12 research outputs found
ΠΠΊΠ°Π·Π°Π½ΠΈΠ΅ ΡΠΊΡΡΡΠ΅Π½Π½ΠΎΠΉ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΎΠΉ ΠΏΠΎΠΌΠΎΡΠΈ Π½Π° Π΄ΠΎΠ³ΠΎΡΠΏΠΈΡΠ°Π»ΡΠ½ΠΎΠΌ ΡΡΠ°ΠΏΠ΅ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°ΠΌ Ρ ΠΎΡΡΡΡΠΌ ΠΈΠ½ΡΠ°ΡΠΊΡΠΎΠΌ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄Π° ΠΈ ΠΎΡΡΡΡΠΌ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΈΠ½ΡΡΠ»ΡΡΠΎΠΌ Π² Π³ΠΎΡΠΎΠ΄Π΅ ΠΠΎΡΠΊΠ²Π΅: ΡΠΎΠ»Ρ Π°Π²ΠΈΠ°ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΈΡ Π±ΡΠΈΠ³Π°Π΄ ΡΠ΅Π½ΡΡΠ° ΡΠΊΡΡΡΠ΅Π½Π½ΠΎΠΉ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΎΠΉ ΠΏΠΎΠΌΠΎΡΠΈ (Π’Π΅ΡΡΠΈΡΠΎΡΠΈΠ°Π»ΡΠ½ΡΠΉ ΡΠ΅Π½ΡΡ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½Ρ ΠΊΠ°ΡΠ°ΡΡΡΠΎΡ)
The increase in the number of patients with complications of cardiovascular diseases and the need for early diagnosis of such complications and the early initiation of treatment already at the prehospital stage leads to an increasingΒ need for more frequent use of helicopter medical equipment, as well as for equipping aviation medical teams with highly qualified specialists. TheΒ formation of a network of vascular invasive centers in the Moscow region,Β modern equipment and its use in air ambulance conditions require constant improvement of skills among medical workers. All this undoubtedly leads to positive results, the mortality rate from heart attacks and strokes decreases, the duration of treatment and the period of rehabilitation of patients areΒ reduced. It should be noted that even 10 years ago, medical helicopters were used in the elimination of medical consequences in road accidents, fires and emergencies. Today, aviation medical teams are involved in more than 50% of cases with cardiovascular diseases, which undoubtedly speaks of theΒ prospects for the development of medical aviation in large cities.Β Π ΠΎΡΡ ΡΠΈΡΠ»Π° ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΠ΅ΡΠ΄Π΅ΡΠ½ΠΎ-ΡΠΎΡΡΠ΄ΠΈΡΡΡΠΌΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΠΌΠΈ, Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎΡΡΡ Π±ΡΡΡΡΠΎΠΉ ΡΡΠ°Π½ΡΠΏΠΎΡΡΠΈΡΠΎΠ²ΠΊΠΈΒ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Π² ΡΡΠ°ΡΠΈΠΎΠ½Π°Ρ Ρ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠ΅ΠΌ ΡΠ°Π½Π½Π΅ΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈΒ ΠΈ ΡΠ²ΠΎΠ΅Π²ΡΠ΅ΠΌΠ΅Π½Π½ΠΎΠ³ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΡ Π½Π° Π΄ΠΎΠ³ΠΎΡΠΏΠΈΡΠ°Π»ΡΠ½ΠΎΠΌ ΡΡΠ°ΠΏΠ΅ ΠΎΠ±ΡΡΠ»Π°Π²Π»ΠΈΠ²Π°ΡΡ Π²ΠΎΠ·ΡΠ°ΡΡΠ°ΡΡΡΡ ΠΏΠΎΡΡΠ΅Π±Π½ΠΎΡΡΡ Π² Π±ΠΎΠ»Π΅Π΅ ΡΠ°ΡΡΠΎΠΌΒ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠΈ Π²Π΅ΡΡΠΎΠ»Π΅ΡΠ½ΠΎΠΉ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΎΠΉ ΡΠ΅Ρ
Π½ΠΈΠΊΠΈ ΠΈΒ Π½Π°Π»ΠΈΡΠΈΠ΅ ΡΠΏΠ΅ΡΠΈΠ°Π»ΠΈΡΡΠΎΠ² Π²ΡΡΠΎΠΊΠΎΠΉ ΠΊΠ²Π°Π»ΠΈΡΠΈΠΊΠ°ΡΠΈΠΈ Π² ΡΠΎΡΡΠ°Π²Π΅Β Π°Π²ΠΈΠ°ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΈΡ
Π±ΡΠΈΠ³Π°Π΄. Π€ΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΡΠ΅ΡΠΈ ΡΠΎΡΡΠ΄ΠΈΡΡΡΡ
Β ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΡΡ
ΡΠ΅Π½ΡΡΠΎΠ² Π² ΠΌΠΎΡΠΊΠΎΠ²ΡΠΊΠΎΠΌ ΡΠ΅Π³ΠΈΠΎΠ½Π΅, ΡΠΎΠ²ΡΠ΅ΠΌΠ΅Π½Π½ΠΎΠ΅ ΠΎΠ±ΠΎΡΡΠ΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ Π΅Π³ΠΎ Π² ΡΡΠ»ΠΎΠ²ΠΈΡΡ
ΡΠ°Π½ΠΈΡΠ°ΡΠ½ΠΎΠΉ Π°Π²ΠΈΠ°ΡΠΈΠΈ ΡΡΠ΅Π±ΡΡΡ ΠΏΠΎΡΡΠΎΡΠ½Π½ΠΎΠ³ΠΎ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΡ Π½Π°Π²ΡΠΊΠΎΠ² ΡΡΠ΅Π΄ΠΈΒ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΈΡ
ΡΠ°Π±ΠΎΡΠ½ΠΈΠΊΠΎΠ². ΠΡΠ΅ ΡΡΠΎ ΠΏΡΠΈΠ²ΠΎΠ΄ΠΈΡ ΠΊΒ ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΡΠΌ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ°ΠΌ, ΡΠ°ΠΊ ΠΊΠ°ΠΊ ΡΠ½ΠΈΠΆΠ°Π΅ΡΡΡ ΡΠΌΠ΅ΡΡΠ½ΠΎΡΡΡΒ ΠΎΡ ΠΈΠ½ΡΠ°ΡΠΊΡΠΎΠ² ΠΈ ΠΈΠ½ΡΡΠ»ΡΡΠΎΠ², ΡΠΎΠΊΡΠ°ΡΠ°ΡΡΡΡ ΡΡΠΎΠΊΠΈ Π»Π΅ΡΠ΅Π½ΠΈΡ ΠΈ ΡΠ΅Π°Π±ΠΈΠ»ΠΈΡΠ°ΡΠΈΠΈ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ². Π‘Π»Π΅Π΄ΡΠ΅Ρ ΠΎΡΠΌΠ΅ΡΠΈΡΡ, ΡΡΠΎ Π΅ΡΠ΅ 10 Π»Π΅Ρ Π½Π°Π·Π°Π΄ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΈΠ΅ Π²Π΅ΡΡΠΎΠ»Π΅ΡΡ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π»ΠΈΡΡ ΠΏΡΠΈ Π΄ΠΎΡΠΎΠΆΠ½ΠΎ-ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ½ΡΡ
ΠΏΡΠΎΠΈΡΡΠ΅ΡΡΠ²ΠΈΡΡ
, ΠΏΠΎΠΆΠ°ΡΠ°Ρ
ΠΈΒ ΡΡΠ΅Π·Π²ΡΡΠ°ΠΉΠ½ΡΡ
ΡΠΈΡΡΠ°ΡΠΈΡΡ
. Π‘Π΅Π³ΠΎΠ΄Π½Ρ Π°Π²ΠΈΠ°ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΈΠ΅Β Π±ΡΠΈΠ³Π°Π΄Ρ Π±ΠΎΠ»Π΅Π΅ ΡΠ΅ΠΌ Π² 50% ΡΠ»ΡΡΠ°Π΅Π² Π·Π°Π΄Π΅ΠΉΡΡΠ²ΠΎΠ²Π°Π½Ρ ΠΏΡΠΈΒ ΡΠ²Π°ΠΊΡΠ°ΡΠΈΠΈ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΡΠ΅ΡΠ΄Π΅ΡΠ½ΠΎ-ΡΠΎΡΡΠ΄ΠΈΡΡΡΠΌΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΠΌΠΈ,Β ΡΡΠΎ Π±Π΅Π·ΡΡΠ»ΠΎΠ²Π½ΠΎ Π³ΠΎΠ²ΠΎΡΠΈΡ ΠΎ ΠΏΠ΅ΡΡΠΏΠ΅ΠΊΡΠΈΠ²Π΅Β ΡΠ°Π·Π²ΠΈΡΠΈΡ ΡΠ°Π½ΠΈΡΠ°ΡΠ½ΠΎΠΉ Π°Π²ΠΈΠ°ΡΠΈΠΈ Π² ΠΊΡΡΠΏΠ½ΡΡ
Π³ΠΎΡΠΎΠ΄Π°Ρ
.
