[The fatty acids of membranes of erythrocytes in women with ischemic heart disease under effect of statins].

The technique of evaluation of metabolism of fatty acids in vivo consists in detection of content of fatty acids in phospholipids of membranes of erythrocytes. The fatty acids are received with food, through synthesis on liver from carbohydrates and by katabolism of very long-chain polyolefinic fatty acids of food in peroxisomes of hepatocytes (oxidation, saturation and desaturation). In position sn-1 phospholipids more often than palmitic fatty acid (14%) stearic fatty acid is esterified (21% of all fatty acids). The palmitic, stearic and lignoceric saturated fatty acids are esterified into sn-1 phospholipids as 2:3:1. The simvastatin (80 mg per day) increased content of margarine, tricosanoic and hexacosanoic fatty acids by decrease of level of palmitic fatty acid. The ratio omega-3 polyolefinic fatty acids/omega-6 polyolefinic fatty acids reliably increased. The statins increase content of omega-3 polyolefinic fatty acids. In practice, it is necessary to differentiate the terms "atherosclerosis" and "atheromatosis". The atherosclerosis is a syndrome of intracellular deficiency of polyolefinic fatty acids, derangement of function of cells in vivo under decrease of biological availability for all cells (absorption blockage). The atheromatosis is such most significant clinically symptom of atherosclerosis as accumulation of non-saturated and polyolefinic fatty acids in pool of collection and utilization of biological "garbage" from blood plasma, in intima of elastic type arteries. The statins activate absorption of low density lipoproteins by cells and normalize biological availability of polyolefinic fatty acids which have a positive effect under atherosclerosis and on formation of atheromatosis.

[Rokitansky's theory of humoral pathology, virchow's theory of cellular pathology, and new phylogenetic theory of diseases. Etiology and pathogenesis of "metabolic pandemics"].

Virchow's theory of cellular pathology contains indirect indications that a) there are in vivo structural and functional units between the cell and the organ and b) common mechanisms operate in health and disease. It is proposed to use the phylogenetic theory to obtain an insight into the unified pathogenetic mechanism of atherosclerosis, diabetes mellitus, metabolic syndrome. and obesity. It includes 1) consideration of in vivo physiological and pathological processes in the context of biological functions and reactions, 2) phylogenesis of metabolic regulation at three levels: a) cellular (autocrine), b) paracrine cell communities (structural and functional units of each organ), c) organismic. Biological functions are trophologic, homeostatic, endoecological ("cleanliness" of intercellular medium), adaptive, locomotor reproductive and cognitive. 3) consideration of the successive three-step development of biological functions and reactions of pathological process in phylogenesis. Technical tools in phylogenesis include a) continuity, of formation of biological functions and reactions, b) biological subordination (later formed humoral mediators can not reverse effect of the phylogenetically earlier ones). Inconsistency of humoral regulation at different phylogenetic levels (autocrine, paracrine, organismic) constitutes the basis for common pathogenesis of all metabolic pandemics inclutding essential AH and insulin resistance.

[Stromal progenitor cells and blood leukocytes after implantation of drug-eluting stents].

Aim of the study was to assess participation in development of restenosis of circulating in blood progenitor cells of stromal line of differentiation and polymorphonuclear granulocytes. We compared levels of osteonectin positive progenitor cells, neutrophils, eosinophils, and basophils in blood of patients with ischemic heart disease (IHD) in whom according to data of angiographic study after endovascular myocardial revascularization with the help of stents with drug coating (Cypher, Cordis Corp, USA) restenosis was detected (n=15), in patients without restenosis (n=23), and in healthy persons (n=17). Levels of stromal progenitor cells and polymorphonuclear granulocytes in blood were measured with the help of methods of flow cytometry. In groups of patients with IHD with and without restenosis number of osteonectin positive cells in blood was higher than in healthy subjects (2.4+/-0.7 and 2.5+/-0.9 vs 1.5+/-0.5 cells/ microL, respectively, p=0.004) without significant differences between groups (p=0.59). These 2 groups of patients did not differ by numbers of leukocytes, neutrophils, and basophils in blood. At the same time we found that in patients with restenosis number of eosinophils in blood was significantly greater than in the group of patients without restenosis (262+/-68 vs 124+/-67 cells/ microL, respectively p<0.001). Moreover in patients with level of eosinophils exceeding 170 cells/ microL rate of development of restenosis was 74% against 5% in patients with number of eosinophils less than 170 cells/ microL (p<0.001). Thus level of stromal progenitor cells in blood of patients with IHD was higher than in healthy persons and remained equally high in groups with and without restenosis. Number of blood eosinophilic leukocytes in patients who had been subjected to coronary stenting in whom later restenosis developed was significantly higher than in patients without restenosis. The data obtained indicate at the presence of link between development of in - stent restenosis and elevated content of eosinophilic granulocytes in blood of patients with IHD.

