Therapeutic effect of hyperbaric oxygen in hepatic artery thrombosis and functional cholestasis after orthotopic liver transplantation.

Among the postoperative complications, hepatic artery thrombosis can occur in up to 10% of adult orthotopic liver transplants and intervention is indicated when this occurs within 30 days by retransplantation. Primary graft dysfunction, which can occur in up to 30% of the cases and is another potential complication, although reversible, has a relatively high mortality rate. Hyperbaric therapy, an efficient mode of tissue oxygenation, is being used in an increasing number of clinical situations. We report here two cases where hyperbaric oxygen therapy greatly benefited patients with complications after orthotopic liver transplantation: one with hepatic artery thrombosis and the other with primary graft dysfunction. Both patients showed rapid clinical recovery with gradual reduction of liver and canalicular enzymes soon after commencing hyperbaric oxygen therapy.

Effect of hyperbaric oxygen on liver regeneration in a rat model.

Hyperbaric oxygen therapy is a treatment that has been gradually implemented for the treatment of several pathologic conditions. The present study evaluated the effect of hyperbaric oxygen therapy for hepatic regeneration and its relationship to mitochondrial function. Male Wistar rats underwent partial hepatectomy (70%) and subsequently underwent two sessions of hyperbaric oxygen (90 minutes each, at a pressure of 2 ATA). The animals were sacrificed at 24 and 48 hours after surgery. Hepatic regeneration was evaluated by the dry weight of the remaining liver, the hepatic regeneration rate, the hepatic DNA content, and the hepatocyte proliferation rate using the "proliferating cell nuclear antigen" (PCNA) content. Function of the mitochondria was evaluated by its oxygen consumption during respiratory states 3 and 4, its respiratory control ratio (RCR), its membrane potential, as well as its osmotic swelling. We also measured serum levels of aminotransferases. The results revealed an increased dry weight of the remaining liver, regeneration rate, and DNA content at 24 and 48 hours after hepatectomy. The hepatocyte proliferation rate was significantly higher among animals treated with hyperbaric oxygen therapy at 48 hours after surgery. There was no significant difference in aminotransferase levels. Mitochondrial respiration revealed reduced oxygen consumption in state 3 after 48 hours. These results demonstrated that hyperbaric oxygen stimulates hepatic regeneration at 24 and 48 hours after 70% hepatectomy. The effect of hyperbaric oxygen on hepatic tissue occurs without tissue damage and protects mitochondria after 48 hours.

Spectral response for laser enhancement in hepatic regeneration for hepatectomized rats.

BACKGROUND AND OBJECTIVES: The low intensity laser therapy (LILT) has been widely used in all medical fields due to its therapeutic effects in reparative process, pain relief, and biostimulation. Even though there is a therapeutic window of wavelengths for clinical application, little has been done concerning the frequency spectrum response to biological effects. In this work, we investigate the dependence of different wavelengths irradiation in the enhancement of the tissue regeneration after partial hepatectomy in Wistar rats. STUDY DESIGN/MATERIALS AND METHODS: The proliferating cell nuclear antigen (PCNA) labeling index and the respiratory control (oxygen consumption in extracted mitochondria) were the tests used to evaluate the liver regeneration after laser irradiation with different wavelengths. RESULTS AND CONCLUSIONS: The results show a correlated spectral response that can be explained based on the combined effect of light penetration on biological tissues and the biomolecular excitation efficiency for each wavelength used.

Effect of a necrogenic dose of diethylnitrosamine on vitamin E-deficient and vitamin E-supplemented rats.

In order to evaluate the effects of a necrogenic dose of diethylnitrosamine (DEN) on vitamin E-deficient and vitamin E-supplemented rats, a single dose of the drug (200 mg/kg body weight) was injected intraperitoneally at the end of 10 weeks of treatment with the diets. The hepatic necrosis and lipoperoxidation provoked by DEN were evaluated 24, 48, 72 and 120 hours after the injection and were found to be more intense in the deficient group (thiobarbituric acid reactive substances (TBARS): 5.20 +/- 1.48 nmol/mg protein; necrosis volume: 68.99 +/- 8.36%; P < 0.05) during the second period. Also, in the same group and during the same period, mean plasma and hepatic vitamin E concentrations and mean liver glutathione concentration were the lowest detected, suggesting the occurrence of antioxidant consumption due to the toxic action of DEN. In contrast to vitamin E deficiency, which permitted the drug to exert stronger toxic effects, 20-fold supplementation with vitamin E did not provide additional protection against the lipoperoxidation and necrosis provoked by DEN (P < 0.05). The results suggest that other mechanisms in addition to lipoperoxidation provoked by free radicals originating from the metabolism of nitrosamines by the cytochrome P-450-dependent enzymatic system may be involved in the hepatotoxic action of these substances.

[Morphological study of the small intestine in rats with experimental zinc deficiency]. / Estudo morfológico do intestino delgado de ratos com carência experimental de zinco.

Rats were maintained 4 weeks on a zinc deficient diet from the time of weaning. A control group received the same basic diet supplemented with zinc. Zinc deficiency, was indicated by poor weight gain, diarrhea, exudative vesicular dermatitis around ears, eyes, nose and extremities, and lowering of blood zinc levels. The morphometric study of the small intestine showed: 1) decreased thickness of the intestinal wall and of the mucosa; 2) significant decrease of the mean villies length and of the mean crypt depth; 3) no alterations in the height of the enterocytes from the middle one third of the villis and in the number of Paneth cells; 4) a decreased mitotic index; 5) a diminished number of epithelial cells living the ville, and 6) a decreased population of intraepithelial lymphocytes, both in the proximal jejunum and distal ileum. These findings are compatible with an impairment of cell replication in the small intestine in experimental zinc deficiency in rats, and allow us to speculate that the diarrhea usually seen in states of zinc malnutrition, at least in part, could be dependent on these changes.

Hepatic damage produced by long-term alcohol consumption in well-nourished rats.

A study of the effect of long-term alcohol consumption on the liver of well-nourished rats is described. Rats fed for 16 weeks on a semipurified diet supplemented with high levels of vitamins and lipotropic factors and alcohol corresponding to 35% of the total caloric intake developed marked fatty changes of the liver. Mild fatty changes were observed in pair-fed controls receiving as isoenergetic equivalent of sucrose instead of alcohol. Intracellular hyaline bodies, corresponding ultrastructurally to giant mitochondria were abundantly found in the hepatocytes of alcoholic rats, while in the controls they were not seen. Te findings in this investigation are postulated to provide further evidence that the long-term intake of alcohol exerts a direct causative role in the pathogenesis of liver damage.