A model for cerebral ischemia that requires injection of emboli into the internal carotid artery of the rabbit is commonly used. However, in our experience we have found the anatomy of the cervical carotid to be highly variable. If not appreciated, this may result in unexpectedly high variability in the severity of ischemic injury. We undertook this experimental protocol to determine whether it was possible to characterize the anatomy of the rabbit cervical carotid artery. We examined and recorded the architecture of the cervical carotid arteries of 105 consecutive rabbits involved in experimental protocols to evaluate the role of tissue-type plasminogen activator during embolic stroke. Two basic patterns of origin of the internal carotid artery were identified: lateral origin, classified as type I, and dorsomedial origin, classified as type II. In addition, there were three subsequent variations in the origin and morphology of the occipital artery in relation to the internal carotid artery: origin from the external carotid artery (subtype A); origin proximal on the internal carotid artery (subtype B); and origin distal on the internal carotid artery (subtype C). The classification of the anatomy of the cervical carotid artery of the rabbit into these easily recognized types will assist those attempting to use this embolization model. Failure to recognize the origin of the occipital artery from the internal carotid artery can result in the misdirection of embolic material into the occipital artery and significantly reduce the effectiveness of this stroke model.
Background and PurposeThe efficacy of thrombolytic therapy for treatment of embolic stroke has been a subject of both experimental and clinical examination. The aim of this study was to compare the efficacy, in regard to reduction of volume of ischemic brain, of two different modes of administration (ie, intra-arterial and intravenous) of tissue-type plasminogen activator (TPA) given 30 minutes after experimental embolic stroke in rabbits.Methods A randomized, blinded, controlled experimental trial was undertaken. Embolic stroke was simulated in rabbits by injecting fragments of autologous arterial thrombus into one internal carotid artery. Thirty minutes after embolization, the rabbits were blindly treated with 2 mg/kg intra-arterial TPA, 2 mg/kg intravenous TPA, or saline (alln=10). Six hours after embolization the rabbits were killed. The brains were perfused with triphenyltetrazolium chloride and cut into 0.5-cm-thick coronal sections, and the areas of ischemia were measured.
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