Interleukin-1 exacerbates focal cerebral ischemia and reduces ischemic brain temperature in the rat.
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 microg/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 degrees 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.
Parry-Jones
Adrian R
AR
Faculty of Life Sciences, University of Manchester, Manchester, UK.
Liimatainen
Timo
T
Kauppinen
Risto A
RA
Gröhn
Olli H J
OH
Rothwell
Nancy J
NJ
D000704:Analysis of Variance; D000818:Animals; D001831:Body Temperature / Q000187:drug effects; D002545:Brain Ischemia / Q000473:pathology*; D007375:Interleukin-1 / Q000633:toxicity*; D016014:Linear Models; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D019047:Phantoms, Imaging; D051381:Rats; D017208:Rats, Wistar
D007375:Interleukin-1