Post-ischemic hypothermia delayed neutrophil accumulation and microglial activation following transient focal ischemia in rats
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Updated: Oct 13, 2026

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
Published on: March 1, 2019
1Department of Neurosurgery, Keio University School of Medicine, Shinanomachi 35, Shinjuku-ku, 160-8582, Tokyo, Japan. georges@med.keio.ac.jp
Abstract:
Following ischemia, inflammation has been demonstrated to be involved in the progression of the tissue damage. Intra-ischemic hypothermia has been shown to attenuate the adverse activities of neutrophils and microglia. We investigated whether neutrophil accumulation and/or microglial activation is attenuated in post-ischemic hypothermia following transient focal ischemia in rats. After 1 h of ischemia, the neutrophil accumulation and the microglial activation was evaluated immunohistochemically. Percent infarct area was compared at 1, 2, 3, 5, and 7 days after ischemia/reperfusion. In hypothermia, the neutrophil accumulation was delayed but not attenuated. In normothermia, the accumulation reached the peak at 2 days after ischemia. The peak shifted to 3 days in hypothermia. Similarly, the microglial activation was delayed in hypothermia. Comparison of the infarct area showed significant protection by hypothermia at 1 and 2 days after reperfusion. However, hypothermia failed to show significant protection after 3 days and later. These results show that the delayed neutrophil accumulation and the microglial activation can be responsible for the loss of persistent protection in post-ischemic hypothermia.