Π₯ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠ°Ρ ΠΎΠ±ΡΡΡΡΠΊΡΠΈΠ²Π½Π°Ρ Π±ΠΎΠ»Π΅Π·Π½Ρ Π»Π΅Π³ΠΊΠΈΡ ΠΈ COVID-19: Π°ΠΊΡΡΠ°Π»ΡΠ½ΡΠ΅ Π²ΠΎΠΏΡΠΎΡΡ
The problem of comorbidity of new coronaviral infection (COVID-19) and chronic obstructive pulmonary disease (COPD) is acute, considering similarity of clinical manifestations, diagnostic difficulties, the potential severe disease course. Patients with COPD represent a vulnerable group of infected SARS-CoV-2, with a complicated disease course and frequent adverse outcome. Features of the spread of the virus limit treatment and diagnosis for patients with COPD, making it difficult to provide medical care during the pandemic. The negative results of some clinical studies of antiviral drugs for patients with COVID-19 indicate the need for a search for new drugs; for this reason, analysis of the anti-inflammatory effect on the lungs in infection COVID-19 of drugs of basic COPD therapy is promising.ΠΠΊΡΡΠ°Π»ΡΠ½ΠΎΡΡΡ ΠΏΡΠΎΠ±Π»Π΅ΠΌΡ ΠΊΠΎΠΌΠΎΡΠ±ΠΈΠ΄Π½ΠΎΡΡΠΈ Π½ΠΎΠ²ΠΎΠΉ ΠΊΠΎΡΠΎΠ½Π°Π²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ COVID-19 ΠΈ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΎΠ±ΡΡΡΡΠΊΡΠΈΠ²Π½ΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π»Π΅Π³ΠΊΠΈΡ
(Π₯ΠΠΠ) ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½Π° ΡΡ
ΠΎΠΆΠ΅ΡΡΡΡ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ, ΡΠ»ΠΎΠΆΠ½ΠΎΡΡΡΡ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ, ΠΏΠΎΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ ΡΡΠΆΠ΅ΡΡΡΡ ΡΠ΅ΡΠ΅Π½ΠΈΡ ΠΈ Π²Π·Π°ΠΈΠΌΠΎΠΎΡΡΠ³ΠΎΡΠ΅Π½ΠΈΠ΅ΠΌ ΡΡΠΈΡ
ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΠΉ. ΠΠΎΠ»ΡΠ½ΡΠ΅ Π₯ΠΠΠ, ΠΈΠ½ΡΠΈΡΠΈΡΠΎΠ²Π°Π½Π½ΡΠ΅ SARS-CoV-2, ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΡΡ ΡΠΎΠ±ΠΎΠΉ ΡΡΠ·Π²ΠΈΠΌΡΡ Π³ΡΡΠΏΠΏΡ Π»ΠΈΡ Ρ ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½Π½ΡΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΈ ΡΠ°ΡΡΠΎ Π½Π΅Π±Π»Π°Π³ΠΎΠΏΡΠΈΡΡΠ½ΡΠΌ ΠΈΡΡ
ΠΎΠ΄ΠΎΠΌ Π±ΠΎΠ»Π΅Π·Π½ΠΈ. ΠΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½ΠΈΡ Π²ΠΈΡΡΡΠ° Π½Π°ΠΊΠ»Π°Π΄ΡΠ²Π°ΡΡ Π·Π½Π°ΡΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΠΎΠ³ΡΠ°Π½ΠΈΡΠ΅Π½ΠΈΡ Π½Π° ΠΌΠ½ΠΎΠ³ΠΎΡΠΈΡΠ»Π΅Π½Π½ΡΠ΅ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ Π»Π΅ΡΠ΅Π±Π½ΡΠ΅ ΠΌΠ΅ΡΠΎΠΏΡΠΈΡΡΠΈΡ ΠΏΡΠΈ Π₯ΠΠΠ, Π·Π°ΡΡΡΠ΄Π½ΡΡ ΠΎΠΊΠ°Π·Π°Π½ΠΈΠ΅ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΎΠΉ ΠΏΠΎΠΌΠΎΡΠΈ Π±ΠΎΠ»ΡΠ½ΡΠΌ Π΄Π°Π½Π½ΠΎΠΉ ΠΊΠ°ΡΠ΅Π³ΠΎΡΠΈΠΈ Π² ΠΏΠ΅ΡΠΈΠΎΠ΄ ΠΏΠ°Π½Π΄Π΅ΠΌΠΈΠΈ Π½Π° Π²ΡΠ΅Ρ
Π΅Π΅ ΡΡΠ°ΠΏΠ°Ρ
. ΠΠ΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎΡΡΡ ΠΏΠΎΠΈΡΠΊΠ° Π½ΠΎΠ²ΡΡ
ΡΠ΅ΡΠ°ΠΏΠ΅Π²ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ΅ΡΠ΅Π½ΠΈΠΉ ΠΏΡΠΎΠ΄ΠΈΠΊΡΠΎΠ²Π°Π½Π° ΠΎΡΡΠΈΡΠ°ΡΠ΅Π»ΡΠ½ΡΠΌΠΈ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ°ΠΌΠΈ ΡΠ΅ΠΊΡΡΠΈΡ
ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΉ ΠΏΠΎ ΠΈΠ·ΡΡΠ΅Π½ΠΈΡ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΡΠ΄Π° ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠ² Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
