Once brain ischemia was induced in the gerbil cerebral fronto‐parietal cortex, serial changes occurred in energy metabolites and various lipids. The amounts of inosi‐tol‐containing phospholipids began to decrease immediately after energy failure, followed by an increase in the amount of 1,2‐diacylglycerol with a subsequent liberation of arachidonic acid and other free fatty acids. The fatty acid compositions of inositol‐containing phospholipids, of 1,2‐diacylglycerols produced by ischemia, and of free fatty acids liberated during ischemia were quite similar. The amount of stearic acid liberated was much larger than that of arachidonic acid between 30 s and 1 min of ischemia. On the other hand, there was no significant decrease in the amount of the other phospholipids except for phosphatidic acid. Furthermore, there was also no change in the fatty acid composition of phosphatidylcholine or phosphatidylethanol‐amine throughout 15 min of ischemia. The amount of cytidine‐monophosphate reached a peak (36.7 nmol/g wet wt) at 2 min of ischemia. These results indicated that arachidonic acid was predominantly liberated from inositol‐containing phospholipids by phospholipase C, and by the diglyceride lipase and monoglyceride lipase system rather than from phosphatidylcholine or phosphatidylethanolam‐ine by phospholipase A2 or plasmalogenase or choline phos‐photransferase during the early period of ischemia.
Liver cirrhosis (LC), which may result in hepatic failure or cancer, has been reported in patients after Fontan procedure. The purpose of this study was to clarify the frequency and histological characteristics of LC, and to evaluate the risk factors and serological markers of LC with Fontan circulation. Retrospective review of contrast-enhanced CT scans (CT) of the liver was carried out in 57 patients after Fontan procedure. Patients were divided into two groups: LC group (n = 31) and no LC group (n = 26). Age at Fontan procedure, duration after Fontan procedure, catheterization data, and history of failing Fontan circulation were compared between groups. Serological data including γ-GTP and hyaluronic acid were compared. Histology of autopsy specimens was assessed when available. Duration after Fontan procedure was significantly longer in LC group than no LC group. History of failing Fontan circulation was more frequent in LC group than in no LC group. There was no correlation between type of procedure (APC/Bjork/lateral tunnel/TCPC) and LC in this series. Serum hyaluronic acid, γ-GTP, and Forns index were significantly higher in LC group. Significant risk factors for LC were duration after Fontan procedure (>20 years). In autopsy specimens, histopathological changes of LC were observed predominantly in the central venous area. LC diagnosed with CT is frequent in patients long after Fontan procedure, especially after 20 years. Hyaluronic acid and γ-GTP could be useful markers to monitor the progression of liver fibrosis in Fontan patients.
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