[Features of the course and adverse events risk of coronavirus infection COVID-19 in hematological diseases (data from the CHRONOS19 register for the Primorsky Territory, intermediate stage)].

AIM: To assess the characteristics of the course of coronavirus infection COVID-19 and to determine the risk factors for adverse events in patients of the regional hematological center. MATERIALS AND METHODS: As part of an observational prospective cohort study, data from 144 medical records of patients in Primorsky Krai with hematological diseases and COVID-19 were analyzed. The data of the developed standardized questionnaire of the CHRONOS19 study were used. The primary endpoint (adverse outcome) was a composite point that included mortality from any cause during the observation period, development of acute respiratory distress syndrome, hospitalization in the intensive care unit, and the need for mechanical ventilation. RESULTS: A study of the features of the course of COVID-19 in hematological patients showed an increase in the number of adverse events in patients with neoplastic blood diseases, especially in chronic lymphoproliferative diseases and acute myeloid leukemia. Significant predictors of an unfavorable course of COVID-19 include a refractory/recurrent variant of the course of a blood tumor, glucocorticoid therapy as part of the protocol for the treatment of the underlying disease, stage 3-4 lung damage according to computerised tomography scans at the onset of COVID-19, and the presence of diabetes mellitus. CONCLUSION: Predictors of an unfavorable course of COVID-19 in hematological patients have been identified. Hematological patients in the context of the COVID-19 pandemic require a coordinated interdisciplinary approach involving hematologists and therapists, careful monitoring of clinical and laboratory parameters to reduce the risk of adverse events.

[Markers of redox potential of blood leukocytes in acute coronary syndrome, depending on the presence of type 2 diabetes mellitus].

Aim      Evaluating the redox potential of white blood cells (WBC) in acute coronary syndrome (ACS) depending on the presence or absence of type 2 diabetes mellitus (DM2).Material and methods  The study included 100 men and women aged 35 to 65 years who were managed for ACS at the Primary Vascular Department (PVD) of the Vladivostok Clinical Hospital #1. The control group consisted of 30 healthy volunteers matched with ACS patients in major anthropometric characteristics. Examinations were performed according to clinical recommendations. Blood was withdrawn for measuring cell activity of enzymes (superoxide dismutase, SOD; succinate dehydrogenase, SDH; and glutathione reductase, GR) and serum concentration of malonic dialdehyde (MDA). Based on the ACS type, all patients were divided into 3 main ACS groups, and then the groups were subdivided into subgroups based on the presence of DM2.Results Development of ACS was associated with changes in WBC redox potential. These changes were characterized by a significant decrease in SDH activity in all ACS patients, irrespective of their ACS type, and a moderate decease in GR in patients with myocardial infarction compared to patients with unstable angina and healthy volunteers. At the same time, the SOD activity and MDA concentration were practically unchanged compared to the control group. There were practically no significant differences in the enzyme activities between the ACS subgroups with or without DM2.Conclusion      The WBC activities of SDH and GR on day 1 of ACS can be considered as the indicators for early diagnosis of mitochondrial dysfunction resulting from the cardiovascular catastrophe as well as the markers for impaired primary cell defense. MDA and SOD values are not informative for determining the intensity of oxidative stress and further damage of the antioxidant system.

HIF-1α- and HIF-2α-Immunopositive Neurons and Capillaries in the Prefrontal Cerebral Cortex of Rats with Experimental Myocardial Infarction.

The quantitative content of HIF-1α- and HIF-2α-immunopositive brain neurons in Wistar rats was studied 1, 15, and 30 days after modeling of myocardial infarction. In rats of the control group, the immunohistochemical markers HIF-1α and HIF-2α in the prefrontal cortex of the brain were determined in few pale-colored neurons and capillaries. One day after myocardial infarction simulation, the number of HIF-1α+ neurons increased, and on day 15 it reached the maximum level: the concentration of immunopositive neurons and capillaries increased by 24.7 and 18.4%, respectively, in comparison with the control. After 30 days, the number of HIF-1α+ structures decreased, but remained above the control values. The number of neurons and capillaries positively stained for HIF-2α peaked only on day 30 of the postinfarction period.

[Chronic obstructive pulmonary disease as a model of premature aging: the pathogenetic role of mitochondria.]

