Correlating tissue outcome with quantitative multiparametric MRI of acute cerebral ischemia in rats

Predicting tissue outcome remains a challenge for stroke magnetic resonance imaging (MRI). In this study, we have acquired multiparametric MRI data sets (including absolute T1, T2, diffusion, T1ρ using continuous wave and adiabatic pulse approaches, cerebral blood flow (CBF), and amide proton transfer ratio (APTR) images) during and after 65 mins of middle cerebral artery occlusion (MCAo) in rats. The MRI scans were repeated 24 h after MCAo, when the animals were killed for quantitative histology. Magnetic resonance imaging parameters acquired at three acute time points were correlated with regionally matching cell count at 24 h. The results emphasize differences in the temporal profile of individual MRI contrasts during MCAo and especially during early reperfusion, and suggest that complementary information from CBF and tissue damage can be obtained with appropriate MRI contrasts. The data show that by using three to four MRI parameters, sensitive to both hemodynamic changes and different aspects of parenchymal changes, the fate of the tissue can be predicted with increased correlation compared with single-parameter techniques. Combined multiparametric MRI data and multiparametric analysis may provide an excellent tool for preclinical testing of new treatments and also has the potential to facilitate decision-making in the management of acute stroke patients

Magnetic resonance imaging of regional hemodynamic and cerebrovascular recovery after lateral fluid-percussion brain injury in rats

Hemodynamic and cerebrovascular factors are crucially involved in secondary damage after traumatic brain injury (TBI). With magnetic resonance imaging, this study aimed to quantify regional cerebral blood flow (CBF) by arterial spin labeling and cerebral blood volume by using an intravascular contrast agent, during 14 days after lateral fluid-percussion injury (LFPI) in rats. Immunohistochemical analysis of vessel density was used to evaluate the contribution of vascular damage. Results show widespread ipsilateral and contralateral hypoperfusion, including both the cortex and the hippocampus bilaterally, as well as the ipsilateral thalamus. Hemodynamic unrest may partly be explained by an increase in blood vessel density over a period of 2 weeks in the ipsilateral hippocampus and perilesional cortex. Furthermore, three phases of perilesional alterations in CBF, progressing from hypoperfusion to normal and back to hypoperfusion within 2 weeks were shown for the first time in a rat TBI model. These three phases were similar to hemodynamic fluctuations reported in TBI patients. This makes it feasible to use LFPI in rats to study mechanisms behind hemodynamic changes and to explore novel therapeutic approaches for secondary brain damage after TBI