices in the normal and cirrhotic livers in preischemia during reperfusion.

Cited by 4 publications

References 30 publications

Acute liver injury induced by low dose dimethylnitrosamine alters mediators of hepatic vascular flow

Acute liver injury induced by low dose dimethylnitrosamine alters mediators of hepatic vascular flow

Progress in experimental study on inhibitory effect of traditional Chinese medicine on liver fibrosis

Cordyceps mycelia extract decreases portal hypertension in rats with dimethylnitrosamine-induced liver cirrhosis: a study on its histological basis

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