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F Crafa

Publications and source records attributed to F Crafa.

21 records · Page 2Linked to original sources

Protective effects of prostaglandin E1 on normothermic liver ischemia.

Effects of treatment with prostaglandin E1 (PgE1) on normothermic liver ischemia were studied in male Lewis rats. Animals were subjected to 90 min of warm liver ischemia. Two groups of rats were constituted: group A (no treatment) and group B (PgE1 treatment). PgE1 (100 micrograms/kg) was given as a bolus 2 min before induction of ischemia and 2 min before the end of ischemia. Survival rates were assessed and, 6 h after the end of ischemia, serum transaminases, histology of the liver, Kupffer cell activity were evaluated. PgE1 treatment significantly improved survival rate (80%) in comparison with the nontreated group (40%). A significant reduction in transaminase levels was observed after PgE1 The extent of necrosis and congestion was improved by PgE1 treatment. Sheep red blood cell 51Cr liver uptake was deeply depressed 6 h after the end of ischemia in group A (6 +/- 2.3%/g tissue), and was significantly higher (p less than 0.001) after PgE1 administration in group B (32.98 +/- 11.7%/g tissue). Our results demonstrate that PgE1 is able to protect the liver from ischemic insult. The mechanism by which prostaglandins exert this beneficial effect on normothermic liver ischemia may be related to their action on hepatic macrophages.

Alprostadil↗

Normothermic ischemia induces major histocompatibility complex class I expression in hepatocytes.

The hepatic expression of major histocompatibility complex (MHC) antigens is normally limited. However aberrant expression may occur in cholestatic diseases or following liver transplantation. The aim of this work was to investigate the effect of normothermic ischemia on hepatocellular MHC expression. Temporary (90-min) normothermic ischemia of the liver was induced in inbred rats. There was a significant elevation of aspartate aminotransferase and alanine aminotransferase levels after ischemia, rising to their maximum by 6 h. Histologic findings showed large, confluent areas of necrosis, and preserved areas were seen with centrolobular congestion and macrovacuolar steatosis. Expression of MHC class I and II antigens was detected using the immunoperoxidase technique, 1 h, 12 h, 3 days, 7 days and 1 month after the end of intervention. A marked induction of the expression of class I, but not of class II, MHC antigens was observed on the hepatocyte membranes after ischemia. We suggest that normothermic ischemia can occur postoperatively in human liver transplantation and may cause increased expression of class I MHC antigens on hepatocytes, leading to increased sensitivity of liver allografts to rejection by cytotoxic T cells.

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