Genophenotypic analysis of angiotensinogen gene M235T polymorphism and preeclampsia.

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.

[Microbiocenosis and activity of the inflammatory process in the colon of the patients with chronic cardiac failure].

The aim of this work was to study colonic microbiocenosis, endotoxin level, intensity of systemic inflammation and the state of matrix metalloproteinase (MMP) system and MMP tissue inhibitors (TIMP) in 75 patients with post-infarction cardiosclerosis at different stages of chronic cardiac failure (CCF). The patients were examined by clinical, echocardiographic and laboratory methods including bacteriological analysis of feces and measurement of amino-terminal brain natriuruetic peptide, endotoxin, TNF-alpha, MMP-9, and TIMP-4. The progress of CCF was shown to be associated with increasing colonic dysbiosis, endotoxin and TNF-alpha levels, disbalance in the MMO and TIMP systems.

[Immune mechanisms in pathogenesis of chronic heart failure].

In the review the new information about a participation of immune mechanisms in a pathogenesis of a chronic heart failure (CHF) is presented. Significance of a bacterial endotoxin, as inductor of activation of immune system at CHF, and factors of a system inflammation in a pathogenesis of the disease, breaking balance of matrix metalloproteinases and tissue inhibitors of metalloproteinases system, leading to change of structure of an extracellular matrix of a myocardium, are discussed.

[The activity of components of system of matrix metalloproteinase and tissue inhibitors of metalloproteinase on different stages of chronic cardiac failure].

The article discusses the results of detection of activity of matrix metalloproteinase-9, tissue inhibitors of metalloproteinases-4, endotoxin, tumor necrosis factor-alpha, C-reactive protein, sE-selectine in blood of patients with chronic cardiac failure depending on severity of disease. It is demonstrated that progressing of chronic cardiac failure is associated with the increase of level of endotoxemia, activation of systemic inflammation and misbalance in the system of matrix metalloproteinase and tissue inhibitors of metalloproteinase.

[Clinic pathogenetic features of gastroduodenal erosions and ulcers in patients with unstable stenocardia].

OBJECTIVE: To reveal the clinical, morphological and pathogenic features of gastroduodenal erosions and ulcers in unstable angina. METHODS: 135 patients with unstable angina were examined and divided into 2 groups, depending on the presence of a pathological process in the gastroduodenal zone. The state of microcirculation in the tissues of the gastroduodenal zone, secretory and motor function of the stomach were estimated by complex of techniques, adapted to the severity of the patients. RESULTS: It is found that the pathological process in the gastroduodenal zone in patients with unstable angina was presented primarily by acute erosions, less - acute ulcers or recurrent peptic ulcer disease. In this case, the leading symptom of acute erosions was dyspepsia, that as a rule prevailed over the indistinct abdominal pain, and often disappeared in the first few days of treatment. Clinical picture of acute ulcers was determined by gastric dyspepsia and was often combined with abdominal pain and symptoms of gastrointestinal bleeding. The recurrence of peptic ulcer disease was characterized by the combination of moderate abdominal pain, often with migration in retrosternal and cardiac area and loss of circadian rhythm inherent in anthro-duodenal ulcer localization, and dyspeptic disorders. The severity of symptoms of ulcerous process was gradually decreased with time, but in most patients, they had remained by the end of the 2nd week of treatment. The basis of development of erosions and ulcers in unstable angina were the focal mainly thrombohaemorrhagic disorders of the terminal blood flow in the gastroduodenal mucosa. Its were combined with changes in the functional state of the stomach, manifested with an increase activity of acid-peptic factor, reduced production of gastromucoproteins, hypomotor dyskinesia and discoordination of anthro-duodenal propulsion on the hypotonic type. CONCLUSION: Erosive and ulcerative lesions of gastroduodenal zone in unstable angina have a number of clinical and pathogenetic features that should be considered in the process of diagnosis and treatment.

[Features of intestine microbiocenosis and systemic inflammation factors in chronic heart failure patients].

AIM: Intestine microbiocenosis structure, endotoxinemia level, C-reactive protein (CRP) and TNFalpha concentration in chronic heart failure patients (CHF) were studied depending on disease severity. MATERIALS AND METHODS: Clinical, echocardiographic and laboratory examination of 104 patients was performed: 75 CHF patients and 29 healthy volunteers. Laboratory examination included bacteriologic analysis of feces for dysbiosis, determination of endotoxin (ET) levels, CRP and TNFalpha levels in blood serum. RESULTS: More expressed alterations in large intestine microbiocenosis and an increase of endotoxinemia and systemic inflammation factors (TNFalpha and CRP) levels were detected in patients with CHF in comparison to individuals without circulatory system pathology. CHF progression is associated with an increase of intestine dysbiosis, and ET, TNFalpha and CRP levels in blood. CONCLUSION: Endotoxinemia in CHF patients, that is caused by an increase in intestine wall permeability during development of venous congestion in systemic circulation, results in immune system activation manifesting in an increase of systemic inflammation factor level in blood that can aggravate the CHF course.

