Kato Gregory J
Sickle Cell Vascular Disease Section, Pulmonary and Vascular Medicine Branch, National Heart, Lung, and Blood Institute, and Critical Care Medicine Department, Clinical Center, National Institutes of Health, Maryland 20892-1476, USA.
J Clin Invest. 2009 Aug;119(8):2140-2. doi: 10.1172/JCI40258. Epub 2009 Jul 20.
Hemoglobin (Hb) is crucial to the function of the red blood cell. However, when it is released during intravascular hemolysis from the cell into blood plasma, it produces a state of NO depletion, oxidant stress, and vascular dysfunction, including hypertension. In their study reported in this issue of the JCI, Boretti and colleagues used canine and guinea pig models to demonstrate that pharmacological doses of glucocorticoid can increase the plasma levels of haptoglobin (Hp), the principal plasma-binding protein for free Hb (see the related article beginning on page 2271). Hp prevented Hb-induced hypertension and the generation of oxidant damage to the kidney. Neutralization of free Hb appears to be part of the downstream antiinflammatory properties of glucocorticoid.
血红蛋白（Hb）对红细胞的功能至关重要。然而，当它在血管内溶血过程中从细胞释放到血浆中时，会导致一氧化氮（NO）耗竭、氧化应激以及包括高血压在内的血管功能障碍。在本期《临床研究杂志》（JCI）上报道的研究中，博雷蒂及其同事使用犬类和豚鼠模型证明，药理剂量的糖皮质激素可提高血浆中触珠蛋白（Hp）的水平，Hp是游离Hb的主要血浆结合蛋白（见第2271页开始的相关文章）。Hp可预防Hb诱导的高血压以及对肾脏的氧化损伤。游离Hb的中和似乎是糖皮质激素下游抗炎特性的一部分。
