Peritoneal dialysis (PD) is a well established method of depuration in uremic patients. Standard dialysis solutions currently in use are not biocompatible with the peritoneal membrane. Studying effects of dialysate on peritoneal membrane in humans is still a challenge. There is no consensus on the ideal experimental model so far. We, therefore, wanted to develop a new experimental non-uremic rabbit model of peritoneal dialysis, which would be practical, easy to conduct, not too costly, and convenient to investigate the long-term effect of dialysis fluids. The study was done on 17 healthy Chinchilla male and female rabbits, anesthetized with Thiopental in a dose of 0.5 mg/kg body mass. A catheter, specially made from Tro-soluset (Troge Medical GMBH, Hamburg, Germany) infusion system, was then surgically inserted and tunneled from animals' abdomen to their neck. The planned experimental procedure was 4 weeks of peritoneal dialysate instillation. The presented non-uremic rabbit model of peritoneal dialysis is relatively inexpensive, does not require sophisticated technology and was well tolerated by the animals. Complications such as peritonitis, dialysis fluid leakage, constipation and catheter obstruction were negligible. This model is reproducible and can be used to analyze the effects of different dialysis solutions on the rabbit peritoneal membrane., S. Zunic-Bozinovski, Z. Lausevic, S. Krstic, N. Jovanovic, J. Trbojevic-Stankovic, B. Stojimirovic., and Obsahuje bibliografii a bibliografické odkazy
The activity of lipoprotein lipase (LPL) is increased after alcohol consumption and can contribute to an increased level of HDL-cholesterol, which is considered to play a key role in the ethanol-mediated protective effect against cardiovascular disease. The increase in HDL-cholesterol concentration can be also due to an ethanol-enhanced synthesis and secretion of apolipoprotein A-I (apo A-I) from hepatocytes. Therefore, the hypothesis that ethanol consumption affects the LPL and apo A-I gene (LPL and APOA1, respectively) expression was tested in male C57BL/6 mice drinking 5 % ethanol or water and fed a standard chow or high-fat (HF) diet for 4 weeks. The LPL expression was determined in the heart, epididymal and dorsolumbal adipose tissues, the APOA1 expression in the liver. Alcohol consumption did not affect lipid and lipoprotein concentrations in the serum. The LPL expression was increased in the heart of mice given ethanol and HF diet compared to mice on chow and ethanol (p<0.001) and was also increased in epididymal fat in mice given ethanol and HF diet compared to mice on water and HF diet (p<0.05). Neither LPL expression in dorsolumbal fat nor APOA1 expression in the liver were affected by ethanol consumption. Our data suggest that ethanol consumption upregulate LPL expression in a tissue- and diet-dependent manner., E. Mudráková, J. Kovář., and Obsahuje bibiografii a bibliografické odkazy
The effect of oral supplementation with glycosaminoglycans (GAG) and radical scavengers (vitamin E/selenium) on the regeneration of osteochondral defects was investigated in rabbits. After introduction of defined osteochondral defects in the knee joint, groups of ten animals were given a GAG/vitamin E/selenium mixture or a placebo (milk sugar) for 6 weeks. Following sacrifice, histological and histochemical analysis was performed. The amount of synovial fluid was increased in the placebo group, while the viscosity of the synovial fluid was significantly enhanced in the GAG group. The amount of sulfated GAG in the osteochondral regenerates (8.8±3.6 % vs. 6.0±5.6 %; p<0.03) was significantly higher in the GAG group. In both groups, the GAG amount in the cartilage of the operated knee was significantly higher than in the non-involved knee (p<0.05). Histological analysis of the regenerates in the GAG group was superior in comparison with the placebo group. For the first time, a biological effect following oral supplementation with GAG was demonstrated in healing of osteochondral defects in vivo. These findings support the known positive clinical results., M. Handl, E. Amler, K. Bräun, J. Holzheu, T. Trč, A. B. Imhoff, A. Lytvynets, E. Filová, H. Kolářová, A. Kotyk, V. Martínek., and Obsahuje bibliografii a bibliografické odkazy