The protective effect of mild hypothermia in cerebral ischemia and reperfusion in rats
LI Cheng-ya
Abstract
LI Cheng-ya
Abstract
Objective To investigate the protective effect of mild hypothermia during cerebral ischemia and reperfusion. Methods After 3 hours of middle cerebral artery occlusion (MCAO) in rats, the myeloperoxi-dase (MPO) activity, the positive expression of intercellular adhesion molecule-1 (ICAM-1) , and the leukocyte integrin Mac-1 (CD11b/CD18) level in the ischemic regions were determined at different times (6 h,12 h,24 h, 48 h and 72 h) during and after 24 h of reperfusion. Cerebral infarction volume and neurological function were also evaluated in a control group, in addition to the above variables, at 24 hours of reperfusion. Results The MPO activity and the expression of ICAM-1 and Mac-1 were significantly elevated at 6 h after cerebral ischemia during reperfusion. These variables peaked at 48 h. There was a remarkable difference between the various groups and a sham-operated group ( P 0. 05 ,P 0. 01). Mild hypothermia reduced MPO activity and the positive expression of ICAM-1 and Mac-1 in brain tissue ( P 0. 05 ,P 0. 01 ). Conclusion Mild hypothermia can ameliorate any neurological deficit and decrease the infarct volume induced by cerebral ischemia and reperfusion. During cerebral ischemia-reperfusion, mild hypothermia could play an important role in decreasing the early onset of any inflammatory cascade reaction, which might be one of the neuroprotective mechanisms of mild hypothermia.
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Objective To investigate the protective effect of mild hypothermia during cerebral ischemia and reperfusion. Methods After 3 hours of middle cerebral artery occlusion (MCAO) in rats, the myeloperoxi-dase (MPO) activity, the positive expression of intercellular adhesion molecule-1 (ICAM-1) , and the leukocyte integrin Mac-1 (CD11b/CD18) level in the ischemic regions were determined at different times (6 h,12 h,24 h, 48 h and 72 h) during and after 24 h of reperfusion. Cerebral infarction volume and neurological function were also evaluated in a control group, in addition to the above variables, at 24 hours of reperfusion. Results The MPO activity and the expression of ICAM-1 and Mac-1 were significantly elevated at 6 h after cerebral ischemia during reperfusion. These variables peaked at 48 h. There was a remarkable difference between the various groups and a sham-operated group ( P 0. 05 ,P 0. 01). Mild hypothermia reduced MPO activity and the positive expression of ICAM-1 and Mac-1 in brain tissue ( P 0. 05 ,P 0. 01 ). Conclusion Mild hypothermia can ameliorate any neurological deficit and decrease the infarct volume induced by cerebral ischemia and reperfusion. During cerebral ischemia-reperfusion, mild hypothermia could play an important role in decreasing the early onset of any inflammatory cascade reaction, which might be one of the neuroprotective mechanisms of mild hypothermia.
Key concepts: Ischemia, Medicine, Hypothermia, Neuroprotection, Anesthesia, Reperfusion injury, Middle cerebral artery, Cerebral infarction