A Lacunar Infarction Model With Proximal MCA Embolization Using Autologus Clot In Beagle Dogs

Backgraund and PurposeLacunar infarcts account for one quarter of ischemic stroke. Presenting forms of lacunar infarction include asymptomatic lacunar infarcts, episodes of transient cerebral ischemia and clinical lacunar syndromes. The exact etiology of lacunar infarction is still unknown. Most lacunar strokes are thought to arise secondary to an abnormality in the walls of the small, deep perforating (lentic-ulostriate) arteries. The arterial wall changes have been referred to as "segmental arteriolar disorganization" or "lipohyalinosis" or "fibrinoid necrosis". However, recent years some controversy have arised. Some researchers insisted that large-artery embolism accounting for lacunar infarcts in variable proportions of patients instead of small-perforating-artery disease.In this study, we try to establish a cerebral infarction model with proximal MCA embolization using autologus clot in beagle dogs. Meanwhile we will (1) evaluate the location, the time course of the ischemic stroke, and the stability of this stroke model in beagle dogs.(2) disscuss the potential causes of lacunar infarction.Materials and methodsSix adult beagle dogs were embolized using interventional technique with relatively large thrombus (about1.7mm in diameter). The DWI-MR scanning was performed to evaluate the processing of ischemic lesions, including the location, the diameter, and the detecting time at30minutes interval within6hours after cerebral artery occlusion, respectively. The cerebral angiogram and MR examinations were repeated at24hours and7days post procedure. The volume of infarctions and the neuro-behavior scoring were recorded for statistical analysis. Then these animals were sacrificed for pathological evaluation.ResultsThe left proximal MCA was successfully occluded in all dogs using single autologus clot. The solitary or multiple ischemic lesions of high intensity in DWI were detected in the basilar ganglion and white matter area. The mean time of detecting was1.18±0.42hours. There were total15lesions were observed with the maximum diameter of9.6mm in6h-DWI after occlusion. The mean diameter and volume of these lesions were6.07±0.56mm and125.72±127.46mm3, respectively. The mean diameter and volume of these lesions were5.37±0.66mm and125.74±145.47mm3at24hours T2image, respectively. The statistical analysis showed significant difference in the diameter between the two time points (P=0.0134, t=2.8305). Toltal13abnormal lesions were detected with mean volume of91.26±110.69mm3at7days T2evaluation. There was no statistical meaning among the three time points in the volume. All dogs survived at7days post embolization. The neuro-behavioral scores were4.25±1.67at24hours and2.63±0.92at7days after procedure (P<0.05). The ischemic infarctions located in the basilar ganglion area were most frequent in pathological examination.Conclusions(1)The reliable proximal MCA occlusion can be established using about1.7mm clot. These DWI abnormalities can be detected in the early phase afer the onset of lacunar infarction.(2)The lacunar infarctions can be induced with embolism in dogs because of the aboundant anastomasis between the ECA and ICA. Thus, embolism may be a potentiao cause of lacunar infarction.