| Background: Cerebral vasospasm (CVS) remains a major complication in patients who experience aneurysmal subarachnoid hemorrhage (SAH). The lack of adequate medical treatments for SAH-induced vasospasm continues to sitimulate preclinical and clinical studies of this disorder. Such studies seek to identify the mechanisms underlying SAH-induced CVS and to develop effective therapeutic strategies for limiting vasospasm. There is a controversy about whether SAH induced CVS is caused by simple functional contraction of smooth muscle cells (SMCs) or pathological changes of blood vessles. Ecdysterone (EDS) is a kind of steroid. Our previous study showed that EDS might prevent CVS following SAH in vitro. However, there is no study about antispastic effect of EDS on CVS in vivo.Objective: Our aim is to establish a simple and inexpensive experimental model of symptomatic CVS after SAH in rabbits and to study the antispastic effects of EDS in the treatment of CVS on this model. Methods:1. Autologous arterial blood was injected into cisterna magna twice after ligation of right common carotid artery in rabbits to establish the symptomatic CVS model.2. The amount of food intaking and neural behavior score of Endo's were investigated in this model.3. Blood flow changes of basilar artery in the symptomatic CVS model was examined by transcranial Doppler ultrasonography (TCD).4. Pathological change of basilar arteries and hippocampal neurons was observed by light microscope and transmission electron microscope after symptomatic CVS.Results: 1. The two-hemorrhage model established by injecting autologous arterial blood into cisterna magna 48 hours apart after ligation of right common carotid artery is a successful symptomatic CVS rabbit model with low mortality rate;2. Changes of vascular hemodynamic indexes were showed by TCD. Vs indexes were 62.18±6.22, 84.53±10.15, 83±14.90, 72.33±11.02, before hemorrhage and 1day, 3 days and 7 days after two-hemorrhage respectively; Vm indexes were 52.43±4.90, 69.58±6.83, 62.98±12.25, 56.43±8.37, before hemorrhage and 1day, 3 day and 7 day after two-hemorrhage respectively; PI indexes were 0.36±0.034, 0.43±0.077, 0.54±0.051, 0.56±0.12, before hemorrhage and 1day, 3 day and 7 day after two-hemorrhage respectively; RI indexes were 0.32±0.025, 0.36±0.052, 0.43±0.024, 0.46±0.075, before hemorrhage and 1day, 3 day and 7 day after two-hemorrhage respectively;3. Morphological structural changes of the basilar arterial wall, including VEC lesions, emergence of inflammatory cells and disorder of VSMC structure, were detected by light microscope and transmission electron microscope observation, while EDS inhibited these changes after SAH;4. Ischemic changes of hippocampus tissue after CVS, including edema of neurons and gliacytes, were observed by light microscope and transmission electron microscope observation. EDS inhibited these changes after SAH.Conclusion: The two-hemorrhage model established by injecting autologous arterial blood into cisterna magna 48 hours apart after ligation of right common carotid artery might be a proper model to show the process of symptomatic CVS after SAH.TCD could investigate the blood flow changes of this symptomatic cerebral vasospasm model.There are vascular endothelial cells lesion, emergence of inflammatory cells and phentypical modulation of smooth muscle cells on basilar artery following SAH-induced vasospasm.There are hypoxic and ischemia pathological changes in hippocampus SAH-induced vasospasm.EDS might have some protective effects on endothelial cells, smooth muscle cells and hippocampus neurons. ...
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