Rodnenkov O V, Luneva O G, Ulyanova N A, Maksimov G V, Rubin A B, Orlov S N, Chazov E I
A.L. Myasnikov Institute of Clinical Cardiology, Russian Cardiological Research Complex, Moscow, Russia.
Pathophysiology. 2005 May;11(4):209-213. doi: 10.1016/j.pathophys.2004.12.001.
This study examined the possible involvement of abnormal erythrocyte oxygen (O(2)) transport in the pathogenesis of heart failure. Haemoglobin (Hb) haemoporphyrin conformation was assessed by Raman spectroscopy (RS) of blood samples, whereas membrane fluidity was estimated at depths of 0.6-0.8 and 2.2nm by electron-paramagnetic resonance spectroscopy of erythrocytes loaded with spin-labeled 5-doxylstearic acid and 16-doxylstearic acid, respectively. The fluidity of erythrocyte membranes from patients with heart failure was decreased in the area near the membrane surface and remained unchanged in the deeper hydrophobic membrane regions. The same differences were also detected in healthy controls subjected to chronic high-altitude hypoxia. RS demonstrated that in heart failure the total content of Hb-ligand complexes and the relative content of Hb-nitric oxide (NO) complexes with cleaved Fe(2+)-globin bond was decreased, whereas content of Hb-NO complexes with preserved Fe(2+)-globin bond was increased. We propose that this phenomenon contributes to the reduced O(2) tissue supply seen in patients with heart failure.
本研究探讨了异常红细胞氧（O₂）运输在心力衰竭发病机制中的可能作用。通过对血样进行拉曼光谱（RS）评估血红蛋白（Hb）血红素卟啉构象，而分别通过对装载自旋标记的5-脱氧硬脂酸和16-脱氧硬脂酸的红细胞进行电子顺磁共振光谱，在0.6 - 0.8纳米和2.2纳米深度处估计膜流动性。心力衰竭患者红细胞膜的流动性在膜表面附近区域降低，而在更深的疏水膜区域保持不变。在经受慢性高原缺氧的健康对照中也检测到了相同的差异。RS表明，在心力衰竭中，Hb-配体复合物的总含量以及具有断裂Fe²⁺-珠蛋白键的Hb-一氧化氮（NO）复合物的相对含量降低，而具有保留Fe²⁺-珠蛋白键的Hb-NO复合物的含量增加。我们认为这种现象导致了心力衰竭患者中观察到的O₂组织供应减少。
