Effects of P38 Mitogen-Activated Protein Kinase Signal Transduction Pathway in Delayed Cerebral Vasospasm After Subarachnoid Hemorrhage

Objective: To study the role of P38 MAPK in the development of delayed cerebral vasospasm after subarachnoid hemorrhage(SAH).Methods: Thirty-five New Zealand white rabbits were divided randomly into four group: control(n=5),SAH(n=10),SAH+DMSO(n=10),and SAH+SB203580(n=10) groups.The SAH model was established by using blood injection via cisternal puncture twice.The perfusion-fixation was performed respectively on the 5th and 7th day after blood-injection in vivo and the entire length of basilar artery was harvested.The degree of cerebral vasospasm was evaluated by measuring the cross-sectional area of each basilar arterial lumen,and the expression of P38 MAPK in the vascular wall was examined with immunohistochemistry.Results: In the SAH group and SAH+DMSO group,the cross-sectional area of rabbits basilar arterial lumen on the 5th day was statistically smaller than that in the control group(P0.01),and the expression of P38 MAPK in the vascular wall was statistically higher than that in the control group(P0.01).The cross-sectional area of arterial lumen in the SAH+SB203580 group on the 5th day was statistically larger than in SAH and SAH+DMSO groups in the same period,and P38 MAPK could not be detected in the vascular smooth muscle cell layer.Conclusion: Activated P38 MAPK in rabbits smooth muscle cells after SAH could induce the development of delayed cerebral vasospasm,and P38 MAPK specific inhibitor SB203580 is able to attenuate effectively the persistent contraction of arterial smooth muscle.