The immunomodulatory mechanism of brain injury induced by hyperhomocysteinemia in spontaneously hypertensive rats

2019 ◽  
Vol 120 (6) ◽  
pp. 9421-9429 ◽  
Author(s):  
Yu Zhang ◽  
Lin Wang ◽  
Xin Zhou ◽  
Jie Geng ◽  
Xin Li
Keyword(s):  
Brain Injury ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

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

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.

scholarly journals Reduction of Tissue Plasminogen Activator-Induced Hemorrhage and Brain Injury by Free Radical Spin Trapping after Embolic Focal Cerebral Ischemia in Rats

2000 ◽  
Vol 20 (3) ◽  
pp. 452-457 ◽  
Author(s):  
Minoru Asahi ◽  
Kazuko Asahi ◽  
Xiaoying Wang ◽  
Eng H. Lo
Keyword(s):  
Free Radical ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Cerebral Hemorrhage ◽  
Spontaneously Hypertensive Rats ◽  
Neurological Deficits ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tissue Plasminogen

Thrombolytic stroke therapy with tissue plasminogen activator (tPA) remains complicated by serious risks of cerebral hemorrhage and brain injury. In this study, a novel model of tPA-induced hemorrhage was used in spontaneously hypertensive rats to examine the correlates of hemorrhage, and test methods of reducing hemorrhage and brain injury. Homologous blood clot emboli were used to occlude the middle cerebral artery in spontaneously hypertensive rats, and delayed administration of tPA (6 hours postischemia) resulted in high rates of cerebral hemorrhage 24 hours later. Compared with untreated rats, tPA significantly increased hemorrhage volumes by almost 85%. Concomitantly, infarction and neurological deficits were worsened by tPA. A parallel experiment in normotensive Wistar-Kyoto rats showed markedly reduced rates of hemorrhage, and tPA did not significantly increase hemorrhage volumes. To examine whether tPA-induced hemorrhage was caused by the delayed onset of reperfusion per se, another group of spontaneously hypertensive rats was subjected to focal ischemia using a mechanical method of arterial occlusion. Delayed (6 hours) reperfusion via mechanical means did not induce hemorrhage. However, administration of tPA plus delayed mechanical reperfusion significantly increased hemorrhage volumes. Since reperfusion injury was implicated, a final experiment compared outcomes in spontaneously hypertensive rats treated with tPA plus the free radical spin trap α-phenyl tert butyl nitrone (α-PBN) versus tPA alone. tPA-induced hemorrhage volumes were reduced by 40% with α-PBN, and infarction and neurological deficits were also decreased. These results indicate that (1) blood pressure isanimportant correlate of tPA-induced hemorrhage, (2) tPA interacts negatively with reperfusion injury to promote hemorrhage, and (3) combination therapies with anti-free radical treatments may reduce the severity of tPA-induced hemorrhage and brain injury after cerebral ischemia.

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