Effects of chronic tabacco smoking on the cerebral blood flow

Захарчук, Н. В.; Невзорова, В. А.; Черток, В. М.; Sarafanova, Natalia

doi:10.17116/jnevro201711721124-129

Cited by 6 publications

(5 citation statements)

References 28 publications

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“…More significant changes of cerebral hemodynamics were found in the medium velocity of blood flow. There was also a significant drop in pulsation index and slight reduction of resistance index (Tables 1 and 2), as it has been shown earlier [33].…”

Section: Carotid Arteries Condition In Copd Depending On the Smoking supporting

confidence: 81%

“…Breathholding test (hypercapnic test) and hyperventilation test (hyperoxia test) allow to calculate the indexes of endothelium-dependent reaction of those vessels in terms of their dilatatory and constricting functions, respectively [45,46]. The obtained results show an existing imbalance of endothelial vasomotor activity in small pial and cerebral vessels where vasospastic reactions are intensified with unchanged or slightly reduced endothelial dilatation ability of these vessels in patients with smoking-induced COPD ( Figure 4) [33]. The value of vascular responsiveness index (VRI) was calculated as: VRI = (Vps 2 À Vps 1 )/Vps 1 Â 100%, Vps 1 is peak systolic velocity in the MCA under investigation and Vps 2 is peak systolic velocity in the MCA after the appropriate tests.…”

Section: Carotid Arteries Condition In Copd Depending On the Smoking mentioning

confidence: 98%

“…Structural deterioration of conductance arteries causes alterations in blood flow velocity. At the same time, the resistance of peripheral vessels and elastic properties of vessel wall decrease which is indicated by lower pulsation index and, to a lesser extent, resistance index [33].…”

Section: Carotid Arteries Condition In Copd Depending On the Smoking mentioning

confidence: 99%

“…Exposure to smoke induces a significant thickening of intima-media complex in conductance arteries, atherosclerotic plaques in the CCA bifurcation area and internal carotid artery mouth that leads to partial artery stenosis [33]. Long-term exposure to toxic products of tobacco combustion causes hypertrophy of smooth muscle cells, disorganization of arterial myoelastic tissue, faster lipid peroxydation leading to thickening of vessel walls, deterioration of their mechanic properties and atherogenesis [23,40].…”

Section: Carotid Arteries Condition In Copd Depending On the Smoking mentioning

confidence: 99%

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Smoking, Respiratory Diseases and Endothelial Dysfunction

Невзорова¹,

Brodskaya²,

Захарчук³

2018

Endothelial Dysfunction - Old Concepts and New Challenges

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Vascular endothelium actively participates in inflammatory reactions in the majority of chronic respiratory diseases. Smoking is a major risk factor for bronchopulmonary diseases, and it plays an important role in endothelial dysfunction development. Some experiments prove that aggressive pollutants of tobacco smoke (benzopyrene, peroxynitrite, acrolein, cyanides, peroxides, etc.) can cause direct damage to endothelial cells due to expression of adhesion molecules on their surface and intensification of lipid peroxidation. In turn, oxidized lipoproteins in the tunica intima of the vessel work as attractants for chemotaxis of leukocytes and monocytes that start to produce pro-inflammatory cytokines in big amounts. These processes trigger systemic inflammatory response that leads to irreversible thickening of the vessel walls and deterioration of their mechanical properties. Chronic exposure to tobacco smoke and the products of combustion of tobacco leads to chronic system inflammatory reaction, oxidative stress, endothelial dysfunction and morpho-functional damage of target organs. Nowadays, the connection between chronic obstructive pulmonary disease (COPD) and some cardiovascular and cerebrovascular diseases has been well established. Studying the mechanisms of endothelial dysfunction in brain blood vessels of patients with smoking habits and COPD can be very important for preventing acute vascular events.

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Section: Carotid Arteries Condition In Copd Depending On the Smoking supporting

confidence: 81%

Section: Carotid Arteries Condition In Copd Depending On the Smoking mentioning

confidence: 98%

Section: Carotid Arteries Condition In Copd Depending On the Smoking mentioning

confidence: 99%

Section: Carotid Arteries Condition In Copd Depending On the Smoking mentioning

confidence: 99%

See 2 more Smart Citations

Smoking, Respiratory Diseases and Endothelial Dysfunction

Невзорова¹,

Brodskaya²,

Захарчук³

2018

Endothelial Dysfunction - Old Concepts and New Challenges

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“…Animal tests show that systemic inflammation in COPD releases pro-inflammatory mediators that facilitate inflammatory cells migration into atherosclerotic plaques, increasing the level of lipids there and, thus creating unstable plaques [14]. Exposure to smoke induces a significant thickening of intimamedia complex in conductance arteries, atherosclerotic plaques in the CCA bifurcation area and internal carotid artery mouth that leads to partial artery stenosis [15]. Long-term exposure to toxic products of tobacco combustion causes hypertrophy of smooth muscle cells, disorganization of arterial myoelastic tissue, faster lipid peroxidation leading to thickening of vessel walls, deterioration of their mechanic properties and atherogenesis [16,17].…”

Section: Carotid Arteries Condition In Copdmentioning

confidence: 99%

Chronic Obstructive Pulmonary Disease and Cardiovascular Comorbidity

Захарчук¹,

Nevzorova²,

Brodskaya³

et al. 2018

JLPRR

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

2018

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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.

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Effects of chronic tabacco smoking on the cerebral blood flow

Cited by 6 publications

References 28 publications

Smoking, Respiratory Diseases and Endothelial Dysfunction

Smoking, Respiratory Diseases and Endothelial Dysfunction

Chronic Obstructive Pulmonary Disease and Cardiovascular Comorbidity

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

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