Metabolic T1 dynamics and longitudinal relaxation enhancement in vivo at ultrahigh magnetic fields on ischemia

J Cereb Blood Flow Metab. 2014 Nov;34(11):1810-7. doi: 10.1038/jcbfm.2014.149. Epub 2014 Sep 10.


Interruptions in cerebral blood flow may lead to devastating neural outcomes. Magnetic resonance has a central role in diagnosing and monitoring these insufficiencies, as well as in understanding their underlying metabolic consequences. Magnetic resonance spectroscopy (MRS) in particular can probe ischemia via the signatures of endogenous metabolites including lactic acid (Lac), N-acetylaspartate, creatine (Cre), and cholines. Typically, MRS reports on these metabolites' concentrations. This study focuses on establishing the potential occurrence of in vivo longitudinal relaxation enhancement (LRE) effects-a phenomenon involving a reduction of the apparent T1 with selective bandwidth excitations- in a rat stroke model at 21.1 T. Statistically significant reductions in Cre's apparent T1s were observed at all the examined post-ischemia time points for both ipsi- and contralateral hemispheres, thereby establishing the existence of LREs for this metabolite in vivo. Ischemia-dependent LRE trends were also noted for Lac in the ipsilateral hemisphere only 24 hours after ischemia. Metabolic T1s were also found to vary significantly as a function of post-stroke recovery time, with the most remarkable and rapid changes observed for Lac T1s. The potential of such measurements to understand stroke at a molecular level and assist in its diagnosis, is discussed.

MeSH terms

  • Animals
  • Aspartic Acid / analogs & derivatives
  • Aspartic Acid / metabolism
  • Brain Ischemia* / diagnostic imaging
  • Brain Ischemia* / metabolism
  • Brain Ischemia* / physiopathology
  • Cerebral Angiography*
  • Cerebrovascular Circulation*
  • Choline / metabolism
  • Creatine / metabolism
  • Female
  • Lactic Acid / metabolism
  • Magnetic Resonance Angiography*
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Stroke* / diagnostic imaging
  • Stroke* / metabolism
  • Stroke* / physiopathology


  • Aspartic Acid
  • Lactic Acid
  • N-acetylaspartate
  • Creatine
  • Choline