[Trends in systemic inflammatory factors and aminoterminal brain natriuretic propeptide in the treatment of chronic heart failure].

AIM: To study trends in systemic inflammatory factors and aminoterminal brain natriuretic propeptide (NT-proBNP) in the blood of patients with stage IIA and IIB chronic heart failure (CHF) during therapy aimed at reducing venous congestion. MATERIAL AND METHODS: The study enrolled 52 patients with postinfarction cardiosclerosis (PICS). Clinical, echocardiographic and laboratory studies were conducted. The levels of TNF-alpha, IL-6, IL-10 and C-reactive protein (CRP) were measured by enzyme immunoassay. The concentration of endotoxin (ET) was estimated by the end-point chromogenic LAL test, that of NT-proBNP--by immunochromotographic assay. RESULTS: In the patients with CHF, clinical signs of pulmonary venous congestion are associated with a statistically significant increase in the blood levels of TNF-alpha and CRP, those of systemic venous congestion are related to a further rise in TNF-alpha levels and elevation of blood concentrations of NT-proBNP, ET and IL-10. Treatment-related reduction in pulmonary venous congection is associated with a decrease in the levels of TNF-alpha, CRP and IL-6; that in systemic venous congestion--with lower concentrations of NT-proBNP, TNF-alpha and ET. CONCLUSION: Specific changes in the levels of systemic inflammatory factors and NT-proBNP were found in patients with CHF in the presence of pulmonary and systemic venous congestion. Treatment aimed at elimination of the latter leads to reduction in the levels of systemic inflammatory factors and NT-proBNP.

[Endotoxinemia and systemic inflammation in pathogenesis of chronic heart failure].

Large intestine microbiocenosis, levels of endotoxinemia, tumor necrosis factor alpha, C-reactive protein, sE-selectin, matrix metalloproteinase-9 (MMP) and tissue inhibitor of metalloproteinases-4 (TIMP) in chronic heart failure (CHF) patients was studied. Association of dysbiosis and endotoxinemia levels increase, systemic inflammation activation and an imbalance of MMP-TIMP system with progression of CHF has been shown. It can be a reason of a myocardium extracellular matrix structure disturbance and heart remodeling at CHF.

[The influence of the experimental hyperlipoproteinemia on lipid composition and infrared spectrum of hypothalamic and hippocampal tissues]. / Vliianie éksperimental'noi giperlipoproteinemii na lipidnyi sostav i pokazateli infrakrasnogo spektra tkanei gipotalamusa i gippokampa.

Lipid composition and parameters of infrared (IR) spectrum of the tissues controlling heart activity (hypothalamus and hippocamp) were studied in rabbits with experimental hyperlipoproteinemia. Thin-layer chromatography discovered that in atherogenic dislipoproteinemia hypothalamic and hippocampal cholesterol, triglycerides, free fatty acids and phospholipids occurred in higher quantities while the levels of phosphatidylcholines and phosphatidylserines were subnormal. Altered parameters of IR-spectrum of hypothalamic and hippocampal tissue homogenates in atherogenesis were seen in the regions reflecting specific features of structural organization of water molecules. The analysis of the data allows the conclusion that disturbed structural transformation of water in the central nervous system in atherosclerosis is an important link of pathogenesis of electric heart unstability which may result in a sudden cardiac death.

[Non-specific resistance and immune responsiveness in patients with ischemic heart disease and cardiac arrhythmias]. / Nespetsificheskaia rezistentnoct' organizma i immunologicheskaia reaktivnost' u bol'nykh ishemicheskoi bolezn'iu serdtsa s narusheniiami serdechnogo ritma.

Nonspecific resistance (peripheral leukogram, integral leukocytic indices, types of adaptive responses, and phagocytosis) and immunological responsiveness (T- and B-immunity systems) were studied in 30 patients with chronic coronary heart disease (CHD) concurrent with various cardiac arrhythmia. In the patients, there was an increase in the relative counts of band neutrophils and lymphocytes, a decrease in the counts of segmented granulocytes and monocytes. A number of integral leukocytic indices (leukocytic index, lymphocytic-and-granulocytic index, total index, and deviation index) were increased and the neuthrophil/lymphocyte ratio was decreased. A higher frequency of a reactivation response and a lower frequency of a training response were revealed in the structure of their adaptive reactions. The patients with CHD concurrent with arrhythmia were also found to have increased granulopectic and phagocytic indices and higher tetrazolium nitroblue test values than healthy individuals. Their immunological responsiveness was characterized by a reduction in the absolute and relative counts of theophylline-sensitive T lymphocytes and an elevation of immunoglobulins A concentrations.

