Receptor-dependent and receptor-independent degradation of low density lipoprotein in normal rabbits and in receptor-deficient mutant rabbits

Low density lipoprotein (LDL) catabolism was studied using WHHL rabbits, an inbred strain deficient in LDL receptor activity and, thus, an animal model for homozygous familial hypercholesterolemia. WHHL and normal rabbits were injected with [14C]sucrose-LDL and the tissue sites of LDL degradation were determined 24 h later. On degradation of [14C]sucrose-LDL, the [14C]sucrose ligand remains trapped within tissues as a cumulative measure of degradation. The fractional catabolic rate of [14C]sucrose-LDL in Watanabe heritable hyperlipidemic (WHHL) rabbits was reduced (0.024 +/- 0.010 versus 0.063 +/- 0.026 h-1) but, by virtue of the increased plasma pool, total LDL flux was increased (33.5 +/- 9.6 versus 10.6 +/- 4.4 mg of LDL protein/kg/day). Liver was the predominant site of catabolism in both WHHL and normal rabbits (52.7 +/- 6.9 and 56.6 +/- 6.2% of total degradation). About 90% of hepatic catabolism was attributable to parenchymal cells in both cases. Thus, Kupffer cells, a major component of the reticuloendothelial system, do not play a major role in LDL catabolism in WHHL rabbits. Despite receptor deficiency, the relative contribution of various tissues to overall LDL degradation was not greatly altered and the absolute rate of delivery of LDL to all tissues was increased with the exception of the adrenal. Thus, there was no evidence that the increased degradation occurred in any special subset of "scavenger" cells. Nevertheless, local scavenger cell uptake may be critically important, especially in atherogenesis. If it is assumed that receptor-independent degradation occurs at the same rate in the tissues of WHHL and normal rabbits and that catabolism in the absence of receptors is a linear function of concentration, then one can estimate the fraction of uptake in normal tissues mediated by receptors. The difference in the fraction of the plasma LDL pool cleared per unit of time in normal and WHHL rabbits would reflect the contribution of receptors to fractional clearance. By this calculation, receptor-mediated degradation in normal rabbits was 62% overall, 63% in liver, 92% in adrenal, and 83% in gut.     

Environmental enrichment for laboratory rodents and rabbits: requirements of rodents, rabbits, and research

Environmental conditions such as housing and husbandry have a major impact on the laboratory animal throughout its life and will thereby influence the outcome of animal experiments. However, housing systems for laboratory animals have often been designed on the basis of economic and ergonomic aspects. One possible way to improve the living conditions of laboratory animals is to provide opportunities for the animals to perform a species-specific behavioral repertoire. Environmental enrichment should be regarded both as an essential component of the overall animal care program and equally important as nutrition and veterinary care. The key component of an enrichment program is the animal staff, whose members must be motivated and educated. It is critically important to evaluate environmental enrichment in terms of the benefit to the animal by assessing the use of and preference for a certain enrichment, the effect on behavior and the performance of species-typical behavior, and the effect on physiological parameters. At the same time, it is necessary to evaluate the impact on scientific outcome, how the enrichment influences the scientific study, and whether and how the statistical power is affected. The result will depend on the parameter measured, the type of enrichment used, and the animal strain. In this article, goals of enrichment are defined and discussed. Animal behaviors and needs are described, along with the translation of those needs into environmental enrichment programs. Specific types of environmental enrichment are outlined with examples from the literature, and an evaluation of environmental enrichment is provided.     

Skeletal muscle fibre composition in new Zealand white rabbits, wild rabbits and wild rabbits bred in captivity: effect of heredity

1. The muscle composition of 3 breeds of rabbit was investigated histochemically in 3 muscle groups in order to identify whether heredity or environment was the predominant factor in dictating composition. 2. In the biceps femoris, differences between the breeds in myosin ATPase activity were due to heredity, whereas differences in oxidative potential were due to environment. 3. In the flexor digitorum longus, the wild rabbit possessed the highest percentage of type I fibres. This was environmentally induced.     

