[Cardiovascular diseases and gene polymorphisms]. / Onemocnení kardiovaskulárního systému a genové polymorfizmy.

Cardiovascular diseases rank among the most important mortality causes in the Czech population. Although the unhealthy living style plays a key role in their development and progression, impacts of the hereditary predisposition can not be denied. This article characterizes the gene polymorphisms and results of mutations in general. An overview of the most important findings presented in papers published in the Czech Republic and worldwide follows. Issues of concrete gene polymorphism associations with such pathological conditions as acute or chronic heart failure, essential hypertension or heart rhythm disorders are discussed. Attention is paid to genes that participate on beta-adrenergic signalling, to genes for angiotensin, to ACE-gene and to angiotensin II receptor gene. A table summarizing the most important data is attached to the article.

[Study of a newly synthesized substance with a potential to stimulate beta3-adrenergic receptors]. / Testování nove syntetizované látky s potencionálním beta-adrenergne agonistickým úcinkem.

beta3-Adrenoreceptor agonists can stimulate lipolysis in the white adipose tissue and thermogenesis in the brown adipose tissue. These activities could be useful in the treatment of obesity and the associated metabolic syndrome. The effects of six-week oral administration of the newly synthesized substance B496 (methyl-4-[2-[2-hydroxy-3-(4-ethylcarbamoyl)phenoxyprophyl]amino]etyl)-phenoxyacetate hydrochloride) on serum glucose, triglycerides, total cholesterol, and leptin levels were studied in male Wistar rats fed with a high-fat diet. The animals were divided into a group treated with B496 (5 mg dissolved in 1 litre of water) and a control group. The results indicated a significant reduction in serum glucose levels (-26 %, p<0,01), triacylglyceride levels (-21 %, p<0,05) and leptin levels (-43 %, p<0,01). Further the effect of a single intraperitoneal dose (1 mg/kg) of B496 and BRL-37344 on serum leptin levels in the C57Bl/6J mouse was investigated. Administration of BRL-37344 resulted in a significant decrease in serum leptin levels (-55 %, p<0,001). This reduction was not demonstrated by newly synthesized substance B496.

[Morin in the therapy of the ischemia-reperfusion damage model of the rat kidney]. / Morin v terapii ischemicko-reperfuzního poskození ledvinné tkáne laboratorního potkana.

The aim of this study was to analyze the protective effects of morin administered during the therapy of reperfusion injury of the laboratory rat kidney. Animals were randomly divided into five groups (n= 10). One group was left intact. Three medicated groups and one placebo group were subjected to ischemia (60 min) and reperfusion of the left kidney. Morin was suspended in a 2 ml of 0.5% Avicel solution and administered orally by a gastric probe at doses of 5, 10, and 20 mg.kg(-1) once a day for 15 days. The placebo group was given only 2 ml of 0.5% Avicel in the same way. On the 15th day, all the animals were exsanguinated and the reperfused kidneys were recovered. Selected biochemical markers in blood were assessed: superoxide dismutase, glutathion peroxidase, total antioxidative capacity, malondialdehyde, creatinine, urea, and uric acid. Creatinine, urea, and total protein were analyzed in urine, and a 24-hour diuresis was recorded. The kidney tissue samples were used for histopathological examination. Morin supported the organism's own defensive reactions against free radicals and decreased lipid peroxidation in the cell membranes and contributed to the recovery of kidney functions. The histopathological results confirm 20 mg x kg(-1) as the most effective dose.

[Prophylactic administration of homoisoflavonoid in ischemic-reperfusion damage of the renal tissue in the laboratory rat]. / Profylaktické podávání homoizoflavonoidu u ischemicko- reperfuzního poskození ledvinné tkáne laboratorního potkana.

The study aimed to examine the antioxidizing effect of homoisoflavonoid in prophylactic administration under the conditions of renal ischemia-reperfusion in the laboratory rat. The pathological model for the in vivo experiment was unilateral renal ischemia-reperfusion of the laboratory rat. The animals were randomized into 5 groups. Homoisoflavonoid was administered to treated groups orally in doses of 5, 10 and 20 mg/kg once a day in 0.5% Avicel solution. The placebo group received Avicel only, and the intact group was without medication and intervention. On day 15 of the experiment, renal tissue ischemia/reperfusion (60/10 mins) was induced in the treated and placebo groups. Then the animals were exsanguinated, biochemical parameters in the blood (superoxidismutase, glutathionperoxidase, total antioxidizing capacity and malondialdehyde) were assayed, and renal samples were withdrawn for histopathological examination. A biochemical examination demonstrated a dependence of the effect of homoisoflavonoid on the dose administered. An obvious effect was demonstrated in the values of GSHPx, AOC, and MDA. On the other hand, a negative dependence was found between the dose of administered homoisoflavonoid and SOD and GSHPx values. The results of biochemical examination correlate with the histopathological pictures of the renal tissue and support the assumption about a protective effect of homoisoflavonoid under the conditions of artificially induced pathological state--renal tissue ischemia-reperfusion.