Cerebral T1ρ relaxation time increases immediately upon global ischemia in the rat independently of blood glucose and anoxic depolarization

Time-dependent changes of T-1 in the rotating frame (T-1 rho), diffusion, T-2, and magnetization transfer contrast on cardiac arrest-induced global ischemia in rat were investigated. T-1 rho, a 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-1 rho response coincided with the drop of water diffusion coefficient in normoglycemic animals. However, unlike the rate of diffusion, the kinetics of T-1 rho 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-1 rho and T-2 immediately increased in concert on induction of ischemia. In contrast to the T-1 rho 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-1 rho immediately increases following ischemia and that the pathophysiological mechanisms affecting this relaxation time may not directly involve magnetization transfer. The mechanisms prolonging T-1 rho differ from those affecting water diffusion with respect to their sensitivities to glucose and are apparently independent of membrane depolarization. (C) 2001 Wiley-Liss, Inc.