Chronic obstructive pulmonary disease (COPD) is a disease with typical features of premature aging. Modern theories of the pathogenesis of COPD include a number of interrelated concepts that dominate in different time periods. In this work, based on the analysis of the results of our own and published scientific studies, it is demonstrated that the mitochondria-mediated component seems to be the link of most of the recognized theories of the pathogenesis of COPD as a model of early premature aging. The issues of mitochondrial involvement in the pathogenesis of COPD are actively studied, but are not fully understood and do not always have an unambiguous interpretation. The paper systematizes information on the contribution of mitochondrial dysfunction to various aspects of the pathogenesis of COPD, including the relationship between inflammation, hypoxia, oxidative stress, protease imbalance, damage to tissue and cellular phenotype with reprogramming of metabolism and accumulation of a pool of cells with an «aged¼ phenotype. Observations suggest that mitochondrial dysfunction may be a key factor contributing to the initiation and progression of COPD, the accumulation of systemic effects, the formation of comorbidity, and premature aging. The argumentation of this concept provides an evidence-based basis for the development of promising, pathogenetically substantiated targeted strategies for the prevention and control of COPD at the topical and systemic levels.

[The assessment of renal function during the therapy of arterial hypertension with azilsartan medoxomil in patients with obesity or overweight and concomitant metabolic disorders].

AIM: To assess the influence of the therapy of arterial hypertension with azilsartan medoxomil on the renal function in overweight or obese patients with concomitant metabolic disorders. MATERIALS AND METHODS: An international multicenter observational nonintervention prospective study included 1945 patients, taking azilsartan medoxomil in accordance with approved prescribing information. The observation period reached 6 months. RESULTS: In patients with an initial glomerular filtration rate (GFR)60 ml/min/1.73 m2 or 60 ml/min/1.73 m2 mean change in systolic blood pressure after 6 months of therapy reached -32.511.1 and -30.413.6 mmHg, correspondingly, while the change in diastolic blood pressure was -13.78.8 and -14.29.4 mmHg, respectively. No decrease in renal function was observed. Moreover, in patients with an initial GFR60 ml/min/1.73 m2 GFR increased significantly (p0.001). CONCLUSION: Azilsartan medoxomil, prescribed as monotherapy or in free combinations, provided an effective control of blood pressure in patients with arterial hypertension with both normal or moderately reduced and initially significantly reduced renal function. High efficacy and acceptability of the drug was associated with a beneficial effect on renal function, which allows to consider azilsartan medoxomil as the drug of choice for the treatment of hypertension in patients with concomitant metabolic disorders.

[Aortic stiffness and content of adipokines in the serum in persons of European and South Asian ethnic].

AIM: To evaluate the cardiovascular risk (CVR) based on arterial stiffness and content of adipokines in young-aged persons of different ethnicity (European and South Asian). MATERIALS AND METHODS: 290 persons of European (Slavic) and South Asian (Korean) ethnicity aged from 19 to 49 years with and without arterial hypertension (AH) were examined. Clinical, anthropometric, laboratory examinations were performed, levels of resistin and adiponectin of blood were assessed. Total CVR was assessed by SCORE scale, patients under the age of 40 years were assessed by relative risk scale. Aortic stiffness was examined by non-invasive arteriography. RESULTS: Patients of European ethnicity had higher blood pressure (BP), body mass index (BMI), waist circumference (WC), levels of resistin and adiponectin. Pulse wave velocity in the aorta (PWVA) did not differ significantly in ethnic groups. According to the SCORE scale in individuals of the European and South Asian races in general groups and groups with arterial hypertension a moderate absolute risk was determined, in individuals under 40 years of age a moderate relative risk was determined without a significant difference between the groups. However increased levels of PWVA (more than 10 m/s) were registered more often in Korean ethnicity (46.9% compared to Slavic ethnicity, 22.2%). Closer reliable correlations between the level of BP and BMI, WC, PWVA were revealed in Korean ethnicity. Ethnic differences in correlation of adipokines in blood and their dependence on anthropometric and hemodynamic characteristics were described. CONCLUSION: The assessment of CVR according to traditional scales does not always accurately represent its real level. New information was obtained on the features of adipokine metabolism and its connections with early manifestations of vascular remodeling in young-aged depending on the race. Taking into account ethnic differences, we recommend in-depth diagnostics of CVR in South Asians. The data can be useful for the design of personalized programs for the diagnostics and assessment of CVR.

