Major hepatectomy can be considered as a possible treatment for liver metastases or primary cancer of the liver. Unfortunately, the extent of liver resection must be kept below 80% for regeneration to occur. When 90% hepatectomy is performed in the rat, there is no regeneration of the 10% remnant. Instead, the major finding is overwhelming steatosis, and the animals do not survive beyond the 40th hr posthepatectomy (1,2). Since testosterone has been reported to reduce liver fat content after partial hepatectomy (3), we decided to ascertain whether, after 90% hepatectomy in the rat, testosterone would reduce steatosis and thereby allow regeneration to occur with ultimate survival of the animal. Histological evidence suggests that testosterone offers protection against steatosis. Moreover, the liver remnant was found to regenerate, accompanied by increased liver weight and survival.Two groups of 50 rats underwent 90% hepatectomy, one treated with testosterone oenanthate (Group 2), the other untreated (Group 1). A survival study was undertaken in 20 rats of each group. The others were sacrificed at different times posthepatectomy to determine liver remnant weight and histology.Survival time was strikingly different for the two groups: in Group 1, 100% of rats died before the 40th hr; in Group 2, 80% survived beyond the 40th hr, among these, 50% presented a normal life span. Moreover, as shown in Table 1, liver remnant weight was significantly higher in the treated group, even as early as 24 hr posthepatectomy. The testosterone-treated rats which survived showed marked liver remnant mass restoration: 400% at 72 hr and 600% at 96 hr posthepatectomy.

According to perioperative ECG changes and/or specific cardiac troponin I measurements, we did not identify specific myocardial damage following gastroesophageal reflux laparoscopic surgery. Unexpectedly, the incidence of hepatic cytolysis was frequent (62%) and has not previously been reported in the literature.

Abstract. Arginine aspartate was administered orally (250 mg/kg/day) for one week to 5 healthy male human volunteers aged 20–35. After this period, the 24 h patterns of growth hormone (GH) and prolactin (Prl) secretion were determined by radioimmunoassay on blood samples withdrawn every 20 min and correlated with the polygraphic recordings of electroencephalogram, electromyogram and electrooculogram. The results were compared to data obtained in identical conditions with the same subjects but after a week of placebo administration. In all 5 subjects the slow wave sleep related GH peak was about 60% higher after a week of arginine aspartate administration than in the control period, with individual changes of + 24, + 25, + 42, + 47 and + 162%. The nocturnal mean plasma Prl of each subject was higher after arginine aspartate than before. The nocturnal rise of plasma Prl increased from a mean value of + 21.5% during the placebo period to + 95% at the end of the arginine aspartate treatment. These hormonal modifications were not accompanied by any detectable alteration of sleep organization and specially of the slow wave sleep pattern, suggesting a direct neuroendocrine action of the drug.

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