[The activity of nonspecific inflammation in hypertensive patients].

AIM: To study the indices of nonspecific inflammation (C-reactive protein--CRP, interleukine 6--IL-6) in patients with essential hypertension (EH) as compared to a circadian profile of blood pressure (BP); changes of CRP in the course of therapy with indapamide-retard and ACE inhibitor perindopril. MATERIAL AND METHODS: The trial enrolled 81 patients with hypertension of stage I-II, moderate and high risk, aged 45.1 +/- 1.3 years, free of chronic inflammatory disease exacerbation, 2 months and more after acute respiratory diseases and 2-week absence of antihypertensive therapy. CRP was estimated by turbidimetry, IL-6--by ELISA, circadian BP monitoring was made using TM 2421 device. Seventeen patients were randomized to receive ariphon retard (Servier), twenty patients--prestarium. The data were processed with STATISTICA 6 programs. RESULTS: CRP level in the patients was 7.0 +/- 1.6 mg/l; an elevated CRP concentration (> 3 mg/l) was registered in 55% patients. These patients demonstrated a positive correlation of CRP concentration with the data of 24-h systolic BP (r = 0.37, p < 0.05) and 24-h diastolic BP (r = 0.43, p = 0.003) monitoring, abnormal circadian rhythm of BP (nondippers). IL-6 in the examinees was 6.7 +/- 1.3 pg/ml. An elevated IL-6 concentration was detected in 30%. In such patients a positive correlation was found between IL-6 and 24-h systolic and diastolic BP (r = 0.88; p < 0.05 and r = 0.97; p < 0.01, respectively). CONCLUSION: A positive correlation between CRP, IL-6 and BP may evidence for involvement of nonspecific inflammation in the course of EH. Patients with elevated CRP responded to ariphon retard with positive CRP dynamics. This can be explained by a relief of chronic hemodynamic stress. A positive CRP dynamics in response to prestarium can be mediated by block of angiotensin II.

[Insulin as a humoral factor of energy supply for the biological function of locomotion]. / Insulin - gumoral'nyi faktor obespecheniia energiei biologicheskoi funktsii lokomotsii.

From the point of view of general biology the author considers hyperglycemia and glucagon to have in the course of phylogenesis provided cells with a capability of in vivo glucose (GLU) uptake and depositing it in the form of glycogen. At the same time gluconeogenesis, facilitated GLU uptake via transporters and passive non-etherified fat acid (FA) uptake by myocytes were formed. Millions years later changes in dietary habits and motion initiated beta-cells and insulin system in order to provide energy for biological function of locomotion (migrations). Glucagon-regulated processes are not affected by insulin (INS). Myocytes became INS-independent cells; in cases of functional INS-resistance, which prevented them from depositing large amount of GLU, the hormone initiated lipogenesis i.e. conversion of GLU into saturated palmitic fat acid FA and its etherification into triglycerides. To deposit them INS initiated the differentiation of adipocytes (the second INS-independent cell). INS initiated the synthesis of apoE and active receptor uptake of FA by cells in the form of triglycerides through apoE/B- 100 receptor endocytosis. Since myocytes oxidize unsaturated FA more rapidly, INS initiated the system of elongases and desaturases and the conversion of saturated palmitic FA into unsaturated oleic FA in adipocytes. The contractile activity of myocytes is the main physiologic counter-regulator of INS. Within millions of years of phylogenesis INS had been forming the system of supplying myocytes with energy and perfecting the biological function of locomotion which Homo sapiens virtually lost in a moment.