[Severe bronchial asthma patient care organization in various regions of the Russian Federation. From endotypes and phenotypes of bronchial asthma to personalized choice of therapy].

The meeting of the Expert board was held in Moscow on June 24, 2019, at which the following issues were considered: the applicability of a new terminology characterizing asthma endotypes and phenotypes in real clinical practice, the effect of phenotypes and biomarkers in patients with bronchial asthma on the choice of biological drug, as well as the optimal clinical profiles of patients for whom dupilumab is most effective, taking into account the data of the III phase clinical trials, regional features of medical care and changes in updated international clinical guidelines for the diagnosis and treatment of asthma. The Expert board included members of leading Russian scientific and educational medical institutions: S.N. Avdeev, corresponding member of the Russian Academy of Sciences, prof., MD; O.A. Volkova, Ph.D.; I.V. Demko, prof., MD; G.L. Ignatova, prof., MD; I.V. Leshchenko, prof., MD; Kanukova N.A.; Kudelya L.M., prof., MD; V.A. Nevzorova, prof., MD; N.G. Nedashkovskaya; O.P. Ukhanova, prof., MD; L.V. Shulzhenko, prof., MD; R.S. Fassakhov, prof., MD.

[Endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease].

Emphysema is one of the main manifestations of chronic obstructive pulmonary disease (COPD), and smoking is one of the most significant risk factors. The results of studies in humans and animals show the vascular endothelium initiates and modulates the main pathological processes in COPD and smoking is an important factor initiating, developing and persisting inflammation and remodeling of blood vessels and tissues, including the destruction of small respiratory tracts with the development of lung tissue destruction and emphysema. The latest studies describe mechanisms not just associated with the endothelium, but specific neuro-mediated mechanisms. There is reason to believe that neuro-mediated and neuro-similar mechanisms associated and not related to endothelial dysfunction may play the significant role in the pathogenesis of COPD and emphysema formation. Information about components and mechanisms of neurogenic inflammation in emphysema development is fragmentary and not systematized in the literature. It is described that long-term tobacco smoking can initiate processes not only of cells and tissues damage, but also become a trigger for excessive release of neurotransmitters, which entails whole cascades of adverse reactions that have an effect on emphysema formation. With prolonged and/or intensive stimulation of sensor fibers, excessive release of neuropeptides is accompanied by a number of plastic and destructive processes due to a cascade of pathological reactions of neurogenic inflammation, the main participants of which are classical neuropeptides and their receptors. The most important consequences can be the maintenance and stagnation of chronic inflammation, activation of the mechanisms of destruction and remodeling, inadequate repair processes in response to damage, resulting in irreversible loss of lung tissue. For future research, there is interest to evaluate the possibilities of therapeutic and prophylactic effects on neuro-mediated mechanisms of endothelial dysfunction and damage emphysema in COPD and smoking development.

[Effect of arterial hypertension and hyperlipidemia on remodeling of articular cartilage and the development of osteoarthritis (experimental study).]

Osteoarthritis (OA) is a degenerative-inflammatory disease of the synovial joints associated with age, cardiovascular comorbidity, and other factors, based on cartilage (AC) and subchondral bone (SCB) damage. Recent studies have shown that age-related changes, cardiovascular diseases and OA may have a number of common molecular mechanisms. At the same time, the conditions and the degree of influence of arterial hypertension (AH) and hyperlipidemia (HL) on the tissues of the joints remain unclear. The purpose of the study is to study the effect of arterial hypertension and hyperlipidemia on the processes of cellular stress, remodeling of AC and the development of OA. An experimental study was carried out on 18 adult males of purebred guinea pigs (28-30 weeks old, weight 750-900 g). The 1st group (model AH) - 6 individuals, the 2nd (model with HL) - 6 individuals, the 3rd group (control) - 6 individuals. The results of the study allowed to establish that AH and HL have a direct effect on the tissues of the joints, causing cellular stress, manifested in changes in the morphofunctional characteristics of chondrocytes. Changes in the phenotype of cells leads to degradation of AC and SCB, ectopic angioproliferation. However, cardiometabolic factors influence AC remodeling processes in different ways. Thus, with isolated hypertension, hypertrophic differentiation of chondrocytes, destruction of articular cartilage, loss of cambial cells are observed. In HL, cell death processes, pathological mineralization of articular cartilage and enhanced pathological angiogenesis are observed. The greatest changes in articular cartilage are caused by the combination of AH and HL. With a combination of cardiometabolic factors, necrotic destruction of AC and replacement of SCB with osteopod-like matrix is observed.

