Hemoglobin-water interactions in normal and sickle erythrocytes by proton magnetic resonance T1ϱ measurements

Zipp, Adam; Kuntz, Irwin D.; James, Thomas Leroy

doi:10.1016/0003-9861(77)90213-2

Cited by 16 publications

(9 citation statements)

References 14 publications

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“…T 1ρ evidently senses oxygen saturation (and oxygen content) in the whole blood in vitro, contrary to an earlier report from packed erythrocytes studied at B 0 of 1T using B 1 fields up to 7 G (39). The effect of blood oxygen saturation on the rotating frame relaxation is linear, in contrast to the behavior of T 2 .…”

Section: Discussioncontrasting

confidence: 99%

Effects of intracellular pH, blood, and tissue oxygen tension on T_1ρ relaxation in rat brain

Kettunen

Gröhn

Silvennoinen

et al. 2002

Magnetic Resonance in Med

110

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The effects of intracellular pH (pH i ), paramagnetic macroscopic, and microscopic susceptibility on T 1 in the rotating frame (T 1 ) were studied in rat brain. Intracellular acidosis was induced by hypercapnia and pH i , T 1 , T 2 , diffusion, and cerebral blood volume (CBV) were quantified. Taking into account the CBV contribution, a prolongation of parenchymal T 1 by 4.5% was ascribed to a change in tissue water relaxation caused by a one unit drop in pH i . Blood T 1 was found to prolong linearly with blood oxygenation saturation (Y). The macroscopic susceptibility contribution to parenchymal T 1 was assessed both through BOLD and an iron oxide contrast agent, AMI-227. The T 1 data from these experiments could be described by intravascular effects with insignificant effects of susceptibility gradients on tissue water. Tissue oxygen tension (PtO 2 ) was manipulated and monitored with microelectrodes to assess its plausible contribution to microscopic susceptibility and relaxation. Parenchymal Acute ischemia results in subtle and almost instantaneous changes in cerebral MR relaxation times, including prolongation of T 1 (1,2) and T 1 in the rotating frame (T 1 ) (3,4), shortening of T* 2 (5), and T 2 (1,6,7). These relaxation changes are expressed in global forebrain ischemia when there is no possibility for edema formation (2) and also almost immediately after the occlusion of the middle cerebral artery (3,8). The time-dependency of these relaxation changes reveals that net water accumulation to the ischemic brain tissue is not responsible for the depicted MR changes. Early T* 2 and T 2 reductions in ischemic brain have been ascribed to local increases in the level of deoxyhemoglobin, i.e., a blood oxygenation level-dependent (BOLD) phenomenon (5,6,9) and, furthermore, T 2 effects have been quantitatively modeled as intravascular susceptibility effects reflecting elevated oxygen extraction in the flow-compromised tissue (7). The presence of negative BOLD in flow-compromised brain is an index of ongoing oxidative metabolism; thus, it can reveal potentially viable tissue (10).While the transverse relaxation changes in the early moments of ischemia can be explained by both intra-and extravascular susceptibility effects, the longitudinal relaxation alterations might have a different pathophysiological background. From a general principle, tissue R 1 relaxation rate (R 1,obs ) has been proposed to receive contributions from the following physical factors:where subscripts exch, rot, and diff indicate exchange, rotational, and diffusion contributions to R 1 , respectively, and b is the fraction of bound water (11). The same relation has commonly been regarded as being applicable throughout the resonance frequency range, thus also including T 1 relaxation in the rotating frame (11,12). Knispel et al. (11) quantitatively explored T 1 relaxation and relaxation dispersion, i.e., T 1 as a function of B 1 , in tissue phantoms and they concluded that three distinct correlation times, falling into the three physical categor...

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Section: Discussioncontrasting

confidence: 99%

Effects of intracellular pH, blood, and tissue oxygen tension on T_1ρ relaxation in rat brain

Kettunen

Gröhn

Silvennoinen

et al. 2002

Magnetic Resonance in Med

110

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“…Our data indicate that tissue displaying reduced T 2 but no change in T 1 and/or D av corresponds to a ''signature'' with good outcome; thus, these MRI signs may represent reversible penumbra. Our finding that T 1 is not sensitive to BOLD effect in acutely hypoperfused cerebral cortex is in line with a previously study of blood in vitro (24).…”

Section: Discussionsupporting

confidence: 93%

“…To extend the list of potential parameters probing tissue viability, we investigated the suitability of the on-resonance T 1 in the rotating frame, generally termed as T 1 (20)(21)(22), to distinguish reversible and irreversible ischemia in rats. This relaxation parameter is thought to probe water protons in close interaction with macromolecules, thus sensing spins with much longer rotational correlation times ( c ) than those of bulk water (20,23,24). We have quantified T 1 together with Hahn-echo T 2 and the diffusion coefficient (D av ϭ 1 ⁄3TraceD ញ ) in the acute phase of the insult and determined tissue histology 24 hours later.…”

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confidence: 99%

Quantitative magnetic resonance imaging assessment of cerebral ischemia in rat using on-resonance T1 in the rotating frame

et al. 1999

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“…Measurements by x-ray diffraction and electron microscopy have been used to study the structure of the intracellular hemoglobin gel (8,9). More recently, NMR spectroscopy has been used to study the intracellular gelation process through measurements of water relaxation rates (10)(11)(12)(13). Despite these studies, a quantitative description of the intracellular gelation process has not been achieved.…”

mentioning

confidence: 99%

“…Laboratory, Lexington, MA) and equilibrating with various gas mixtures (0-20% oxygen, 5.6% carbon dioxide, and the balance nitrogen) for [10][11][12][13][14][15][16][17][18][19][20] lisec.…”

mentioning

confidence: 99%

Determination of deoxyhemoglobin S polymer in sickle erythrocytes upon deoxygenation.

Noguchi¹,

Torchia²,

Schechter³

1980

Proc. Natl. Acad. Sci. U.S.A.

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Hemoglobin-water interactions in normal and sickle erythrocytes by proton magnetic resonance T1ϱ measurements

Cited by 16 publications

References 14 publications

Effects of intracellular pH, blood, and tissue oxygen tension on T_1ρ relaxation in rat brain

Effects of intracellular pH, blood, and tissue oxygen tension on T_1ρ relaxation in rat brain

Quantitative magnetic resonance imaging assessment of cerebral ischemia in rat using on-resonance T1 in the rotating frame

Determination of deoxyhemoglobin S polymer in sickle erythrocytes upon deoxygenation.

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Hemoglobin-water interactions in normal and sickle erythrocytes by proton magnetic resonance T1ϱ measurements

Cited by 16 publications

References 14 publications

Effects of intracellular pH, blood, and tissue oxygen tension on T1ρ relaxation in rat brain

Effects of intracellular pH, blood, and tissue oxygen tension on T1ρ relaxation in rat brain

Quantitative magnetic resonance imaging assessment of cerebral ischemia in rat using on-resonance T1 in the rotating frame

Determination of deoxyhemoglobin S polymer in sickle erythrocytes upon deoxygenation.

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Effects of intracellular pH, blood, and tissue oxygen tension on T_1ρ relaxation in rat brain

Effects of intracellular pH, blood, and tissue oxygen tension on T_1ρ relaxation in rat brain