[The role of certain sections of the central nervous system in the genesis of sudden death]. / Rol' nekotorykh otdelov tsentral'noi nervnoi sistemy v geneze vnezapnoi smerti.

Hypothalamic and hippocampal lipid composition in sudden death from coronary heart disease is studied. Thin-layer chromatography was the main method of biochemical analysis. Disorders in the lipid component of hippocampal cytostructures involved mainly the cholesterol fractions. Metabolic disorders in the hypothalamus involved the phospholipid metabolism. The above-mentioned biochemical changes were paralleled by ultrastructural abnormalities. Analysis of the data demonstrates a probable metabolic basis of a central mechanism of sudden cardiac death.

[Lipid composition of the hypothalamus and hippocampus in sudden cardiac death]. / Lipidnyi sostav gipotalamusa i gippokampa pri vnezapnoi serdechnoi smerti.

The study was made of hypothalamic and hippocampal lipid composition in sudden death of ischemic heart disease. Biochemical findings rest on the evidence obtained at thin-layer chromatography. Lipid disorders of the hippocampal cell structures were primarily related to cholesterol fractures. Hippocampal metabolism was impaired in phospholipids metabolism. These biochemical changes entailed changes in ultrastructure which may represent one of the central mechanisms of a sudden cardiac death.

[Mechanism of self-maintenance of experimental atherogenic hyperlipoproteinemia]. / O mekhanizme samopodderzhaniia éksperimental'noi aterogennoi giperlipoproteinemii.

Disorders of lipid catabolism in the liver and increased formation and intensified secretion into the blood of lipoproteins synthesized in the liver evidently play a significant role in the maintenance of experimental atherogenic hyperlipoproteinemia induced in rabbits by prolonged administration of atherogenic lipoproteins.

[Role of the patho-autokinetic element in the pathogenesis of disturbances of myocardial lipid composition induced by experimental atherogenic dyslipoproteinemia]. / Rol' patoautokineticheskogo élementa v patogeneze narushenii lipidnogo sostava miokarda, indutsirovannykh éksperimental'noi aterogennoi dislipoproteidemiei.

The lipid and phospholipid composition of the myocardium and mitochondria of cardiac myocytes of rabbits was studied after correction of atherogenic dyslipoproteinemia induced by intravenous infusion of atherogenic lipoproteins. Discontinuation of lipoprotein infusions and subsequent normalization of the blood lipoprotein spectrum was not attended by removal of lipidosis of the cardiac muscle characteristic of hyperlipoproteinemia. The disturbance of the lipid composition of the mitochondria of the cardiac myocytes also persisted after disappearance of atherogenic dyslipoproteinemia. The results of the study provide evidence of the existence of a patho-autokinetic element of the pathogenesis of disturbances of myocardial lipid metabolism occurring in atherogenesis.

[The metabolic changes in myocardial subcellular fractions in the pathogenesis of ischemic heart disease]. / Metabolicheskie izmeneniia subkletochnykh fraktsii miokarda v patogeneze ishemicheskoi bolezni serdtsa.

In the myocardial mitochondria (MCh) of persons who had died from ischemic heart disease (IHD) the content of phosphatidylcholine (PCh) and cardiolipin reduces while the amount of the products of their hydrolysis--free fatty acids (FFA) and lysophospholipids--increases. This is evidence of the breakdown of the membrane MCh phospholipids (PL). The content of PL, protein, FChS, FFA, and lysophosphatidylethanolamine in the sarcoplasmic reticulum increases. The increase in the amount of PL, protein, and free cholesterol (FChS) may be explained by an increase of their synthesis due to myocardial hypertrophy which was encountered in all of the cases studied. The accumulation of FFA and lysophosphatidylethanolamine is probably not linked with PL hydrolysis (their amount in this subcellular fraction increases) but is a consequence of other changes in myocardial lipid metabolism. Thus, in IHD hydrolysis of PL prevails in the myocardial MCh and their synthesis in the sarcoplasma reticulum. These changes in the metabolism of the subcellular fractions may lead to damage of the membranes of the cardiomyocyte MCh, which may be the cause of disorders of electrolyte metabolism and contractile properties of the myocardium in IHD.

[Effect of experimental dyslipoproteinemia of atherogenic nature on the lipid composition of the rabbit myocardium and peripheral blood leukocytes]. / Vliianie éksperimental'noi dislipoproteidemii aterogennogo kharaktera na lipidnyi sostav miokarda i leikotsitov perifericheskoi krovi krolikov.

Content of total lipids, phospholipids, total-, free- and ester-bound cholesterol, free fatty acids and triglycerides were increased in myocardium of left ventricle of rabbits with atherogenic dyslipoproteinemia as compared with intact animals. In polymorphonuclear leukocytes content of total lipids and phospholipids was increased only, while in mononuclear leukocytes concentration of total lipids, free-, total- and ester-bound cholesterol and of free fatty acids was elevated.