Effects Of Transection Of Cervical Sympathetic Trunk On Astrocytes Activation After Subarachnoid Hemorrhage In Rats

Objective:To investigate effects of transection of cervical sympathetic trunk on astrocytesactivation after subarachnoid hemorrhage in rats,for further ascertaining itsneuroprotective mechanism.Methods:Ninety-six male Sprague Dawley (SD) rats of clean grade were randomized intofour groups: group A (shame operation group)、group B (SAH)、group C (TCST+SAH) and group D (control group). The model of SAH was set up by injecting ofautologous blood into the cisterna magna twicely. Rats of group A just servedneedle，not injection of blood. In group D cervical sympathetic trunk was exposed,not transection,and the rest part of group D were done as group B. After modeling，all rats of each group were killed respectively12h、24h、48h and72h. The histologicalchange of brain tissue slice was observed with HE staining,and the concentration ofGFAP and IL-1β in brain tissue was detected.Results:Levels of GFAP of group B、group C and group D began to go up at12h，reached the peak at48h and were still higher than normal at72h；the contents ofIL-1β of group B and group D began to go up at12h，reached the peak at72h. Ateach time point, both levels of GFAP and the contents of IL-1β of group B、group Cand group D were specifically higher than group A (P<0.05). At the same time point,both the levels of GFAP and the contents of IL-1β of group C were specifically lowerthan group B (P<0.05). At each time point，the diffrences of group B and group D didnot have statistical significance（P>0.05）. HE staining found：the degree of neureedema and cellular structure in the group C were better than those in the group B;activity of astrocytes proliferation in the group C were more weak than that in thegroup B; those of group B were worse than those of group A,appearing nuclear solidshrinkage and nuclear fragmentation.Conclusion: TCST impaired astrocytes activation after subarachnoid hemorrhage inrats, reducing the release of inflammatory medium IL–1β,which produces aneuroprotective effect.