Abstract
The proinflammatory cytokine interleukin‐1 (IL‐1) is a key mediator of inflammation in cerebral ischemia, but its precise mechanisms of action remain elusive. Temperature is critical to outcome in brain injury and given the importance of IL‐1 in pyrogenesis this has clear mechanistic implications. IL‐1 exacerbates ischemia independently of core (rectal) temperature. However, it is temperature in the ischemic brain that influences outcome and rectal temperature is likely to be a poor surrogate marker. This study tested the hypothesis that IL‐1 exacerbates cerebral ischemia by increasing ischemic brain temperature. Wistar rats undergoing transient middle cerebral artery occlusion received either 4 μg/kg IL‐1 (n = 9) or vehicle (n = 10) intraperitoneally. NMR‐generated maps of brain temperature, tissue perfusion, and the trace of the diffusion tensor were collected during occlusion, early reperfusion, and at 24 hr. IL‐1 significantly increased ischemic damage at 24 hr by 35% but rectal temperature did not vary significantly between groups. However, ischemic brain was 1.7°C cooler on reperfusion in IL‐1‐treated animals (vs. vehicle) and a corresponding reduction in cerebral blood flow was identified in the ischemic striatum. Contrary to the stated hypothesis, IL‐1 reduced ischemic brain temperature during reperfusion and this may be due to a reduction in tissue perfusion. Magn Reson Med, 2008. © 2008 Wiley‐Liss, Inc.