Experimental Study Of Protective Effect Of Ecdysterone On Early Brain Injury Following Subarachnoid Hemorrhage

Objective: To establish a subarachnoid hemorrhage(SAH) model with simulate pathophysiological processes of clinic intracranial aneurysm rupture in rats .To study mechanisms of early brain injury following subarachnoid hemorrhage and discuss its protective mechanisms of ecdysterone effects.Methods:This study consists of two parts.Part one: SAH was produced by passing a nylon thread through the right external carotid artery to internal carotid artery and piercing its furcation .Dynamic monitor of electroencephalogram and regional cerebral blood flow were made in operation, the mortality and neurological deficits, brain water content, pathologic change were observed in 24 hours after the operation.Part two: According to part one, to establish noncraniotomy model of Subarachnoid hemorrhage in rats ,90 Sprague-Dawley rats were divided randomly into three groups including control group,SAH group and EDS-treatment group. Dynamic monitor of electroencephalogram and regional cerebral blood flow were made in operation, meanwhile pathological anatomy were verificated succeed to produce the SAH model after operation. the mortality and neurological deficits, brain water content,pathologic change were observed by light microscope and transmission electronic microscope, the chang of Bcl-2 and Caspase were observed by immunohistochemistry and apoptosis were observed by TUNEL at 24h.Results:1.The achievement ratio of SAH model is 96.7%.There was much blood or blood clots found in subarachnoid cavity of SAH model rats.2.Neurological deficits were observed after SAH .The amplitude of EEG significantly decreased andδwave increased following SAH . The change of rCBF has biphasic response, which decreased obviously following SAH (78.00±2.39%),and increased to (89.85±5.72%) of preoperative leve in 10min and then decreased again to reach a stable lever(47.68±4.72%) within 2h,which lasted for 24h. Brain water content increased in SAH group in 24h. nerve cell had hydropic degeneration. basilar artery coarctation turned smaller, tunica intima showed crenation and some basal lamina had segmentation. Immunohistochemistry detection showed that Bcl-2 decreased and Caspase increased.TUNEL detection showed that some typical apoptotic cell were detected in SAH group.3. Neurological deficits were improved in EDS group. The amplitude of EEG significantly increased at 2h and rCBF increased at 12h after SAH. Brain water content and nerve cell hydropic degeneration had improved in some degree. Immunohistochemistry manifested that Bcl-2 increased and Caspase decreased compared with SAH group.Conclusions:1. The noncraniotomy model of SAH in rats is reliable.It can effectively simulate clinic intracranial aneurysm rupture pathophysiological processes.2. The dynamic change of EEG and rCBF can be taken as a criterion to judge whether it is successful in producing SAH or not. It also can indirectly estimate subarachnoid hemorrhagic volume and velocity. 3. Early brain injury is taken place following SAH including increased intracranial pressure, cerebral edema, decreased rCBF, cerebral vasospasm, nerve cell and vascular endothelial cell apoptosis and so on.4.EDS can relieve Early brain injury following SAH.Its protective mechanisms maybe including relieving vasospasm, vascular endothelial cell injury, anti-cerebral edema and anti-apoptosis.