Comparative Study of HIF-1α- and HIF-2α-Immunopositive Neurons and Capillaries in Rat Cortex under Conditions of Tissue Hypoxia.

We measured the content of HIF-1α and HIF-2α-immunopositive neurons and microvessels in the brain of Wistar rats during the first 24 h of tissue hypoxia induced by subcutaneous injection of cobalt dichloride (50 mg/kg). In control rats (without hypoxia), immunohistochemical marker HIF-2α in cortex of parietal lobe was not detected, and HIF-1α was detected only in few weakly stained pale neurons and capillaries. In 30 min after injection of the cobalt salt, the number of HIF-1α+ neurons increased by 25.6% (in capillaries by 12.3%), many of these were characterized by intensive reaction; the quantitative parameters reached their maximum level within 1-3 h. However, the concentration of immunopositive neurons returned to the control values in 6 h after hypoxia modeling (capillaries in 9 h). In contrast to HIF-1α, the number of neurons and capillaries containing HIF-2α reached a maximum level in 6-12 h of hypoxia. The relative density of HIF-2α+ capillaries increased most pronouncedly (by 23.6%); the relative density of neurons increased by 18.9%. The relative density of HIF-2α+ cells did not change significantly to the end of the experiment. Thus, HIF-1α is more essential for regulation of adaptation to hypoxia in neurons and HIF-2α is more important for the endothelium of microvessels.

[The distribution of matrix metalloproteinases and their tissue inhibitors in the brain vascular bed exposed to chronic tobacco smoke]. / Ékspressiia matriksnykh metalloproteinaz i ikh tkanevykh ingibitorov v sosudistom rusle golovnogo mozga pri khronicheskoi intoksikatsii tabachnym dymom v éksperimente.

AIM: To study the distribution of MMP-2 and MMP-9 and their inhibitors (TIMP-2 and TIMP-1 respectively) in the brain vascular bed of rats exposed to chronic tobacco smoke. MATERIAL AND METHODS: Localization and expression of MMP-2, MMP-9, TIMP-2 and TIMP-1 in the pial branches (I-V order vessels), intracerebral arteries and capillaries of rats exposed to tobacco smoke were studied for 36 weeks. The level of enzymatic activity was assessed by the relative quantity of enzymopositive arteries and amount of fragments per 1 mm2 and rate of immunohistochemical reaction. Specific capillary density per mm2 of brain tissue and optical density of the immunohistochemical product were calculated. RESULTS: MMP-2 and TIMP-2 were found in all segments of the arterial course in control animals. In rats exposed to tobacco smoking, the expression of MMP-2 increased only in intracerebral arteries and capillaries while TIMP-2 level decreased. MMP-9 and TIMP-1 were noted only in single vessels, mainly small pial and intracerebral arteries, in intact animals. In rats exposed to tobacco smoke, MMP-9 expression significantly increased in all segments of the arterial course whereas the increase in TIMP-1 was observed mainly in large pial arteries. CONCLUSION: In physiological conditions, the dynamic balance between MMP-2 and TIMP-2 maintains basic tissue metabolism. Products of tobacco combustion are inductors of the inducible MMP-9 which promotes morphofunctional changes. The imbalance in MMP-9 - TIMP-1 system causes the degradation of extracellular matrix in different segments of the brain arterial course promoting the development of cerebral dysfunction.

Dynamics of Distribution of Capillaries with Matrix Metalloproteinase-2 and Its Tissue Inhibitor in Rat Brain during Development of Experimental Hypertension.

The capillaries containing MMP-2 and its tissue inhibitor TIMP-2 were examined in cerebral cortex and white matter obtained from intact Wistar rats (n=5) and the rats with progressing experimental renovascular hypertension (n=35). In hypertensive rats, the changes in intensity of the immunohistochemical reaction and in the density of capillaries expressing TIMP-2 significantly differed from the corresponding values in MMP-2-positive capillaries, which resulted in pronounced deviation of MMP-2/TIMP-2 index from the control level (especially in cerebral cortex) probably attesting to enhanced risk of complications in cases with arterial hypertension.

Effects of Chronic Tobacco Smoking on the Distribution of Tachykinin Receptors in Rat Pial Arteries.

