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T Asakura

Publications and source records attributed to T Asakura.

545 records · Page 31Linked to original sources

NMR relaxation times of blood: dependence on field strength, oxidation state, and cell integrity.

The variation with field strength or interecho interval of the T1 and T2 relaxation times of oxyhemoglobin (HbO2), deoxyhemoglobin (Hb), and methemoglobin (MHb) in either intact or lysed red blood cells was studied with a variable field (0.19-1.4 T) nuclear magnetic resonance spectroscopy unit. The T2 relaxation time of intracellular HbO2 decreased slightly with increasing field strength and interecho interval. The T2 relaxation times of intracellular Hb and MHb decreased markedly with increasing field strength and interecho interval. This T2 proton relaxation enhancement increased as the square of the applied field strength and was 1.6 times stronger for intracellular MHb than for intracellular Hb. The T2 relaxation enhancement is secondary to the loss of transverse phase coherence of water protons that diffuse across cellular magnetic field gradients. These field gradients occur when an external field is applied to a region with gradients of magnetic susceptibility. The heterogeneity of magnetic susceptibility is caused by the heterogeneous distribution (only intracellular) of the paramagnetic molecules (Hb or MHb). The T2 relaxation times of red cell lysates (homogeneous magnetic susceptibility) were independent of field strength or interecho interval. There was a decrease in the T1 relaxation times when the red cells were lysed. This may be due to an increase in the slow motional components of water molecules, because of the decrease in the average distance between water and hemoglobin molecules in the lysate. The T1 relaxation times of all the MHb samples were shortened because of proton-electron dipolar-dipolar relaxation enhancement. All the T1 relaxation times increased with increasing field strength.

Blood↗

Hemoglobin gelation.

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Buffers↗

An in vitro study of magnetization transfer and relaxation rates of hematoma.

PURPOSE: To assess, in an in vitro model of acute hematoma, whether hemoglobin immobilization by clot and red cell membrane aging can account for the T2 shortening usually attributed to deoxyhemoglobin. METHODS: Clotted and heparinized blood samples were packed (100% hematocrit). The apparent magnetization transfer rate (AMTR), T1 and T2 relaxation rates of the samples, and images with a volunteer's head were obtained at 1.5 T. RESULTS: The AMTR and T1 and T2 relaxation rates were unaffected by the presence of clot. The AMTR was unaffected by red cell aging. The diamagnetic packed blood samples, which are much denser than brain, were isointense to gray matter on T2-weighted images and had about one-fifth the AMTR of white matter. CONCLUSIONS: Hemoglobin immobilization by clot structure or red cell contraction with aging is insignificant and does not contribute to the T2 shortening of acute hematoma. The low AMTR and T2 relaxation rates of diamagnetic blood appear to be caused by the mobility of hemoglobin and by the red cell's lack of immobile macromolecular structures such as those associated with nucleated brain cells.

Acute Disease↗