دانلود رایگان مقاله لاتین سازگاری عروق از سایت الزویر
عنوان فارسی مقاله:
سازگاری عروق به شرایط شدید: نقش هیپوکسی
عنوان انگلیسی مقاله:
Vascular adaptation to extreme conditions: The role of hypoxia
سال انتشار : 2016
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مقدمه انگلیسی مقاله:
1. Introduction
During human evolution, several homeostatic mechanisms, involving the cardiovascular, respiratory and neuroendocrine system, have been developed in order to maintain stable tissue O2 levels. NO is a key molecule in systemic and pulmonary vascular physiology, for its vasodilating, antithrombotic and antimitotic properties.1 Reduced NO availability in the systemic circulation, which is the main feature of endothelial dysfunction, has been recognized as the first step towards development of atherosclerosis.1 During exposure to hypoxia, NO is crucial to ensure O2 and nutrients delivery to tissues and it is considered the main responsible for early hypoxic vasodilation. For example, NO metabolites such as nitrite are supposed to be converted again to NO under hypoxic conditions and may induce vasodilation both by endothelium-dependent and -independent pathways.2 An increased expression of several NO synthase (NOS) isoforms has also been demonstrated.3 The balance between reactive oxygen species (ROS) and NO pathway seems also to be crucial for successful vascular adaptation to hypoxia, since increased ROS production is the main cause of NO destruction. Indeed, low O2 concentrations may be a cause of overproduction of ROS together with decreased levels of antioxidant capacity, leading to oxidative damage to lipids, proteins, and DNA, and finally to cellular death.4 Under a more prolonged exposure to hypoxia, other regulatory mechanisms take place. After few hours-days, hypoxia-induced peripheral vasoconstriction, sympathetically mediated as a consequence of chemoreflex activation, prevails on direct vasodilation,5 leading to increased blood pressure.6 Sympathetic activation is also able to induce endothelial dysfunction,7 while oxidative stress per se is also able to induce sympathetic activation,8 thus inducing a vicious circle. A late effect of high altitude acclimatization is an increased proliferation of red blood cells, aimed at achieving a greater oxygen-carrying capacity to overcome the low ambient oxygen tension. Subsequent hyperviscosity might also influence negatively cardiovascular homeostasis and vascular function. The key for successful adaptation to hypoxia probably resides in the complex balance between these contrasting forces. In this framework, the study of individuals and populations naturally predisposed to successful acclimation to high altitude, a powerful challenge to the cardiovascular system triggering mechanisms underlying most chronic noncommunicable diseases,9 might suggest novel strategies and therapeutic targets for cardiovascular disease.
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کلمات کلیدی:
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