COVID-19; ΠΏΠ΅ΡΡΠΏΠ΅ΠΊΡΠΈΠ²Π½ΡΠΌ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ΅ΡΡΡ ΠΈΠ·ΡΡΠ΅Π½ΠΈΠ΅ Π΄Π΅ΠΉΡΡΠ²ΠΈΡ Π½Π° SARS-CoV-2 ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠ² Π±Π°Π·ΠΎΠ²ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π₯ΠΠΠ Ρ Π΄ΠΎΠΊΠ°Π·Π°Π½Π½ΡΠΌ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠΌ Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ΠΌ Π½Π° Π±ΡΠΎΠ½Ρ
ΠΎΠ»Π΅Π³ΠΎΡΠ½ΡΡ ΡΠΈΡΡΠ΅ΠΌΡ
ΠΠΎΠ½ΠΎΡΠΈΡΡ ΠΊΡΠΎΠ²ΠΈ Π² ΠΏΠΎΠ΄Π΄Π΅ΡΠΆΠ°Π½ΠΈΠΈ Π±Π°Π»Π°Π½ΡΠ° Π΄Π΅ΡΡΡΡΠΊΡΠΈΠ²Π½ΡΡ ΠΈ ΡΠ΅ΠΏΠ°ΡΠ°ΡΠΈΠ²Π½ΡΡ ΠΏΡΠΎΡΠ΅ΡΡΠΎΠ² Π² ΡΠΎΡΡΠ΄ΠΈΡΡΠΎΠΌ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠΈ ΠΏΡΠΈ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ
Highlights. The features of subsets of monocytes in combination with the levels of desquamated endotheliocytes, endothelial damage and regeneration mediators and progenitor cell migration-enhancing factors in patients with coronary heart disease and with/without ischemic cardiomyopathy were analyzed. For the first time it was shown that in patients with ischemic cardiomyopathy, compared with CHD patients without cardiomyopathy, higher desquamation of the endothelium is associated with a deficiency of non-classical monocytes and reduced migration of progenitor endothelial cells (VEGFR2+-monocytes) with regenerative potential across the bone marrow due to a deficiency of the HIF-1Ξ± mediator in the blood.Background. The development of ischemic cardiomyopathy (ICM) is an understudied process, and one of its elements may be insufficient regeneration of blood vessels due to an imbalance of subsets of monocytes in the blood.Aim. To assess subsets of monocytes and desquamated endothelial cells in combination with endothelial damage and regeneration mediators in the blood of patients with coronary heart disease (CHD) and with/without ICM.Methods. The study included 30 patients with ICM, 22 patients with coronary heart disease without cardiomyopathy aged 55β69 years, and 18 healthy donors. In whole blood, the populations of CD45βCD146+ desquamated endothelial cells and progenitor endothelial cells related to CD14+VEGFR2+Β monocytes, intermediate CD14++CD16+Β Β andΒ non-classicalΒ CD14+CD16++Β Β monocytesΒ wereΒ assessedΒ by flow cytometryΒ usingΒ theΒ appropriateΒ monoclonalΒ antibodiesΒ (BDΒ Biosciens, USA). In blood plasma, the levels of hypoxia-inducible factor HIF-1Ξ±, monocyte chemoattractant protein MCP-1 and matrix metalloproteinase MMP-9 were assessed by enzyme immunoassay. The results of the analysis were considered significant at p<0.05.Results. The number of progenitor and desquamated endothelial cells was increased in both groups of patients with coronary artery disease. At the same time, in patients with ICM, the number of progenitor endothelial cells did not reach the number noted in patients with CHD without cardiomyopathy, while the number of desquamated endothelial cells reached the