Corrigendum to ‘Preconditioning effect of (S)-3,5-dihydroxyphenylglycine on ischemic injury in middle cerebral artery occluded Sprague–Dawley rats” [Neurosci. Lett. 588 (2015) 137–141]

2015 ◽  
Vol 590 ◽  
pp. 132-133
Author(s):  
Nik Nasihah Nik Ramli ◽  
Nursyazwani Omar ◽  
Andrean Husin ◽  
Zalina Ismail ◽  
Rosfaiizah Siran
2015 ◽  
Vol 588 ◽  
pp. 137-141 ◽  
Author(s):  
Nik Nasihah Nik Ramli ◽  
Nursyazwani Omar ◽  
Andrean Husin ◽  
Zalina Ismail ◽  
Rosfaiizah Siran

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.


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.


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.


2004 ◽  
Vol 286 (6) ◽  
pp. H2127-H2132 ◽  
Author(s):  
Marilyn J. Cipolla ◽  
Lisa Vitullo ◽  
John McKinnon

Eclampsia is thought to be similar to hypertensive encephalopathy, whereby acute elevations in intravascular pressure cause forced dilatation (FD) of intrinsic myogenic tone of cerebral arteries and arterioles, decreased cerebrovascular resistance, and hyperperfusion. In the present study, we tested the hypothesis that pregnancy and/or the postpartum period predispose cerebral arteries to FD by diminishing pressure-induced myogenic activity. We compared the reactivity to pressure (myogenic activity) as well as factors that modulate the level of tone of third-order branches (<200 μm) of the posterior cerebral artery (PCA) that were isolated from nonpregnant (NP, n = 7), late-pregnant (LP, 19 days, n = 10), and postpartum (PP, 3 days, n = 8) Sprague-Dawley rats under pressurized conditions. PCAs from all groups of animals developed spontaneous tone within the myogenic pressure range (50–150 mmHg) and constricted arteries at 100 mmHg (NP, 30 ± 3; LP, 39 ± 4; and PP, 42 ± 7%; P > 0.05). This level of myogenic activity was maintained in the NP arteries at all pressures; however, both LP and PP arteries dilated at considerably lower pressures compared with NP, which lowered the pressure at which FD occurred from >175 for NP to 146 ± 6.5 mmHg for LP ( P < 0.01 vs. NP) and 162 ± 7.7 mmHg for PP ( P < 0.01 vs. NP). The amount of myogenic tone was also significantly diminished at 175 mmHg compared with NP: percent tone for NP, LP, and PP animals were 35 ± 2, 11 ± 3 ( P < 0.01 vs. NP), and 20 ± 7% ( P < 0.01 vs. NP), respectively. Inhibition of nitric oxide (NO) with 0.1 mM Nω-nitro-l-arginine (l-NNA) caused constriction of all vessel types that was significantly increased in the PP arteries, which demonstrates significant basal NO production. Reactivity to 5-hydroxytryptamine (serotonin) was assessed in the presence of l-NNA and indomethacin. There was a differential response to serotonin: PCAs from NP animals dilated, whereas LP and PP arteries constricted. These results suggest that both pregnancy and the postpartum period predispose the cerebral circulation to FD at lower pressures, a response that may lower cerebrovascular resistance and promote hyperperfusion when blood pressure is elevated, as occurs during eclampsia.


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