Decompressive craniectomy and mild hypothermia reduces infarction size and counterregulates Bax and Bcl-2 expression after permanent focal ischemia in rats.

Both mild hypothermia (MH) and decompressive craniectomy (CE) have been shown to have neuroprotective effects in brain ischemia. We investigated a possible effect of MH and a combination of CE and MH (CE + MH) on the changes of infarction size, DNA fragmentation, and immunoreactivities for Bcl-2 and Bax after 24 h of permanent middle cerebral artery occlusion (MCAO) in rats. For the estimation of ischemic brain injury, we calculated the infarct size of the MCA region at 24 h after the MCAO. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick labeling (TUNEL) staining was performed for the detection of DNA fragmentation. Immunoreactivities for Bcl-2 and Bax were stained. Infarction size after permanent MCAO was significantly reduced by CE+MH treatment (P < 0.01). Infarction size did not change significantly by application of MH alone (P > 0.05). TUNEL staining was remarkably reduced both in MH-treated animals and in CE + MH-treated animals. Immunoreactivity for Bcl-2 was greatly induced both in MH-treated animals and in CE + MH-treated animals. Induction of immunoreactivity for Bcl-2 was obviously inhibited both in MH-treated animals and in CE + MH-treated animals. It suggests that temporary MH delays infarct evolution and ameliorates neuron apoptosis but does not significantly reduce definite infarction size. CE + MH not only ameliorates neuron apoptosis but also remarkably reduces infarction size.