number noted in CHD patients without cardiomyopathy. There was a deficiency of non-classical monocytes and HIF-1Ξ± in the blood of patients with ICM, and an excess of intermediate monocytes and MCP-1 was observed in CHD patients without cardiomyopathy. The concentration of MMP-9 in patients with CHD corresponded to the norm, regardless of the presence of ICM.Conclusion. In ICM, in contrast to CHD without cardiomyopathy, vascular damage is associated with a deficiency of nonclassical monocytes and reduced endothelial repair due to insufficient migration of progenitor endothelial cells across the bone marrow due to HIF-1Ξ± deficiency in the blood.ΠΡΠ½ΠΎΠ²Π½ΡΠ΅ ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΡ. ΠΠ·ΡΡΠ΅Π½Ρ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΡΠΎΡΡΠ°Π²Π° ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΊΡΠΎΠ²ΠΈ Π² ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ΅ Ρ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ΠΌ Π΄Π΅ΡΠΊΠ²Π°ΠΌΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠΎΡΠΈΡΠΎΠ², ΠΌΠ΅Π΄ΠΈΠ°ΡΠΎΡΠΎΠ² Π΄Π΅ΡΡΡΡΠΊΡΠΈΠΈ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΡ ΠΈ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΌΠΈΠ³ΡΠ°ΡΠΈΠΈ Π΅Π³ΠΎ ΠΊΠ»Π΅ΡΠΎΠΊ-ΠΏΡΠ΅Π΄ΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΈΡ Π² ΠΊΡΠΎΠ²ΠΈ ΠΏΡΠΈ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΠΈ ΡΠ΅ΡΠ΄ΡΠ°, ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½Π½ΠΎΠΉ ΠΈ Π½Π΅ ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½Π½ΠΎΠΉ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠ΅ΠΉ. ΠΠΏΠ΅ΡΠ²ΡΠ΅ ΠΏΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΠΏΡΠΈ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ, Π² ΠΎΡΠ»ΠΈΡΠΈΠ΅ ΠΎΡ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΠΈ ΡΠ΅ΡΠ΄ΡΠ° Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ, Π²ΡΡΠΎΠΊΠ°Ρ Π΄Π΅ΡΠΊΠ²Π°ΠΌΠ°ΡΠΈΡ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΡ Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π° Ρ Π΄Π΅ΡΠΈΡΠΈΡΠΎΠΌ Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΈ ΠΏΠΎΠ½ΠΈΠΆΠ΅Π½Π½ΠΎΠΉ ΠΌΠΈΠ³ΡΠ°ΡΠΈΠ΅ΠΉ ΠΈΠ· ΠΊΠΎΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π° ΠΏΡΠΎΠ³Π΅Π½ΠΈΡΠΎΡΠ½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ (VEGFR2+-ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ²) Ρ ΡΠ΅ΠΏΠ°ΡΠ°ΡΠΈΠ²Π½ΡΠΌ ΠΏΠΎΡΠ΅Π½ΡΠΈΠ°Π»ΠΎΠΌ Π²Π²ΠΈΠ΄Ρ Π΄Π΅ΡΠΈΡΠΈΡΠ° ΠΌΠ΅Π΄ΠΈΠ°ΡΠΎΡΠ° HIF-1Ξ± Π² ΠΊΡΠΎΠ²ΠΈ.ΠΠΊΡΡΠ°Π»ΡΠ½ΠΎΡΡΡ. ΠΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠ°Ρ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΡ (ΠΠΠΠ) ΡΠ°Π·Π²ΠΈΠ²Π°Π΅ΡΡΡ ΠΏΠΎ ΠΌΠ°Π»ΠΎΠΈΠ·ΡΡΠ΅Π½Π½ΡΠΌ Π·Π°ΠΊΠΎΠ½ΠΎΠΌΠ΅ΡΠ½ΠΎΡΡΡΠΌ, Π² ΡΠΈΡΠ»Π΅ ΠΊΠΎΡΠΎΡΡΡ
ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ Π½Π΅Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½Π°Ρ ΡΠ΅ΠΏΠ°ΡΠ°ΡΠΈΡ ΡΠΎΡΡΠ΄ΠΎΠ² Π²ΡΠ»Π΅Π΄ΡΡΠ²ΠΈΠ΅ Π΄ΠΈΡΠ±Π°Π»Π°Π½ΡΠ° ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΉ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² Π² ΠΊΡΠΎΠ²ΠΈ.Π¦Π΅Π»Ρ. ΠΠΏΡΠ΅Π΄Π΅Π»ΠΈΡΡ ΡΠΈΡΠ»Π΅Π½Π½ΠΎΡΡΡ ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΉ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΈ Π΄Π΅ΡΠΊΠ²Π°ΠΌΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ Π² ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ΅ Ρ ΠΌΠ΅Π΄ΠΈΠ°ΡΠΎΡΠ°ΠΌΠΈ Π΄Π΅ΡΡΡΡΠΊΡΠΈΠΈ ΠΈ ΡΠ΅ΠΏΠ°ΡΠ°ΡΠΈΠΈ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΡ Π² ΠΊΡΠΎΠ²ΠΈ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΡΡ ΡΠ΅ΡΠ΄ΡΠ° (ΠΠΠ‘), ΡΡΡΠ°Π΄Π°ΡΡΠΈΡ
ΠΈ Π½Π΅ ΡΡΡΠ°Π΄Π°ΡΡΠΈΡ
ΠΠΠΠ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. Π ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Π²ΠΎΡΠ»ΠΈ 30 Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠΠ ΠΈ 22 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ° Ρ ΠΠΠ‘ Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ Π² Π²ΠΎΠ·ΡΠ°ΡΡΠ΅ 55β69 Π»Π΅Ρ, Π° ΡΠ°ΠΊΠΆΠ΅ 18 Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ½ΠΎΡΠΎΠ². Π ΡΠ΅Π»ΡΠ½ΠΎΠΉ ΠΊΡΠΎΠ²ΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ CD45βCD146+Β Π΄Π΅ΡΠΊΠ²Π°ΠΌΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ ΠΈ ΠΏΡΠΎΠ³Π΅Π½ΠΈΡΠΎΡΠ½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ, ΠΎΡΠ½ΠΎΡΡΡΠΈΡ
ΡΡ ΠΊ CD14+VEGFR2+-ΠΌΠΎΠ½ΠΎΡΠΈΡΠ°ΠΌ, ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
CD14++CD16+ ΠΈ Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² CD14+CD16++ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΏΡΠΎΡΠΎΡΠ½ΠΎΠΉ ΡΠΈΡΠΎΡΠ»ΡΠΎΡΠΈΠΌΠ΅ΡΡΠΈΠΈ Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²ΡΡΡΠΈΡ
ΠΌΠΎΠ½ΠΎΠΊΠ»ΠΎΠ½Π°Π»ΡΠ½ΡΡ
Π°Π½ΡΠΈΡΠ΅Π» (BD Biosciences, Π‘Π¨Π). Π ΠΏΠ»Π°Π·ΠΌΠ΅ ΠΊΡΠΎΠ²ΠΈ ΠΎΡΠ΅Π½ΠΈΠ²Π°Π»ΠΈ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ ΠΈΠ½Π΄ΡΡΠΈΡΡΠ΅ΠΌΠΎΠ³ΠΎ Π³ΠΈΠΏΠΎΠΊΡΠΈΠ΅ΠΉ ΡΠ°ΠΊΡΠΎΡΠ° HIF-1Ξ±, ΠΌΠΎΠ½ΠΎΡΠΈΡΠ°ΡΠ½ΠΎΠ³ΠΎ Ρ
Π΅ΠΌΠΎΡΠ°ΠΊΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π±Π΅Π»ΠΊΠ° ΠΠ‘Π -1 ΠΈ ΠΌΠ°ΡΡΠΈΠΊΡΠ½ΠΎΠΉ ΠΌΠ΅ΡΠ°Π»Π»ΠΎΠΏΡΠΎΡΠ΅ΠΈΠ½Π°Π·Ρ ΠΠΠ -9 ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅ΡΠΌΠ΅Π½ΡΠ½ΠΎΠ³ΠΎ Π°Π½Π°Π»ΠΈΠ·Π°. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ Π°Π½Π°Π»ΠΈΠ·Π° ΡΡΠΈΡΠ°Π»ΠΈ Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½ΡΠΌΠΈ ΠΏΡΠΈ Ρ<0,05.Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π£ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠ‘ ΠΎΠ±Π΅ΠΈΡ
Π³ΡΡΠΏΠΏ Π²ΡΡΠ²Π»Π΅Π½ΠΎ ΠΏΠΎΠ²ΡΡΠ΅Π½Π½ΠΎΠ΅ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ Π΄Π΅ΡΠΊΠ²Π°ΠΌΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
ΠΈ ΠΏΡΠΎΠ³Π΅Π½ΠΈΡΠΎΡΠ½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ Π² ΠΊΡΠΎΠ²ΠΈ. ΠΡΠΈ ΡΡΠΎΠΌ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ ΠΏΡΠΎΠ³Π΅Π½ΠΈΡΠΎΡΠ½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΠΠΠ Π½Π΅ Π΄ΠΎΡΡΠΈΠ³Π°Π»ΠΎ ΡΡΠΎΠ²Π½Ρ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠ‘ Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ, Π° ΡΠΈΡΠ»ΠΎ Π΄Π΅ΡΠΊΠ²Π°ΠΌΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠΎΡΠΈΡΠΎΠ² ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²ΠΎΠ²Π°Π»ΠΎ ΡΠ°ΠΊΠΎΠ²ΠΎΠΌΡ. Π ΠΊΡΠΎΠ²ΠΈ ΠΏΡΠΈ ΠΠΠΠ ΠΎΠ±Π½Π°ΡΡΠΆΠ΅Π½ Π΄Π΅ΡΠΈΡΠΈΡ Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΈ HIF-1Ξ±, ΠΏΡΠΈ ΠΠΠ‘ Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ β ΠΈΠ·Π±ΡΡΠΎΠΊ ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΈ ΠΠ‘Π -1. ΠΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ ΠΠΠ -9 Π² ΠΊΡΠΎΠ²ΠΈ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΠΠ‘ ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²ΠΎΠ²Π°Π»Π° Π½ΠΎΡΠΌΠ΅ Π²Π½Π΅ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ Π½Π°Π»ΠΈΡΠΈΡ ΠΠΠΠ.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΡΠΈ ΠΠΠΠ, Π² ΠΎΡΠ»ΠΈΡΠΈΠ΅ ΠΎΡ ΠΠΠ‘ Π±Π΅Π· ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ, ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΠ΅ ΡΠΎΡΡΠ΄ΠΎΠ² Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½ΠΎ Ρ Π΄Π΅ΡΠΈΡΠΈΡΠΎΠΌ Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΈ ΠΏΠΎΠ½ΠΈΠΆΠ΅Π½Π½ΠΎΠΉ ΡΠ΅ΠΏΠ°ΡΠ°ΡΠΈΠ΅ΠΉ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΡ, ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½Π½ΠΎΠΉ Π½Π΅Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½ΠΎΠΉ ΠΌΠΈΠ³ΡΠ°ΡΠΈΠ΅ΠΉ ΠΏΡΠΎΠ³Π΅Π½ΠΈΡΠΎΡΠ½ΡΡ
ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ ΠΈΠ· ΠΊΠΎΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π° Π²Π²ΠΈΠ΄Ρ Π΄Π΅ΡΠΈΡΠΈΡΠ° HIF-1Ξ± Π² ΠΊΡΠΎΠ²ΠΈ
PROSPECTS FOR CYTOPROTECTORS USE IN THE ELDERLY PATIENTS THROUGH THE EXAMPLE OF CALCIFIED AORTIC STENOSIS AND ISCHEMIC HEART DISEASE
Issues of pathogenesis of the calcified aortic stenosis and ischemic heart disease in the elderly are considered. The relevance of early detection of angina, syncope, and dyspnea in view of their non-specific and subclinical course for early detection of heart disease is specified. Current scientific views on the myocardial bioenergy and its role in the genesis of chronic heart failure are presented. Particular attention is paid to the place of cytoprotectors, especially trimetazidine, in the management of patients with cardiac N.Yu. Karpova1diseases.</p
PROSPECTS FOR CYTOPROTECTORS USE IN THE ELDERLY PATIENTS THROUGH THE EXAMPLE OF CALCIFIED AORTIC STENOSIS AND ISCHEMIC HEART DISEASE
Issues of pathogenesis of the calcified aortic stenosis and ischemic heart disease in the elderly are considered. The relevance of early detection of angina, syncope, and dyspnea in view of their non-specific and subclinical course for early detection of heart disease is specified. Current scientific views on the myocardial bioenergy and its role in the genesis of chronic heart failure are presented. Particular attention is paid to the place of cytoprotectors, especially trimetazidine, in the management of patients with cardiac N.Yu. Karpova1diseases
CORRECTION OF ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH CHRONIC COR PULMONALE BY ANGIOTENSIN II RECEPTORS ANTAGONISTS
