OBJECT: The intraluminal suture model for focal cerebral ischemia is increasingly used, but not without problems. It causes hypothalamic injury, subarachnoid hemorrhage, and inadvertent premature reperfusion. The patency of the posterior communicating artery (PCoA) potentially affects the size of the infarct. In addition, survival at 1 week is unstable. The authors operated on C57Black6 mice to produce proximal middle cerebral artery occlusion (MCAO) so that drawbacks with the suture model could be circumvented. METHODS: The MCA segment just proximal to the olfactory branch was occluded either permanently or temporarily. After 1 hour of MCAO the infarct volume was significantly smaller than that found after 2 hours or in instances of permanent MCAO. The differences were assessed at 24 hours and 7 days after surgery (p < 0.05 and p < 0.001, respectively). The patency of the PCoA, as visualized using carbon black solution, did not correlate with the infarct size. Neurologically, the 1- and 2-hour MCAO groups displayed significantly less severe deficits than the permanent MCAO group on Days 1, 4, and 7 (p < 0.005 and p < 0.01, respectively). Although the infarct size, neurological deficits, and body weight loss were more severe in the permanent MCAO group, the survival rate at Day 7 was 80%. CONCLUSIONS: This model provides not only a robust infarct size (which is not affected by the patency of the PCoA), but also a better survival rate.
OBJECT: The intraluminal suture model for focal cerebral ischemia is increasingly used, but not without problems. It causes hypothalamic injury, subarachnoid hemorrhage, and inadvertent premature reperfusion. The patency of the posterior communicating artery (PCoA) potentially affects the size of the infarct. In addition, survival at 1 week is unstable. The authors operated on C57Black6 mice to produce proximal middle cerebral artery occlusion (MCAO) so that drawbacks with the suture model could be circumvented. METHODS: The MCA segment just proximal to the olfactory branch was occluded either permanently or temporarily. After 1 hour of MCAO the infarct volume was significantly smaller than that found after 2 hours or in instances of permanent MCAO. The differences were assessed at 24 hours and 7 days after surgery (p < 0.05 and p < 0.001, respectively). The patency of the PCoA, as visualized using carbon black solution, did not correlate with the infarct size. Neurologically, the 1- and 2-hour MCAO groups displayed significantly less severe deficits than the permanent MCAO group on Days 1, 4, and 7 (p < 0.005 and p < 0.01, respectively). Although the infarct size, neurological deficits, and body weight loss were more severe in the permanent MCAO group, the survival rate at Day 7 was 80%. CONCLUSIONS: This model provides not only a robust infarct size (which is not affected by the patency of the PCoA), but also a better survival rate.
Authors: K Myojin; A Taguchi; K Umetani; K Fukushima; N Nishiura; T Matsuyama; H Kimura; D M Stern; Y Imai; H Mori Journal: AJNR Am J Neuroradiol Date: 2007-05 Impact factor: 3.825
Authors: Gary P Morris; Amanda L Wright; Richard P Tan; Amadeus Gladbach; Lars M Ittner; Bryce Vissel Journal: PLoS One Date: 2016-02-12 Impact factor: 3.240
Authors: Hongmei Song; Sivakami M Mylvaganam; Justin Wang; Saeyon M K Mylvaganam; Chiping Wu; Peter L Carlen; James H Eubanks; Jiachun Feng; Liang Zhang Journal: Front Cell Neurosci Date: 2018-08-29 Impact factor: 5.505