A new model of temporary focal neocortical ischemia in the rat.

Abstract

Background and Purpose:We describe a new rat model of temporary focal ischemia that produces neocortical ischemia without the need for prolonged anesthesia.Methods: Temporary focal cerebral ischemia was initiated during halothane anesthesia, maintained for varying periods without anesthesia, and reversed by clip removal requiring brief anesthesia. Tandem carotid and middle cerebral artery occlusion for 1-4 hours and permanent occlusion were used to determine the duration and extent of ischemia necessary to produce predictable volumes of neocortical infarction in Wistar and spontaneously hypertensive rats.Results :

Rodent models of focal stroke: Size, mechanism, and purpose

“…These variations include permanent occlusion of the ipsilateral common and middle cerebral carotid arteries, 92 permanent occlusion of the ipsilateral common carotid artery alone, 95 permanent occlusion of the middle cerebral artery alone, 94 and temporary occlusion of all three vessels. 96 A comparison of infarct size across these variations suggests that this approach generates a reproducible infarct volume, especially within the same lab. 94 Ischemic damage involves most of the frontal, parietal, temporal and rostral occipital cortex, the underlying white matter and a small region of dorsolateral striatum.…”

“…94 Ischemic damage involves most of the frontal, parietal, temporal and rostral occipital cortex, the underlying white matter and a small region of dorsolateral striatum. 92,94,96 Importantly, both the Tamura and three-vessel occlusion models involve reperfusion. In the Tamura model, local collaterals from the anterior cerebral artery provide a zone of reflow in medial frontal and parietal cortex.…”

Thrombotic distal middle cerebral artery occlusion produced by topical FeCl3 application: A novel model suitable for intravital microscopy and thrombolysis studies

“…Several models of permanent or temporary and proximal or distal middle cerebral artery (MCA) occlusion have been developed (Ginsberg and Busto, 1989). A large infarct and high mortality rate caused by brain swelling are disadvantages of proximal MCA occlusion models, whereas damage to the duramater and peri-arterial cortex, as well as high cost in some cases (e.g., photothrombosis with laser) limit the use of distal MCA models (Brint et al, 1988;Buchan et al, 1992;Chen et al, 1986;Kaneko et al, 1985). Recently, intravital or multiphoton microscopy and laserspeckle imaging have become popular because they allow live monitoring of several pathophysiological processes during cerebral ischemia.…”

Time-Related Neuronal Changes following Middle Cerebral Artery Occlusion: Implications for Therapeutic Intervention and the Role of Calpain

“…More recently, insight into some of the temporal events associated with focal infarct has come from studies employing occlusions of different durations in conjunction with quantitative histology. CoUec tively, these papers suggest that while reliable cel lular changes occur within 30 min to 1 h of ischemia, they are not lethal (Knight et al , 1991;Buchan et al , 1992;Memezawa et al , 1992;Minematsu et al , 1992a,b). This conclusion is based on the observa tion that reperfusion within a 1-to 2-h window al lowed sufficient cellular recovery to occur so that little or no infarct was observed at 24 h postocclu sion (Kaplan et al , 1991;Memezawa et al , 1992).…”

“…Several reperfusion studies argue that 3 h (but not 1 to 2 h) of MCA-O-induced ischemia leads to near-maximal cell death (Kaplan et al , 1991;Buchan et al , 1992;Memezawa et al , 1992). However, one cannot determine from the experi mental designs employed at what point in time sig nificant, irreversible cell damage actually occurred because none of the reperfusion studies examined tissue from anything less than end-stage, 24-h postocclusion tissue.…”