Previous works showed a significant increase in the rotational correlation time of the water bound to the hemoglobin S during the aggregation process under sickle cell disease. In this case, the contribution of “Curie-Spin” relaxation mechanism to proton relaxation may be expected. The Curie-Spin relaxation mechanism has been well described theoretically but only a few experimental evidences have been presented. Based on the reported correlation times, the contribution of the Curie-spin relaxation mechanism to proton relaxation times (\({T}_{1}\) and \({T}_{2}\)) has been estimated in comparison with the contribution of the dipole–dipole relaxation mechanism at the extreme stages of the aggregation process of the hemoglobin S. This contribution is about 25% and 50% in the spin–spin relaxation rates at the magnetic field of 1.5 T during the latent and ending stages of the aggregation process, respectively. At lower magnetic fields, this mechanism gives an insignificant contribution. The contribution to the spin–lattice relaxation is negligible even at 1.5 T. In particular, this relaxation mechanism should be taken into account when interpreting experiments related to MRI.

以前的工作表明在镰状细胞病的聚集过程中，与血红蛋白S结合的水的旋转相关时间显着增加。在这种情况下，可以预期“居里旋”弛豫机制对质子弛豫的贡献。理论上已经很好地描述了居里-自旋弛豫机理，但是仅给出了一些实验证据。根据报告的相关时间，居里自旋弛豫机制对质子弛豫时间（\（{T} _ {1} \）和\（{T} _ {2} \）的贡献）与在血红蛋白S聚集过程的极端阶段偶极子-偶极子弛豫机制的贡献进行了估算。在磁场强度为15的自旋-自旋弛豫率中，这一贡献约为25％和50％。在聚集过程的潜在阶段和结束阶段分别为1.5T。在较低的磁场下，这种机理的贡献很小。即使在1.5 T时，对自旋-晶格弛豫的贡献也可以忽略不计。特别是，在解释与MRI相关的实验时，应考虑这种弛豫机制。