Abstract TP280: A Bland-new Rat Model of Embolic Cerebral Ischemia Using Micro Catheter Under Fluoroscopic Guide

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Teppei Komatsu ◽  
Hiroki Ohta ◽  
Junichi Hata ◽  
Haruhiko Motegi ◽  
Koshiro Terawaki ◽  
...  

Background: The failure of clinical trials on neuroprotective treatment may be partially caused by unestablished animal models. To verify a trans-arterial regeneration therapy, our project is aimed at developing a brand-new focal stroke model using micro catheter. Methods: Using Sprague-Dawley rats (n=8), a micro catheter (ID 0.26mm, OD 0.35mm) was navigated from the caudal ventral artery to the middle cerebral artery in order to establish local occlusion under digital subtraction angiography apparatus. Results: We succeeded in brain angiography by percutaneous tail artery puncture and occlusion of the middle cerebral artery by a radiopaque micro bead with 6 rats (75%). Ischemic stroke lesion volume is 480.3 mm3±84.2 mm3 on sustained 1% TTC solution after 24 hours occlusion. Conclusion: We present a new rat model for focal stroke using micro catheter under fluoroscopic control. The model is capable of repeated super selective administration of therapeutics directly to cerebral artery, and practice the 3Rs principles in experimental animals because of minimal invasive.Figure Legend- A: A sheath is inserted through the ventral midline, approximately 5 cm from the root of the tail of the rat, with a sharp angle. B: Cerebral angiography of rats. Arrowhead pointe middle cerebral artery. C: Occlusion of the middle cerebral artery by a radiopaque micro bead (arrowhead). D: Brain is sliced and stained 1% TTC solution after 24 hours occlusion.

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Shu-Jen Chang ◽  
Juin-Hong Cherng ◽  
Ding-Han Wang ◽  
Shu-Ping Yu ◽  
Nien-Hsien Liou ◽  
...  

Objective.Postinfarction transneuronal degeneration refers to secondary neuronal death that occurs within a few days to weeks following the disruption of input or output to synapsed neurons sustaining ischemic insults. The thalamus receives its blood supply from the posterior circulation; however, infarctions of the middle cerebral arterial may cause secondary transneuronal degeneration in the thalamus. In this study, we presented the areas of ischemia and associated transneuronal degeneration following MCAo in a rat model.Materials and Methods.Eighteen 12-week-old male Sprague-Dawley rats were randomly assigned to receive middle cerebral artery occlusion surgery for 1, 7, and 14 days. Cerebral atrophy was assessed by 2,3,5-triphenyltetrazolium hydrochloride staining. Postural reflex and open field tests were performed prior to animal sacrifice to assess the effects of occlusion on behavior.Results.Myelin loss was observed at the lesion site following ischemia. Gliosis was also observed in thalamic regions 14 days following occlusion. Differential degrees of increased vascular endothelial growth factor expression were observed at each stage of infarction. Increases in myelin basic protein levels were also observed in the 14-day group.Conclusion.The present rat model of ischemia provides evidence of transneuronal degeneration within the first 14 days of occlusion. The observed changes in protein expression may be associated with self-repair mechanisms in the damaged brain.


1995 ◽  
Vol 15 (3) ◽  
pp. 398-408 ◽  
Author(s):  
Hiroshi Yao ◽  
Myron D. Ginsberg ◽  
David D. Eveleth ◽  
Joseph C. LaManna ◽  
Brant D. Watson ◽  
...  

To ascertain the tempo of progression to irreversible injury in focal ischemia, we subjected halothaneanesthetized Sprague–Dawley rats to photochemically induced distal middle cerebral artery occlusion (dMCAO) combined with permanent ipsilateral and 1 h contralateral common carotid artery occlusions. Head temperature was maintained at 36°C. At times centered at either 1.5 or 3 h post-dMCAO, the rate of local glucose metabolism (lCMRgl) was measured by 2-deoxyglucose autoradiography, and cytoskeletal proteolysis was assessed regionally by an immunoblotting procedure to detect spectrin breakdown products. At 1.5 h (n = 5), the cortical ischemic core was already severely hypometabolic (lCMRgl 15.5 ± 10.8 μmol 100 g−1 min−1, mean ± SD), whereas the cortical penumbral zone was hypermetabolic (69.0 ± 9.7). (The lumped constant was verified to be unchanged by methylglucose studies.) Neutral red pH studies at this time point showed that both the core and penumbral zones were equally acidotic. By 3 h post-dMCAO (n = 6), lCMRgl in the penumbral zone had fallen to low levels (15.4 ± 2.2 μmol 100 g−1 min−1) equal to those of the ischemic core (16.7 ± 4.5). Correspondingly, spectrin breakdown in the ischemic core was advanced at both 2 and 3.5 h post-dMCAO (36 ± 18% and 33 ± 18% of total spectrin, respectively), whereas in the penumbral zone spectrin breakdown was less extensive and more highly variable at both times (22 ± 23% and 29 ± 16%). We conclude that irreversible deterioration of the ischemic core, as evidenced by the onset of local cytoskeletal proteolysis, begins within 2 h of middle cerebral artery occlusion. In the ischemic penumbra, the transition from glucose hyper- to hypometabolism occurs by 3.5 h and is associated with a milder and more variable degree of spectrin breakdown.


2015 ◽  
Vol 588 ◽  
pp. 137-141 ◽  
Author(s):  
Nik Nasihah Nik Ramli ◽  
Nursyazwani Omar ◽  
Andrean Husin ◽  
Zalina Ismail ◽  
Rosfaiizah Siran

1999 ◽  
Vol 19 (4) ◽  
pp. 425-434 ◽  
Author(s):  
Aurel Popa-Wagner ◽  
Eike Schröder ◽  
Harald Schmoll ◽  
Lary C. Walker ◽  
Christoff Kessler

Although stroke in humans usually afflicts the elderly, most experimental studies on the nature of cerebral ischemia have used young animals. This is especially important when studying restorative processes that are age dependent. To explore the potential of older animals to initiate regenerative processes after cerebral ischemia, the authors studied the expression of the juvenile-specific cytoskeletal protein, microtubule-associated protein (MAP) 1B, and the adult-specific protein, MAP2, in male Sprague-Dawley rats at 3 months and 20 months of age. The levels of MAP1B and MAP2 transcripts and the corresponding proteins declined with increasing age in the hippocampus. In the cortex, the levels of the transcripts did not change significantly with age, but the morphologic features of immunostained fibers were clearly affected by age; that is, cortical MAP1B fibers became thicker, and MAP2 fibers, more diffuse, in aged rats. Focal cerebral ischemia, produced by reversible occlusion of the right middle cerebral artery, resulted in a large decrease in the expression of both MAP1B and MAP2 in the infarct core at the messenger ribonucleic acid and protein levels. However, at 1 week after the stroke, there was vigorous expression of MAP1B and its messenger ribonucleic acid, as well as MAP2 protein, in the border zone adjacent to the infarct of 3-month-old and 20 month-old male Sprague-Dawley rats. The upregulation of these key cytologic elements generally was diminished in aged rats compared with young animals, although the morphologic features of fibers in the infarct border zone were similar in both age groups. These results suggest that the regenerative potential of the aged rat brain appears to be competent, although attenuated, at least with respect to MAP1B and MAP2 expression up to 20 months of age.


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