Biomedical subjects

K Z Pachkoriia

Publications and source records attributed to K Z Pachkoriia.

3 recordsLinked to original sources

PubMed2006

[Oxidative stress during thyrotoxicosis and its correction].

Oligocrine is a preparation of vegetable origin characterized by anti-inflammatory, antioxidant, immunomodulating properties. Our study shows that administration of L-thyroxine injections (irrespective of the duration) results in elevated synthesis of thyroid hormones and intensification of oxidative stress in experimental animals. These changes are evidenced by accumulation of membrane phospholipide peroxidation products - lipid peroxides in the blood. At that we should point that while dependence of FT3 and FT4 levels on the duration of L-thyroxine administration was insignificant in the experimental model of thyrotoxicosis, intensity of lipid peroxidation increased along with prolongation of injections. Blood levels of free nitric oxide were decreased likely due to the transformation of nitric oxide into peroxinitrite. Oligocrine facilitates to the stabilization of thyroid status and restriction of NO hyperproduction, hypermetabolism and oxidative stress in the body.

Animals↗

PubMed2005

[Major pathogenic links of atherosclerosis].

The experimental and clinical data concerning pathogenesis of the atherosclerosis are summarized and analyzed in this article. Major concepts that explain initiation and progressive growth of atherosclerosis such as lipid infiltrations, response to disturbing factors, "response on the keeping of particles" and inflammatory processes are discussed. These concepts are considered as base for integral theory of atherosclerosis according which the inflammatory process in atherosclerosis are the result of the universal response reaction of endothelium to the various disturbing risk factors. Chronic inflammation leads to complex cellular and molecular interactions among cells derived from the endothelium, smooth muscle and several blood cell components and causes oxidative stress, proliferation of smooth muscle cells, oxidative modification of LDL, uptake and macrophage foam cell formation, endothelium dysfunction. Major pathogenic links of atherosclerosis, such as inflammation, oxidative stress, oxidative modification of LDL, lipid infiltration, endothelial dysfunction closely interact, forming close vicious circles which leads to metabolic and morphological disturbances, re-modulation of blood vessels, cardiovascular diseases and such complication as cardiac infarction and stroke. Pathogenic peculiarities of atherosclerosis are the theoretic base to the elaboration of therapeutic strategy. Endothelium may be discussed as a new therapeutic target in atherosclerosis. So far as the leukotrienes play an important role in inflammatory processes, it is suggested that the leukotrienes may be as a potential therapeutic target in cardiovascular diseases.

Coronary Artery Disease↗

PubMed2005

[Pharmacological correction of hyperactivity of renin-angiotensin-aldosterone system].

Reference data on the function of renin-angiotensin-aldosterone system (RAAS) and pharmacological correction of its hyperactivity are summarized and analyzed in the paper. RAAS plays important role in the development and worsening of hypertension, facilitates proliferation of smooth muscle and heart cells. The hyperactivity of RAAS promotes the development of cardiovascular complications, such as myocardial infarction, stroke, increases cardiovascular mortality and morbidity. Pharmacological correction of RAAS hyperactivity decreases hypertension, prevents occlusion of heart and blood vessels, provides anti-ischemic action, vascular and cardiac protection, improves life style, prevents cardiovascular mortality, such as fatal stroke, myocardial infarction and sudden death. b-blocker inhibitors, angiotensin converting enzyme (ACE) inhibitors, angiotensin AT1-receptors blockers are reviewed as first line therapy of essential hypertension and congestive heart failure. ACT inhibitors, AT1- receptor blockers decrease total cholesterol, LDL, but increase HDL, beta-blockers decrease HDL. AT1-blockers are alternative drugs for treatment of cardiovascular diseases in those cases where ACE inhibitors are contraindicated or intolerance exists.

Adrenergic beta-Antagonists↗