Cerebral T1rho relaxation time increases immediately upon global ischemia in the rat independently of blood glucose and anoxic depolarization.

Time-dependent changes of T1 in the rotating frame (T1rho), diffusion, T2, and magnetization transfer contrast on cardiac arrest-induced global ischemia in rat were investigated. T1rho, 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 T1rho response coincided with the drop of water diffusion coefficient in normoglycemic animals. However, unlike the rate of diffusion, the kinetics of T1rho 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 T2 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 T1rho and T2 immediately increased in concert on induction of ischemia. In contrast to the T1rho and diffusion changes, a much slower change in magnetization transfer contrast was evident over the first 20 min of ischemia. These data demonstrate that T1rho immediately increases following ischemia and that the pathophysiological mechanisms affecting this relaxation time may not directly involve magnetization transfer. The mechanisms prolonging T1rho differ from those affecting water diffusion with respect to their sensitivities to glucose and are apparently independent of membrane depolarization. Copyright 2001 Wiley-Liss, Inc.