Liver Injury Following Long-Term Administration of Large Doses of Sake to Rats

The hepatotoxic effect on rats of long-term (55 weeks) administration of sake (a rice wine, 17% ethanol by volume) at large doses (average 12.6 g ethanol/kg body weight/day) was investigated in order to gain an insight into the reasons for the high incidence of liver fibrosis in Japanese alcoholics. Rats grew favorably under the experimental conditions, and daily variations in blood ethanol and acetaldehyde levels ranged from 3.8 to 21.1 mM and from O to 3.5 μM, respectively. Fatty and fibrotic liver was shown histologically and biochemically in sake-administered rats

Plasma branched chain amino acid abnormalities in sake-treated rats.

Plasma amino acid abnormalities in rats treated with large doses of sake and whisky for 3 days were investigated under adequate nutritional conditions. A significant decrease in plasma branched-chain amino acid (BCAA) levels was observed in sake- but not whisky-treated rats. However, known factors affecting BCAA levels, such as serum insulin and plasma glucagon levels ahd BCAA-metabolizing enzyme (BCAA transaminase and branched chain alpha-ketoacid dehydrogenase) activities in the liver and skeletal muscle, were not significantly altered in the sake group. Furthermore, ethanol-metabolizing enzyme (alcohol and aldehyde dehydrogenases and the microsomal ethanol-oxidizing system) activities in the liver were not altered in the sake group. Other mechanisms need to be considered for explaining the diminished levels of plasma BCAA in sake-treated rats.</p

Potentiation of carbon tetrachloride hepatotoxicity by beta-phenethyl alcohol.

Carbon tetrachloride (CCl4)-induced hepatotoxicity was potentiated by pretreatment with beta-phenethyl alcohol, abundantly present in sake. The injury was determined by serum GPT levels and histological examination. Similar results were observed in ethanol- and phenobarbital-pretreated rats. Acetaminophen-induced hepatotoxicity was not accentuated by beta-phenethyl alcohol or ethanol pretreatment. The activities of liver microsomal enzymes, such as cytochrome P-450, cytochrome b5 reductase, aniline hydroxylase and aminopyrine demethylase, were not altered in beta-phenethyl alcohol-pretreated rats. Thus, CCl4-induced hepatotoxicity potentiation by beta-phenethyl alcohol administration is postulated to be due to a mechanism other than increased free radical generation.</p

Very Low-pressure Hydrocephalus: A New Clinical Entity and Issues of Treatment

Secondary normal pressure hydrocephalus (NPH) frequently occurs after severe head injury and cerebrovascular disease. This condition is usually treated by surgically implanting a cerebrospinal fluid (CSF) shunt with a pressure-setting valve or programmable valve. However, some patients do not respond to the shunt operation. Among these non-responders, we found 7 patients whose pressure-setting shunts were mechanically patent, but were not functioning due to very low intracranial pressure (ICP). In these 7 cases, continuous ICP monitoring indicated low pressure with occasional negative pressure, and the patients\u27 consciousness improved during negative-pressure CSF drainage. We performed shunt revisions with zero setting on-off valves, which raised the mean functional independence measure (FIM) scores from 26 to 62. Four patients in a persistent vegetative state (PVS) regained their ability to communicate and recovered to the level of severely disabled (SD). We propose very low-pressure hydrocephalus (VLPH) as a new clinical entity, and describe the process of diagnosis and treatment

Cerebral edema associated with acute hepatic failure.

The clinicopathological findings of cerebral edema were investigated in patients with acute hepatic failure autopsied at Okayama University Hospital between 1970 and 1980 retrospectively. Nine (64%) of 14 hepatic failure cases were found to have cerebral edema during a post-mortem examination of the brain. Clinical features of the patients with cerebral edema were not significantly different from those of the patients without cerebral edema. However, general convulsions were observed more frequently in patients later found to have cerebral edema. Moreover, the length of time from deep coma to death was much shorter in the brain edema cases with cerebral herniation than without herniation.</p

Detection of type V collagen-degrading enzyme activity in human liver.

&lt;p&gt;Type V collagen-degrading enzyme activity was detected as a metalloprotease acting at neutral pH in the human liver. Type V collagen extracted from human placenta and labeled with [1-14C] acetic anhydride was used as the substrate in the assay. Four major degradation products with relatively high molecular weights were observed upon polyacrylamide gel electrophoresis of the incubation mixture of type V collagen and liver homogenate. The significance of the measurement of this enzyme activity was discussed in relation to the clarification of the mechanism of liver fibrosis.&lt;/p&gt;</p

Effect of continued drinking on prognosis of alcoholic liver cirrhosis.

The prognoses of patients with alcoholic liver cirrhosis were compared between those who continued to drink and those who stopped. Clinical criteria were strictly set so as to control other variables affecting the prognoses. Four-year survival was significantly higher in the patients who stopped drinking than in those who continued to drink. Continued drinking worsens the prognosis of patients with alcoholic liver cirrhosis.</p