Pial arteries of different diameter were studied in intact rats and after 6-month modeling of chronic tobacco smoking in rats. Expression of tachykinin NK1 receptors in pial arteries was studied by biomicroscopy and immunohistochemical methods. Chronic tobacco smoking induced considerable reorganizations of the arterial bed. The intensity of changes depended on the diameter of vessels. In small pial vessels that directly participate in the blood supply to the brain, pronounced vasodilatation and enhanced expression of NK1 receptors in the endothelium mediating the effects of substance P were observed; the number of these vessels also increased. The intensity of the response to tobacco smoke components decreased with increasing vessel diameter.

[Effects of chronic tabacco smoking on the cerebral blood flow]. / Vliyanie khronicheskogo tabakokureniya na tserebral'nuyu gemodinamiku.

AIM: To study an effect of chronic smoking on cerebral hemodynamics and cerebrovascular reactivity in different segments of the arterial system of the brain in men. MATERIAL AND METHODS: Male patients enrolled in the study were divided into two groups: controls (n=11) and smokers (n=24) with index 30.7 pack-year smoking history. Haemorheological parameters: viscosity of blood, aggregation of erythrocytes, hematocrit, fibrinogen were evaluated in both groups. Using carotid duplex ultrasound (MyLab 50 Esaote, Italy), intima-media thickness (IMT) of common carotid arteries (CCA) was measured. Parameters of cerebral hemodynamics were evaluated using transcranial Doppler ultrasound (Nicolet Companion Biomedikal, USA). Tests of the cerebrovascular reactivity were used to study arteries of three levels: common carotid arteries, middle cerebral arteries (MCA) and pial arteries. RESULTS: An increase in erythrocytes, hemoglobin, hematocrit, viscosity of blood, aggregation of erythrocytes and fibrinogen was found in the group of smokers compared to the control group. There were an increase in IMT of CCA by more than 50% and a decrease in the mean flow velocity in CCA in smokers. Also smoking decreased MCA mean flow velocity, but this decrease was 2-3 times smaller than in the common carotid arteries. Vasoconstrictor reactions prevailed in MCA, as indicated by the increase in the peripheral vascular resistance index. An increase in vasospastic reactions in pial arteries in smokers was discovered. At the same time, the vasodilatation reaction was maintained or not significantly reduced in pial arteries. CONCLUSION: Chronic smoking is one of the significant factors causing changes in haemorheological parameters, damage of vascular wall, initiation of atherogenesis and disturbance of cerebral hemodynamics. The study of velocity characteristics and peripheral vascular resistance indices in the group of smokers revealed different reactions of different segments of the brain arterial system.

[Role of vascular remodeling markers in the development of osteoporosis in idiopathic pulmonary arterial hypertension]. / Rol' markerov remodelirovaniya sosudov v formirovanii osteoporoza pri idiopaticheskoi legochnoi arterial'noi gipertonii.

AIM: To define the role of circulating biomarkers for the metabolism of collagen and intercellular substance and vascular remodeling in the development of osteoporosis (OP) in idiopathic pulmonary arterial hypertension (IPAH). MATERIAL AND METHODS: Functional hemodynamic parameters, bone mineral density (BMD) in the lumbar spine and femoral neck and the serum levels of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), MMP-9/TIMP-1 complex, C-terminal telopeptide of collagen type 1 (CITP), and endothelin-1 (ET-1) were determined in 27 high-risk IPAH patients and 30 healthy volunteers. RESULTS: OP in IPAH was detected in 50% of the examinees. The serum levels of CITP, MMP-9, TIMP-1, and ET-1 proved to be higher in the high-risk IPAH patients than in the healthy volunteers. There was a direct correlation between BMD and six-minute walk test and an inverse correlation with total pulmonary vascular resistance (TPVR). Serum TMIP-1 levels correlated with cardiac index and TPVR; ET-1 concentrations were directly related to pulmonary artery systolic pressure, cardiac index, and TPVR. Inverse relationships were found between BMD and circulating CITP, MMP-9, TMIP-1, MMP-9/TMIP-1, and ET-1. At the same time, there was only a tendency towards a positive correlation between serum CITP and ET-1 concentrations. CONCLUSION: The results of the investigation confirm that endothelin system dysregulation plays a leading role in the development of persistent hemodynamic disorders in high-risk IPAH and suggest that it is involved in the development of osteopenic syndrome. Enhanced ET-1 secretion initiates bone loss possibly via activation of connective tissue matrix destruction.