Aim. To evaluate intensity of endothelial dysfunction, processes of apoptosis, state of central and peripheral hemodynamics and to evaluate how these characteristics are influenced by angiotensin II receptors antagonists (ARA II) β candesartan (Atacand) and losartan (Cosaar) in patients with chronic cor pulmonale (CCP) at different stages of disease.Material and methods. 100 patients with chronic obstructive pulmonary disease (COPD), complicated by CCP were included into the study. Caspase activity as apoptosis induction marker, von Willebrand factor, production of nitric oxide in blood plasma and condensate of breathing out air were assessed. 70 patients received ARA II (50 patients β candesartan 4-8 mg daily, 20 patients β losartan 50-100 mg daily), 30 patients received neither ARA II nor angiotensin converting enzyme inhibitors (ACEI).Results. Significant increase in intensity of endothelial dysfunction and activation of apoptosis processes were registered according to growth of CCP severity. After 6 months of therapy von Willebrand factor decreased by 25,2% and 27,7% in candesartan and losartan groups respectively (p<0.01 for both groups). In the control group only 13.2% of von Willebrand factor reduction was seen.Conclusion. ARA II added to common therapy of COPD complicated by CCP improves functional state of endothelium restricting hyperproduction of nitric oxide and its toxic effects and slowing down apoptotic cell death
CORRECTION OF ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH CHRONIC COR PULMONALE BY ANGIOTENSIN II RECEPTORS ANTAGONISTS
Aim. To evaluate intensity of endothelial dysfunction, processes of apoptosis, state of central and peripheral hemodynamics and to evaluate how these characteristics are influenced by angiotensin II receptors antagonists (ARA II) β candesartan (Atacand) and losartan (Cosaar) in patients with chronic cor pulmonale (CCP) at different stages of disease.Material and methods. 100 patients with chronic obstructive pulmonary disease (COPD), complicated by CCP were included into the study. Caspase activity as apoptosis induction marker, von Willebrand factor, production of nitric oxide in blood plasma and condensate of breathing out air were assessed. 70 patients received ARA II (50 patients β candesartan 4-8 mg daily, 20 patients β losartan 50-100 mg daily), 30 patients received neither ARA II nor angiotensin converting enzyme inhibitors (ACEI).Results. Significant increase in intensity of endothelial dysfunction and activation of apoptosis processes were registered according to growth of CCP severity. After 6 months of therapy von Willebrand factor decreased by 25,2% and 27,7% in candesartan and losartan groups respectively (p<0.01 for both groups). In the control group only 13.2% of von Willebrand factor reduction was seen.Conclusion. ARA II added to common therapy of COPD complicated by CCP improves functional state of endothelium restricting hyperproduction of nitric oxide and its toxic effects and slowing down apoptotic cell death.</p