Dynamics of pial vessels reactivity after brief cerebral ischemia

Gorshkova, O. P.; Lensman, M.V.; Artem'eva, A. I.; Dvoretsky, D. P.

doi:10.24884/1682-6655-2015-14-1-74-78

Cited by 3 publications

(1 citation statement)

References 5 publications

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“…One of the hyperoxic vasoconstriction mechanisms can be NO inactivation by superoxide anions resulting from superoxygenation [24,47]. As a result of those processes, vasorelaxant effect of NO weakens; perfusion reserve and self-regulation potential of resistance vessels are reduced while the risks of cerebrovascular pathology become higher [48].…”

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

confidence: 99%

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 mentioning

confidence: 99%

Smoking, Respiratory Diseases and Endothelial Dysfunction

Невзорова¹,

Brodskaya²,

Захарчук³

2018

Endothelial Dysfunction - Old Concepts and New Challenges

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Effects of chronic tabacco smoking on the cerebral blood flow

Захарчук

Невзорова

Черток

et al. 2017

Z. nevrol. psikhiatr. im. S.S. Korsakova

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The coagulation hemostasis dynamics in rats in the post-ischemic time

Gorshkova

Shuvaeva

Dvoretskii

2019

Regional blood circulation and microcirculation

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Introduction. Ischemic injury to the endothelium influences on a coagulation hemostasis, worsening hemodynamics of cerebral microcirculation as a result of rheological occlusion. The long-term post-ischemic blood clotting system changes are not studied well by now.The work purpose – to study a coagulation hemostasis and endothelial prostacyclin – synthetic activity of pial vessels within 21 days after single short-term transient cerebral ischemia in rat.Material and Methods. Ischemia was reproduced by means of 12-minute time occlusion of both carotids with the simultaneous arterial hypotension. Post-ischemic changes were investigated in 4 groups of rats: on the 3rd, 7th, 14th and 21st day after ischemia. The state of blood clotting system was estimated on time of clot formation in the blood plasma by an automatic optical method with use of screening tests of definition of prothrombin and thrombin clotting time and concentration of fibrinogen. Endothelial prostacyclin – synthetic activity was estimated by pial vessel reaction to indometacin.Results. On the 3rd day after ischemia the increase in prothrombin time was observed. Level of fibrinogen increased on the 3rd and the 14th days of the post-ischemic time. On the 21st day after ischemia thrombin time decreased. The inverse correlation of pial vessel endothelial prostacyclin – synthetic activity with the fibrinogen level and direct correlation with vessel cross-sectional area of these vessels is established.Conclusions. Short-time global cerebral ischemia causes changes of blood clotting system mechanisms lasting for 21 days of the post-ischemic time. Post-ischemic abnormalities in hemostasis system are connected with changes in endothelial prostacyclin – synthetic activity of cerebral vessels that, along with decreased anti-aggregation ability of vascular system, is also the reason of narrowing of the lumen in pial vessels.

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Dynamics of pial vessels reactivity after brief cerebral ischemia

Cited by 3 publications

References 5 publications

Smoking, Respiratory Diseases and Endothelial Dysfunction

Smoking, Respiratory Diseases and Endothelial Dysfunction

Effects of chronic tabacco smoking on the cerebral blood flow

The coagulation hemostasis dynamics in rats in the post-ischemic time

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