The objective of the study was to demonstrate the effect of oral administration of aluminum on the level of hematological and biochemical blood indicators, clinical symptoms and its contents in selected CNS structures in dogs. The study was conducted in two stages. The dogs were assigned to two groups. The experimental group was composed of 7 hybrid dogs (aged 12-17 years, 5 males and 2 females) which received 10 mg/kg aluminum sulphate orally over a period of 6 weeks. The control group was composed of 7 hybrid dogs (aged 13-20 years, 3 males and 4 females) which did not receive the preparation. 1 ml blood samples for hematological tests were collected from the cephalic vein (vena cephalica) to EDTA test tubes. The number of erythrocytes (RBC), hemoglobin concentration (Hb), hematocrit (Ht), the number of leukocytes and platelets were determined. The hematological test was conducted with the automatic analyzer unit by ABX Diagnostic. 5 ml blood samples were collected for the biochemical tests into test tubes with silicone spheres. Serum was obtained from full blood for 5 min. at 1500 × g. Serum was used to assess the activity of alanine aminotransferase (ALAT/GPT), aspartate aminotransferase (AspAT/GOT), alkaline phosphatise (ALP/AP/FA), level of calcium (with the POINTE 180 biochemical analyzer unit), magnesium, organic phosphorus (with the EPOLL 11 analyzer unit), sodium, potassium, and chlorine (with the CIBA CORNING 644 analyzer unit). After 42 days of administration of aluminum, an insignificant decrease in all morphological blood parameters was recorded in the experimental group, with a statistically significant decrease found in the concentrations of calcium and potassium in blood serum between the first day of the study and the 42nd day. The level of calcium in the experimental group was reduced. No statistically significant differences were found in the concentrations of sodium, magnesium, phosphorus and chlorine in the experimental group. However, a statistically significant increase was recorded in the content of aluminum in the cerebral cortex, hippocampus and cerebellum cortex in the experimental group.
The article presents atherosclerotic and inflammatory changes in brain vessels and perivascular tissue leading to ischemic and hypoxic changes which, in consequence, produce strokes and brain hemorrhages. The aim of the study was to examine the morphology of the brain vessels of seven elderly animals from 7-21 years of age (three monkeys, a likaon, wolf and two pigs). The brain vessels of the investigated animals demonstrated atherosclerotic changes such as: fibroid changes and amyloidal angiopathy (CAA) in the cortical and leptomeningeal vessels of the three monkeys, likaon and wolf brain. Fibroid arteritis was present in the meningeal arteries of the two sows. These atherosclerotic and inflammatory processes in the CNS vessels led to strokes and hemorrhages. Subarachnoid (Cebus apella) and intraventricular (Lemur mongoz) hemorrhages were noted in two of the monkey’s brains and fibrinotic arteritis produced massive mesencephalon hemorrhaging in the two 7-year old sows. The advanced stages of infarct necrosis were characterized by a predominance of vacuolated macrophages with proliferating mesodermal and glial components. Small post infarct and post hemorrhages lesions in nervous tissue produced scarring, with astrocytes, whereas large foci liquefied and formed cysts, marked by the presence of macrophages with hemosyderin in their margins. No atheromatosis changes were observed in the brain vessels.
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Recently, we have shown that MK-886 - an inhibitor of five lipoxygenase activating protein (FLAP) inhibits atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. We, therefore, wanted to find out if other FLAP inhibitor - BAYx1005 given at a dose of 1.88 mg per 100 mg of body weight per day during 16 weeks, could also attenuate atherogenesis. In apoE/LDLR - DKO mouse model BAYx1005 inhibited atherogenesis, measured both by "en face" method (23.84 ± 2.7% vs. 15.16 ± 1.4%) and "cross-section" method (497236 ± 31516 µm2 vs. 278107 ± 21824 µm2). This is the first report that shows the effect of BAYx1005 on atherogenesis in gene-targeted mice.