Metabolism of methylmercury in rabbits and hamsters

The metabolism of²⁰³Hg-labeled methylmercury chloride (MeHg) has been studied in rabbits and hamsters. Rabbits were administered 1.6 μmol MeHgCl/kg bw intravenously, and hamsters 40 μmol/kg bw orally. Urine and feces were collected daily and groups of four animals killed after 1 h, 1 d, or 7 d. The concentration of²⁰³Hg in blood, liver, kidney, spleen, lung, heart, and brain was determined by gamma counting. In both animal species, the clearance of²⁰³Hg in the brain was slower than in other tissues. In the rabbits the brain²⁰³Hg concentration increased during the whole experimental period. Rabbits excreted²⁰³Hg primarily in feces (about 20% of the dose within 1 wk), and much less in urine (<2%). In contrast, hamsters very efficiently excreted²⁰³Hg in urine (50% in 1 wk). The fecal excretion was similar to that of the rabbits. Separation of inorganic Hg and MeHg in urine from hamsters by ion exchange chromatography showed that about 90% of the urinary²⁰³Hg was excreted as MeHg.     

Rearing of germfree rabbits

The present work describes in detail experimental procedures and conditions required for rearing of germfree rabbits. Newborn germfree rabbits were obtained using the “wet” hysterectomy technique. The animals were successfully maintained under germfree conditions up to four months after delivery in flexible plastic isolators. Infant rabbits were first fed a sterile VA2-b diet and after weaning, a modifled diet L-478 according to Reddyet al. (1965). Both diets were shown to be suitable as the development of megacoecum was significantly reduced. The infant germfree rabbits were characterized by a good general clinical condition and body weights were comparable to those found in their conventional counterparts fed mother’s milk.     

Density of rabbits (

The density of rabbits (Oryctolagus cuniculus) in the modified tussock grasslands of the Mackenzie Basin, South Island, New Zealand, in August-September 1991 was determined within 26 I-ha quadrats spread over 1000 ha. The area was poisoned with 1080- carrot baits and dead and live rabbits counted. The overall kill rate was 93%. Wide variability in rabbit densities amongst the quadrats was correlated with burrow density, but vegetation was not a significant predictor of rabbit numbers. High density quadrats were not all spatially clumped together. Variation amongst quadrats of 0-43% of rabbits dying underground shows that searching burrows as well as the surface will provide the most accurate rabbit densities. Poisoning efficacy was greater than or equal to 90% in 77% of the quadrats, but two low- density quadrats recorded kill rates <70%. Nine per cent of carcasses had been partly eaten by predators, suggesting a potential for the predators to be killed during rabbit control operations via secondary poisoning. The average density of 19 rabbits per ha confirms the classification of this area as a moderate to high rabbit-prone zone, with the rabbit population imposing grazing pressure equivalent to at least 1-2 sheep per ha at the beginning of spring. Sustainable agriculture cannot be attained in these semi-arid regions of New Zealand without cheap, widespread and effective rabbit control.     

Hematuria in rabbits

A nine year retrospective study of hematuria in 14 New Zealand White rabbits was conducted to classify possible etiologies of this clinical finding. Physical examination, laboratory tests, radiography and postmortem examination were utilized in most cases to verify the presence of hematuria and to determine its etiology. Uterine adenocarcinoma was diagnosed in two rabbits. Three rabbits had uterine polyps with hemorrhage. Renal infarction with hemorrhage was diagnosed in three rabbits. Urolithiasis with secondary urethral obstruction and hemorrhagic cystitis was identified as the cause of hematuria in four rabbits. Other causes of hematuria included chronic cystitis, disseminated intravascular coagulation, bladder polyps and pyelonephritis. Hematuria of undetermined origin was observed in one rabbit. This last [corrected] case was negative for both blood and porphyrin in the urine, but positive for excess levels of urobilin, the oxidative product of urobilinogen. This case illustrates that hyperpigmented urine should be a rule out in all cases of suspected hematuria in rabbits.     

Monocytes and radiation-induced atheromatosis in rabbits

Previous experiments have shown that local irradiation of the carotid arteries of hypercholesterolemic rabbits results in the development of atheromatosis in the irradiated areas of the arteries. The process starts with the adherence of monocytes to the endothelial layer, their entrance into the subendothelial space, and their subsequent transformation into lipophages (foam cells). Prevention of this type of plaque formation can be achieved by prednisolone (in a lower concentration than previously used) (Vos et al. 1981) and by VP16-213 (Vepesid). Differential blood cell counts demonstrated that the animals subjected to treatment with prednisolone developed a moderate relative lymphocytopenia, whereas treatment with Vepesid resulted in a severe monocytopenia. Since prednisolone treatment only partially prevented plaque formation, whereas Vepesid seemed to fully inhibit the development of plaques, we conclude that although a role of the lymphocyte in the process of plaque formation cannot be excluded, the monocyte seems to play a crucial role in the pathogenesis of radiation-induced atheromatosis.