d) function of red blood cells?
Answers
Answer:
red blood cells function maintain hemoglobin
Explanation:
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Abstract
Significance: Recent clinical evidence identified anemia to be correlated with severe complications of cardiovascular disease (CVD) such as bleeding, thromboembolic events, stroke, hypertension, arrhythmias, and inflammation, particularly in elderly patients. The underlying mechanisms of these complications are largely unidentified.
Recent Advances: Previously, red blood cells (RBCs) were considered exclusively as transporters of oxygen and nutrients to the tissues. More recent experimental evidence indicates that RBCs are important interorgan communication systems with additional functions, including participation in control of systemic nitric oxide metabolism, redox regulation, blood rheology, and viscosity. In this article, we aim to revise and discuss the potential impact of these noncanonical functions of RBCs and their dysfunction in the cardiovascular system and in anemia.
Critical Issues: The mechanistic links between changes of RBC functional properties and cardiovascular complications related to anemia have not been untangled so far.
Future Directions: To allow a better understanding of the complications associated with anemia in CVD, basic and translational science studies should be focused on identifying the role of noncanonical functions of RBCs in the cardiovascular system and on defining intrinsic and/or systemic dysfunction of RBCs in anemia and its relationship to CVD both in animal models and clinical settings. Antioxid. Redox Signal. 26, 718–742.
Introduction
The main physiological role of red blood cells (RBCs), or erythrocytes is to transport of gases (O2, CO2) from the lung to the tissues and to maintain systemic acid/base equilibria. In addition, RBCs are well equipped with antioxidant systems, which essentially contribute to their function and integrity. Damage of red cell integrity, defined as hemolysis, has been shown to significantly contribute to severe pathologies, including endothelial dysfunction. Recent clinical and experimental evidence indicates that RBCs may be directly involved in tissue protection and regulation of cardiovascular homeostasis by exerting further noncanonical functions, including nitric oxide (NO) metabolism and control of blood rheology, as well as erythrocrine function (i.e., by releasing bioactive molecules, including NO, NO metabolites, and ATP). Many hypotheses on the role of noncanonical functions of RBCs in cardiovascular homeostasis have been put forward, and evidence of a central role played by RBCs in cardiovascular protection is accumulating. However, many aspects of RBC-mediated control of NO metabolism and ATP release are still speculative or not universally accepted.
Anemia is a pathological condition characterized by a decreased number of circulating RBCs and defined by hemoglobin (Hb) concentrations in whole blood below 12 g/dL in females and 13 g/dL in males (192). There is clinical evidence that anemia is also associated with a series of severe complications in cardiovascular disease (CVD) such as thromboembolic events (e.g., venous thrombosis and stroke). However, therapeutic interventions aimed to increase the circulating number of RBCs (e.g., by transfusion of blood or by administration of erythropoiesis-stimulating agents [ESAs] to stimulate the production of RBCs by the bone marrow), were not always effective in the tested cohorts (48, 91, 156). One possible explanation is that these treatments have side effects and therefore may contribute themselves to the negative outcome, for example, treatment with ESAs was associated with increased thromboembolic events