To study surgical reversibility of intraabdominal cryptorchidism, a study in which weanling rats were made artificially cryptorchid was undertaken. At the same time both sperm ducts were anastomosed into the urine bladder (vasocystostomy) to enable sperm output measurements, which were performed by putting the animals in metabolic cages for 24 hr. Group I animals were reoperated on 2 weeks after the initial cryptorchidism operation to reverse this intervention by an orchiopexy operation; in Group II orchiopexy was carried out after 4 weeks, in Group III after 8 weeks. In Group IV, a control group in which only the vasocystostomy operation was performed, the rats were sham operated. The animals were followed for 3 months after orchiopexy. All control animals showed sperm output between 20 and 30 million of spermatozoa per 24 hr from the age of 13 weeks on. However, experimental animals that had been de facto cryptorchid did not show any sperm output. Three out of 4 animals in which spontaneous descent of one or both testes had taken place showed sperm output from 6 to 8 weeks after orchiopexy. The results show that, notwithstanding the short periods of cryptorchidism, certain irreversible changes had already developed.
In five groups of 15 rats allogeneic kidney transplantations were performed. Four groups received pre- and postoperatively a semisynthetic diet, isocalorically but differing in quantity and quality of fatty acids: group I received a diet high in saturated fat; group II, a diet high in linoleic acid; group III, a diet containing fish oil; group IV, a diet high in monoenoic acid. Finally, the fifth group of rats was fed a standard commercial chow and served as a control for the procedure of technique and immunological regimen. All groups received the same immunosuppressive regimen of immunological enhancement induced by pretreatment with complete donor blood. Survival and several parameters of graft function were studied. The results showed that the technical mortality, i.e. animals dying in the first week after transplantation, was substantially higher in rats on the semisynthetic diets in comparison with the group of rats on the commercial diet. A statistically significant better graft function could be observed in the group of rats on the diet high in linoleic acid in the first period after kidney transplantation, compared to the other groups on semisynthetic diets. This difference disappeared in the course of the study when a number of animals was lost due to graft rejection. Furthermore, in the same diet group mortality due to rejection was significantly decreased as well.
To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two‐stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gasses, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 ± 1.9 h (n = 6, mean ± SEM). Other liver‐failure‐associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 ± 0.4 h (n = 6, mean ± SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta‐activity, and an increase in delta activity). However, these changes were not statistically significant, and non‐specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia‐induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
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