Systematic screening for hepatocellular carcinoma (HCC) in cirrhotic patients by alpha-fetoprotein and ultrasound permits the detection of small asymptomatic tumors. Owing to the small tumor size, more liver resections can now be performed than in the past. These resections are performed in a more economical way in terms of loss of functional parenchyma and in a more appropriate manner with regard to carcinology: surgical techniques of liver segmentectomy and use of intraoperative echography are mandatory. Favorable long-term results obtained in Eastern countries by resecting such lesions are encouraging but remain to be confirmed in the Western hemisphere.

In the present study, subtotal hepatectomy was evaluated as a model of acute liver failure in the rat. Sprague-Dawley rats, weighing 250–300 g, underwent hepatectomy under varying basal conditions of temperature and glucose administration. Rats operated and maintained postoperatively at ambient temperature (25 °C external environment) developed hypothermia with a rate of return to normal temperature which was related to the extent of hepatectomy and the availability of glucose postoperatively. However, no significant difference in survival was observed between groups maintained at ambient temperature and those whose core temperature was maintained at 37 °C by passive external warming. Severe hypoglycemia was observed in rats undergoing 90 and 95% hepatectomy without glucose postoperatively. With 20% glucose available in drinking water the mortality of 90% hepatectomy was reduced from 95 to 40% (p < 0.0001). With increase of the hepatectomy to 95%, 90% mortality was observed despite glucose support. Transplantation of 4 × 10⁷ isolated syngeneic hepatocytes intraperitoneally at the time of hepatectomy did not increase survival after 90 or 95% hepatectomy; addition of testosterone therapy did not improve survival either alone or with hepatocyte transplantation. In this study, hepatectomy exceeding 90% was lethal and did not respond to the supportive measures provided. Hepatocyte transplantation and testosterone pretreatment, both therapies which are thought to increase regeneration, were ineffective in improving survival in this resection model.

Several clinical and experimental findings suggest that liver allografts are less sensitive than other organ allografts to lymphocytotoxic antibodies. In this experimental study in hypersensitized inbred rat recipients, rejection of liver allografts was delayed compared to that of heart allografts. Furthermore, there was a marked decrease in the level of cytotoxic antibodies after liver allografting but not after heart allografting in these animals. The decrease in the level of antibodies also occurred after donor-specific extracorporeal liver hemoperfusion in hypersensitized recipients. Whether the decrease was caused by a massive absorption of antibodies on the liver or related to excretion of major histocompatibility complex antigens in a soluble form remains to be demonstrated. These results support the hypothesis that the liver has a privileged position in regard to rejection and are consistent with clinical observations made following ABO incompatible or crossmatch positive liver transplantations.Experimental studies in pigs (1) and rats (2, 3) have shown that the liver is less sensitive than other organ allografts to acute rejection. In preliminary experiments using rats hypersensitized by multiple skin allografts, we also have observed that liver allografts are less rapidly rejected than heart allografts (4). These experimental observations suggest t h a t the liver has a privileged position in regard to allograft rejection. This hypothesis of a privileged position agrees with two clinical observations: (i) the lesser severity and easier control of acute rejection of liver allografts compared t o that of other organ allografts (5) and (ii) the fact that, at variance with what occurs with kidney or heart allografts, hyperacute rejection of liver transplants is not usually observed in cases of ABO incompatibility or positive T-cell cross-match (6).In Experimental Protocol. Allogeneic hypersensitization was induced using repeated skin allografts according to theprotocol published by Guttmann (7): BN rats were grafted with a LEW skin graft on three successive occasions at 10-day intervals. Subsequent grafts in these animals were called donorspecific when the donor was of the same strain as that previously used to take skin allografts. ANIMALS AND METHODSTen days after the thud skin allograft, these hypersensitized BN rats were grafted, either with a LEW heart (Group 1) or a LEW liver allograft (Group 2). In the control groups, unsensitized BN rats were grafted with a LEW heart (Group 3) or a LEW liver allograft (Group 4). In a second series of experiments, LEW heart allografts were grafted in unsensitized BN rats after transfer of serum from hypersensitized rats just allografted with a LEW heart (Group 5) or a LEW liver allograft (Group 6). In Group 7, a donor-specific (LEW) extracorporeal liver hemoperfusion was performed in hypersensitized BN rats 10 days after the third LEW skin graft. One day later, a donor-specific (LEW) heart allograft was performed in these rats. The same protocol was applied in Group...