scholarly journals Cilostazol, Not Aspirin, Reduces Ischemic Brain Injury via Endothelial Protection in Spontaneously Hypertensive Rats

Stroke ◽  
2011 ◽  
Vol 42 (9) ◽  
pp. 2571-2577 ◽  
Author(s):  
Naoki Oyama ◽  
Yoshiki Yagita ◽  
Miki Kawamura ◽  
Yukio Sugiyama ◽  
Yasukazu Terasaki ◽  
...  
Keyword(s):  
Brain Injury ◽  
Spontaneously Hypertensive Rats ◽  
Ischemic Brain Injury ◽  
Hypertensive Rats ◽  
Ischemic Brain ◽  
Spontaneously Hypertensive

Excitatory and inhibitory amino acid changes in ischemic brain regions in spontaneously hypertensive rats

1991 ◽  
Vol 16 (1) ◽  
pp. 51-56 ◽  
Author(s):  
Hiroaki Ooboshi ◽  
Hiroshi Yao ◽  
Takashi Matsumoto ◽  
Makoto Hirano ◽  
Hideyuki Uchimura ◽  
...  
Keyword(s):  
Amino Acid ◽  
Spontaneously Hypertensive Rats ◽  
Brain Regions ◽  
Hypertensive Rats ◽  
Ischemic Brain ◽  
Spontaneously Hypertensive

scholarly journals Protection of ischemic brain metabolism by CBM 36-733 in spontaneously hypertensive rats.

Nosotchu ◽  
1991 ◽  
Vol 13 (4) ◽  
pp. 244-248
Author(s):  
Seizo Sadoshima ◽  
Yasushi Okada ◽  
Hiroshi Yao ◽  
Setsuro Ibayashi ◽  
Masatoshi Fujishima
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Brain Metabolism ◽  
Hypertensive Rats ◽  
Ischemic Brain ◽  
Spontaneously Hypertensive

A preventive injection of endothelial progenitor cells prolongs lifespan in stroke-prone spontaneously hypertensive rats

2018 ◽  
Vol 132 (16) ◽  
pp. 1797-1810 ◽  
Author(s):  
Cheng Peng ◽  
Xiao-Hui Dong ◽  
Jia-Lin Liu ◽  
Yu-Long Tao ◽  
Chun-Fang Xu ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Spontaneously Hypertensive Rats ◽  
Single Injection ◽  
Ischemic Injury ◽  
Hypertensive Rats ◽  
Ischemic Brain ◽  
Spontaneously Hypertensive ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

There is a pressing need for new approaches to prevent stroke. Endothelial progenitor cells (EPCs) promote vascular repair and revascularization in the ischemic brain. The present study sought to evaluate whether preventive delivery of EPCs could prevent or protect against stroke. Stroke-prone spontaneously hypertensive rats (SHR-SP) received a single injection of EPCs, and their survival time was monitored. In addition, at 28 and/or 42 days after a single injection of EPCs, SHR-SP and mice were subjected to cerebral ischemia, and cerebral ischemic injury, local angiogenesis and in vivo EPC integration were determined. Other experiments examined the effects of EPC conditioned medium, and the distribution of donor EPCs taken from GFP transgenic mice. It was found that EPC-pretreated SHR-SP showed longer lifespans than untreated controls. A single preventive injection of EPCs could produce persistent protective effects against cerebral ischemic injury (lasting at least 42 days), and promote local angiogenesis in the ischemic brain, in two types of animals (SHR-SP and normotensive mice). EPCs of donor origin could be detected in the recipient peripheral blood, and integrated into the recipient ischemic brains. Furthermore, it was suggested that mouse EPCs might exert paracrine effects on cerebral ischemic injury in addition to their direct angiogenic effects. In conclusion, a single preventive injection of EPCs prolonged the lifespan of SHR-SP, and protected against cerebral ischemic injury for at least 7 weeks. It is implied that EPC injection might be a promising candidate for a preventive role in patients at high risk for stroke.

scholarly journals Brain injury after intracerebral hemorrhage in spontaneously hypertensive rats

2011 ◽  
Vol 114 (6) ◽  
pp. 1805-1811 ◽  
Author(s):  
Gang Wu ◽  
Xuhui Bao ◽  
Guohua Xi ◽  
Richard F. Keep ◽  
B. Gregory Thompson ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Neuronal Death ◽  
Spontaneously Hypertensive Rats ◽  
Neurological Deficits ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Autologous Whole Blood

Object Hypertension is the main cause of spontaneous intracerebral hemorrhages (ICHs), but the effects of hypertension on ICH-induced brain injury have not been well studied. In this study, the authors examined ICH-induced brain injury in spontaneously hypertensive rats (SHRs). Methods This 2-part study was performed in 12-week-old male SHRs and Wistar Kyoto (WKY) rats. First, the rats received an intracaudate injection of 0.3 U collagenase, and hematoma sizes were determined at 24 hours. Second, rats were injected with 100 μl autologous whole blood into the right basal ganglia. Brain edema, neuronal death, ferritin expression, microglia activation, and neurological deficits were examined. Results Hematoma sizes were the same in SHR and WKY rats 24 hours after collagenase injection. The SHRs had greater neuronal death and neurological deficits after blood injection. Intracerebral hemorrhage also resulted in higher brain ferritin levels and stronger activation of microglia in SHRs. However, perihematomal brain edema was the same in the SHRs and WKY rats. Conclusions Moderate chronic hypertension resulted in more severe ICH-induced neuronal death and neurological deficits, but did not exaggerate hematoma enlargement and perihematomal brain edema in the rat ICH models.

scholarly journals Pharmacologically increasing collateral perfusion during acute stroke using a carboxyhemoglobin gas transfer agent (Sanguinate™) in spontaneously hypertensive rats

2017 ◽  
Vol 38 (5) ◽  
pp. 755-766 ◽  
Author(s):  
Marilyn J Cipolla ◽  
Italo Linfante ◽  
Abe Abuchowski ◽  
Ronald Jubin ◽  
Siu-Lung Chan
Keyword(s):  
Brain Injury ◽  
Spontaneously Hypertensive Rats ◽  
Time Window ◽  
Artery Occlusion ◽  
Gas Transfer ◽  
Chronic Hypertension ◽  
Collateral Flow ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cerebral Artery Occlusion

Similar to patients with chronic hypertension, spontaneously hypertensive rats (SHR) develop fast core progression during middle cerebral artery occlusion (MCAO) resulting in large final infarct volumes. We investigated the effect of Sanguinate™ (SG), a PEGylated carboxyhemoglobin (COHb) gas transfer agent, on changes in collateral and reperfusion cerebral blood flow and brain injury in SHR during 2 h of MCAO. SG (8 mL/kg) or vehicle ( n = 6–8/group) was infused i.v. after 30 or 90 min of ischemia with 2 h reperfusion. Multi-site laser Doppler probes simultaneously measured changes in core MCA and collateral flow during ischemia and reperfusion using a validated method. Brain injury was measured using TTC. Animals were anesthetized with choral hydrate. Collateral flow changed little in vehicle-treated SHR during ischemia (−8 ± 9% vs. prior to infusion) whereas flow increased in SG-treated animals (29 ± 10%; p < 0.05). In addition, SG improved reperfusion regardless of time of treatment; however, brain injury was smaller only with early treatment in SHR vs. vehicle (28.8 ± 3.2% vs. 18.8 ± 2.3%; p < 0.05). Limited collateral flow in SHR during MCAO is consistent with small penumbra and large infarction. The ability to increase collateral flow in SHR with SG suggests that this compound may be useful as an adjunct to endovascular therapy and extend the time window for treatment.

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