Sprague-Dawley rats were subjected to occlusion of the descending aorta at different duration under normothermia (38.0 ± 0.5) or hypothermia (33.0 ± 0.5°). Neurologic function was assessed. Motor neuron number, glial activation, and cytokine expression in the spinal cord were examined. Minocycline was administered perioperatively by intraperitoneal injection in the rats subjected to the aorta occlusion.
In contrast to normothermia conditions at which immediate paralysis occurred when the duration of aorta occlusion exceeded 11.5 min, hypothermia did not induce immediate paralysis if the duration of aorta occlusion was less than 41 min. However, delayed paralysis was developed when the duration of aorta occlusion exceeded 18 min, and reached peak level when the duration of aorta occlusion was 40 min at hypothermia condition. The number of motoneurons was significantly decreased (P < 0.05) at 30 h postoperation. In addition, microglia was activated, and interleukin-1β and interleukin-6 levels were upregulated, both of which were co-localized in microglia at 24 h postoperation in the hypothermia group. Minocycline treatment attenuated the incidence and degree of paralysis but did not decrease the mortality.
Hypothermia, a neuroprotective strategy in cardiothoracic surgery, increased the incidence of delayed paralysis through activation of spinal microglia and cytokines. Blocking the activated microglia may be a potential intervention to prevent the incidence of delayed paralysis.