[The state of the larynx in the patients presenting with chronic obstructive pulmonary disease].

The objective of the present study was to evaluate the clinical state of the larynx and its microbial population in 49 patients examined at the stage of stable condition of chronic obstructive pulmonary disease. Examination of the larynx was carried out with the use of a rigid laryngoscope having a visual angle of 70 degrees, videofibrolaryngoscopy, and stroboscopy using a «TelePac¼ videocomplex (Karl Storz, Germany). It was supplemented by the study of the bacteriological and mycological paysage. The acoustic analysis of the voice was performed with the help of the Specta PLUS computer program. It was shown that more than 70% of the examined patients presented with various forms of chronic laryngitis. Potentially pathogenic St. pyogenes and yeast-like fungi C. albicans were isolated from 59% and 29% of the patients respectively.

[Dynamics of activity of neurokinine receptors and enzymes of intercellular matrix (MMP9 and TIMP-2) in the nasal mucosa of the chronic cigarette smokers].

The present study was designed to determine localization of substance P and neuroknine receptors in the nasal mucous membrane of the subjects having the history of chronic smoking. The mechanisms underlying reorganization of the mucous tissue were elucidated by measuring the activity of intercellular matrix enzymes (MMP9 and TIMP-2). The activity of neurokinine receptors localized on the cells of ciliary epithelium and in the connective tissue elements of the submucous structures was shown to be significantly increased. It is concluded that the specific dynamics of MMP9 and TIMP-2 activities in the chronic cigarette smokers indicates that the matrix metalloproteinases of this type play an important role in the structural reorganization of the tissues of the nasal mucous membrane.

[Ursodeoxycholic acid-enhanced efficiency and safety of statin therapy in patients with liver, gallbladder, and/or biliary tract diseases: the RACURS study].

AIM: To evaluate the efficiency and safety of using statins in combination with ursodeoxycholic acid (UDCA) in patients with this or another liver disease at high risk for cardiovascular events (CVE). SUBJECTS AND METHODS: A register of 262 patients at high risk for CCE who needed statin therapy and have concomitant chronic liver and biliary tract diseases was created in 5 cities of the Russian Federation. RESULTS: After addition of statins or adjustment of their doses, the patients were recommended to include UDCA into their therapy. Six months after stabilization of the dose of statins, the whole group showed a significant reduction in the levels of total cholesterol and low-density lipoprotein (LDL) cholesterol. Assessment of the laboratory parameters responsible for the safety of statin intake revealed no deterioration in the trend in the activity of alanine aminotransferase, aspartate aminotransferase, creatine phosphokinase, lactate dehydrogenase, as well as an increase in the serum level of bilirubin. The data obtained using a special questionnaire indicated that 196 patients had taken UDCA and 56 had not. The UDCA and non-UDCA subgroups did not differ in age, weight, or baseline lipid metabolic disturbances. An additional analysis showed that by the end of 6 months, the goal levels of LDL cholesterol in the UDCA and non-UDCA groups were reached in 37 and 20%, respectively (p = 0.01). CONCLUSION: UDCA added to statin therapy in patients at high risk for CVE and concurrent liver diseases contributes to an additional reduction in total cholesterol and LDL cholesterol and prevents enhanced hepatic transaminase activities.

[The functional status of the upper respiratory tract in the long-term smokers].

The objective of the present study was to evaluate the functional status of the upper respiratory tract in 50 long-term smokers based on the results of comprehensive medical examination, determination of mucociliary transport time, endoscopic study of the oral cavity and nasopharynx, anterior active rhinomanometry, computed tomography of the nasal cavity and paranasal sinuses, fibroendoscopic study of the larynx, and stroboscopy. It was shown that the most significant changes in the nasal cavity were associated with various forms of chronic rhinitis whereas chronic catarrh and hyperplastic laryngitis caused the most pronounced changes in the larynx.

Vasomotor activity of the aorta during chronic smoking modeling.

We studied vasomotor responses of aortic endothelium in a rat model of chronic smoking. It was found that long-term exposure to tobacco smoke (inhalation) impaired vasomotor function of the aortic endothelium leading to insufficient vasodilator activity and enhanced vasoconstriction. After the cessation of inhalations, vasomotor disturbances were not only preserved, but also exacerbated because of increased pathological endothelium-independent vasoconstriction.