Резюме. Проведено сравнительное изучение уровней эндотоксинемии, фактора некроза опухо-ли α, С-реактивного белка, sE-селектина, матриксной металлопротеиназы 9 (ММР) и тканевых ин-гибиторов металлопротеиназ 4 (TIMP) у больных хронической сердечной недостаточностью (ХСН) в зависимости от стадии заболевания. Показано, что прогрессирование ХСН ассоциируется с актива-цией системного воспаления, а также дисбалансом в системе ММР-TIMP, который может приводить к нарушению структуры экстрацеллюлярного матрикса миокарда и способствовать ремоделирова-нию отделов сердца при данном заболевании. MARKERS OF SYSTEMIC INFLAMMATION AND MATRIX METALLOPROTEINASE / TISSUE INHIBITOR OF METALLOPROTEINASES SYSTEM AT DIFFERENT STAGES OF CHRONIC HEART FAILUREAbstract. A comparative analysis of endotoxinemia grade, tumor necrosis factor α, C-reactive protein, sEselectin, matrix metalloproteinase-9 (MMP) and tissue inhibitor of metalloproteinases-4 (TIMP) levels was performed in a group of patients with chronic heart failure (CHF). An association has been shown between CHF progression and activation of systemic inflammation, like as with an imbalance in MMP/TIMP system. These alterations may represent a factor of structural disturbances in myocardial extracellular matrix, and promote a compartmental heart remodeling in this disorder.

We studied phenotypes of the circulating renin-angiotensin-aldosterone system and circadian BP during preeclampsia depending on polymorphism of angiotensinogen gene M235T. The TT genotype or T allele of angiotensinogen M235T gene polymorphism is associated with the risk of preeclampsia. Plasma renin activity significantly decreases under conditions of preeclampsia. The TT genotype of angiotensin M235T gene polymorphism is associated with highest renin activity and highest 24-h diastolic BP in comparison with MT and MM genotypes in patients with preeclampsia. Plasma aldosterone level is lower in patients with preeclampsia, but this is not related to angiotensinogen M235T gene polymorphism.

The aim: to detect the presence of pathoautokinesis signs in development and maintenance of hyperlipoproteidemia (HLP) in experiments on intact rabbits and the rabbits after long-term intravenous injection of lipoproteids (LP).Material and methods. 3 series of experiments on rabbits which received for 60 days intravenous homologous apo-Bcontaining LP (25–30 mg LP per 1 kg of the body mass) were carried out. Correspondence of calculated and true values of injected LP, duration of HLP maintenance after LP injection termination and the body response to single injection of interlipin as well as character of elimination with J 131 apo-B-LP from blood alteration of the liver homogenates have been studied.Results. It has been shown that in 50% of rabbits with experimental HLP, the true values of intravenously injected LP were higher than calculated ones. In rabbits after LP injection termination HLP arisen lasts for 30–40 days and intralipid injection induces prolonged HLP. The values of radioactivity of plasma LP in HLP testify to their difficult elimination from blood and their accumulation in the liver.Conclusion. Mechanisms of pathoautokinesis are present in HLP development and maintenance.

The association of angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism with plasma ACE, renin activity and endothelial function of skin microvassals were studied. Preeclamptic patients with the DD genotype of ACE I/D gene polymorphism have lowest plasma renin activity level and endothelium-dependent vasodilatation, D allele carriers have highest plasma ACE activity.