Blood-brain Barrier Opening And Vasogenic Brain Edema Of Experimental Acute Ischemia Of Rats: MRI Evaluation, And The Correlation With MMP-9 And VEGF Expression In Infarcted Brain Tissue

Background The main factors which influence the survival rate in acute brain ischemia are ischemic brain edema and hemorrhagic transformation(HT) of the infarction. Thrombolytic treatment may increase the possibility of secondary hemorrhage. The key mechanism of above mentioned pathological changes is related to the disruption or opening of blood-brian barrier(BBB). Previously, the main methods to probe vasogenic brain edema(VBE) and opening of BBB were to study the specimen pathologically. The disadvantages of these studies included : lack of continuity of observation, not suitable to be applied to living case, and difficult to predict the molecular biological changes after ischemia.The purposes of this study are:to observe the dynamic findings of VBE and opening of BBB of infarcted rats, to look into the pathologic changes, and to observe if the MRI findings is correlated well with MMP-9 and VEGF expression of infarcted brain tissue.Parti: Evaluation with Enhanced MRI of Blood-brain Barrier Opening of Rats in Experimental Acute IschemiaObjective To evaluate contrast-MRI findings of BBB opening of acute brain ischemia, and to probe the difference of brain parenchyma enhancement between temporal middle cerebral artery occlusion(tMCAO) and permanent middle cerebral artery occlusion(pMCAO) in rats. We also investigated the temporal features of brain parenchyma enhancement and its ultrastructural features in both series. Materials and Mathods A modified Zea-Longea operation was performed to set up MCAO model of 160 rats. Coronal non-enhanced and Gd-DTPA enhanced brain MRI were made thereafter. We observed the enhancement rate of ischemic brain parenchyma and the increasement of signal intensity on T,WI after contrast medium administration. The ischemic brain specimens which obtained at various time after MCAO were analyzed histologically and electroscopically. Results In t.MCAO series, there was biphasic brain parenchyma enhancement at 3h and 1d-3d after MACO. Whereas there was single phase enhancement in pMCAO rats at ld-3d after ischemia. At 3h, after administration of contrast medium, an obvious increasing delayed enhancement was detected 3h to 21h after injection. In the earlier phase, the enhancement of tMCAO series was more apparent than that of pMCAO series and the second phase of tMCAO series. On electroscopic examination at various time after ischemia, the alteration of BBB included:endothelial cell swelling and increased engulf vesicles, enlarged extravascular space, disruption of basal membrane, and extravascular exudates. 2 days after ischemia, neovascularity were found on specimen of both series. Conculsion On contrast-MRI, BBB opening in acute ischemia manifested as local parenchyma enhancement. There was biphasic parenchyma enhancement to tMCAO rats. However, there was single phase enhancement to pMCAO series. Themain cause of abnormal parenchyma enhancement is the destruction of BBB structures. However,the neovascularity may also be the cause of enhancement 2 days after ischemia in both tMCAO and pMCAO rats. The parenchyma enhancement also depends on the effective blood perfusion of ischema area. The early phase parenchyma enhancement may probably be the mark of re-perfusion of ischemic tissue.Part II:MRI Manifestations of Vasogenic Brain Edema in Acute Ischemia/Reperfusion Rats and MMP-9 Expression of Ischemic Brain TissueObjective To set up the model of vasogenic brain edema(VBE) after ischemia/reperfusion of rats. To investigate the MRI findings of VBE and its correlation with MMP-9 expression of infarcted tissue. Materials and Methods The thread occulsion of right or left middle cerebral artery(MCA) was made to set up VBE models in 70 rats. Dynamic evaluation of VBE with MRI was performed. The specimens were analyzed immunohistochemically at various time. Results High siganl intensity was detected in the right MCA territories on T2WI 3h to 72h after operation. On 12h to 3d LWI, compression of ipsilateral lateral ventricle and displacement of midline structures was foun...