Cerebral T1ρ relaxation time increases immediately upon global ischemia in the rat independently of blood glucose and anoxic depolarization
✍ Scribed by Mikko I. Kettunen; Olli H.J. Gröhn; Markku Penttonen; Risto A. Kauppinen
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 196 KB
- Volume
- 46
- Category
- Article
- ISSN
- 0740-3194
- DOI
- 10.1002/mrm.1228
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✦ Synopsis
Abstract
Time‐dependent changes of T~1~ in the rotating frame (T~1ρ~), diffusion, T~2~, and magnetization transfer contrast on cardiac arrest‐induced global ischemia in rat were investigated. T~1ρ~, as acquired with spin lock amplitudes >0.6 G, started to increase 10–20 sec after cardiac arrest followed by an increase within 3–4 min to a level that was 6–8% greater than in normal brain. The ischemic T~1ρ~ response coincided with the drop of water diffusion coefficient in normoglycemic animals. However, unlike the rate of diffusion, the kinetics of T~1ρ~ were not affected by either preischemic hypoglycemia or hyperglycemia. Similar to diffusion, the kinetics of anoxic depolarization were dependent on preischemic blood glucose levels. Ischemia caused a reduction in the Hahn spin echo T~2~ as a result of blood oxygenation level‐dependent (BOLD) effect; maximal negative BOLD seen by 40 sec. In the animals injected with an ironoxide particle contrast agent, AMI‐227, prior to the insult, both T~1ρ~ and T~2~ immediately increased in concert on induction of ischemia. In contrast to the T~1ρ~ and diffusion changes, a much slower change in magnetization transfer contrast was evident over the first 20 min of ischemia. These data demonstrate that T~1ρ~ immediately increases following ischemia and that the pathophysiological mechanisms affecting this relaxation time may not directly involve magnetization transfer. The mechanisms prolonging T~1ρ~ differ from those affecting water diffusion with respect to their sensitivities to glucose and are apparently independent of membrane depolarization. Magn Reson Med 46:565–572, 2001. © 2001 Wiley‐Liss, Inc.