Acute cerebral ischemia has been shown to be associated with an enhanced transverse relaxation rate in rat brain parenchyma, chiefly due to the blood oxygenation level-dependent (BOLD) effect. In this study, Carr-Purcell R 2 (CP R 2 ), acquired both with short and long time intervals between centers of adiabatic -pulses ( CP ), was used to assess the contributions of BOLD and tissue effects to the transverse relaxation in two brain ischemia models of rat at 4.7 T. R 1 and diffusion MR images were also acquired in the same animals. During the first minutes of global ischemia, the long CP R 2 in brain parenchyma increased, whereas the short CP R 2 was unchanged. Based on the simulations, and using constraints of intravascular BOLD effect on parenchymal R 2 , the former observation was ascribed to be due to susceptibility changes arising in the extravascular compartment. R 1 declined almost immediately after the onset of focal cerebral ischemia, and further declined during the evolution of ischemic damage. Interestingly, short CP CP R 2 started to decline after some 20 min of focal ischemia and declined over a time course similar to that of Several recent studies have shown that in the early minutes of cerebral ischemia the transverse relaxation rate in brain parenchyma increases, leading to negative T* 2 (1,2) and T 2 (3-5) MR signal change. A shortening of transverse relaxation time has been observed in animal models of hypoperfusion (6), and global (7,8) and focal (1,3) ischemia, as well as in human stroke victims (9), at field strengths ranging from 1.5 to 9.4 T. This observation has been generally attributed to the blood oxygenation leveldependent (BOLD) effect, and the known hemodynamic and metabolic adaptations to reduced cerebral perfusion pressure (CPP) support this conclusion. At lowered CPP levels, cerebral blood volume (CBV) and oxygen extraction increase (10), resulting in a situation in which the accumulation of deoxyhemoglobin (Hb) is favored. Increased Hb levels generate local susceptibility gradients, resulting in enhanced transverse relaxation expressed as a negative BOLD effect.The negative BOLD effect in focal cerebral ischemia is interesting as regards tissue assignment, since BOLD is generated only by tissue that is capable of mitochondrial oxidation. On the basis of this mechanism underlying the generation of T 2 /T* 2 change, it has been proposed that the negative BOLD effect may have a role in the assessment of tissue viability in focally ischemic brain (11). Before the role of decreased T 2 and/or T* 2 in acute cerebral ischemia can be explicitly assigned, a deeper understanding of the underlying physiological and physical phenomena must be obtained. Recent studies in our laboratory have suggested that the T 2 changes associated with focal and global rat brain ischemia can be explained by intravascular susceptibility effects at both 1.5 T (6) and 4.7 T (12). These observations are in line with data from human brain BOLD experiments at 1.5 T (13-15) and 4 T (16), as well as with relaxation ...