Synergistic induction of heme oxygenase-1 by nicaraven after subarachnoid hemorrhage to prevent delayed cerebral vasospasm

2009 ◽  
Vol 620 (1-3) ◽  
pp. 16-20 ◽  
Author(s):  
Yasuhito Shimada ◽  
Hiroshi Tsunoda ◽  
Liqing Zang ◽  
Minoru Hirano ◽  
Takehiko Oka ◽  
...  
1999 ◽  
Vol 104 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Hidenori Suzuki ◽  
Kenji Kanamaru ◽  
Hiroshi Tsunoda ◽  
Hiroyasu Inada ◽  
Minoru Kuroki ◽  
...  

2011 ◽  
Vol 31 (11) ◽  
pp. 2231-2242 ◽  
Author(s):  
Tomoyuki Ogawa ◽  
Daniel Hänggi ◽  
Yumei Wu ◽  
Hiroyuki Michiue ◽  
Kazuhito Tomizawa ◽  
...  

A sequence of 11 consecutive arginine residues (11R) is one of the best protein transduction domains for introducing proteins into cell membranes. Heme-oxygenase-1 (HO-1) is involved in heme catabolism and reduces the contractile effect of hemoglobin after subarachnoid hemorrhage (SAH). Therefore, we constructed 11R-fused HO-1 protein to achieve successful transduction of the protein into the cerebral arteries and examined the therapeutic effect of the 11R-HO-1 protein for cerebral vasospasm (CV) after SAH. We injected the 11R-HO-1 protein into the cisterna magna of male rats and, several hours after the injection, performed immunofluorescence staining and western blotting analysis of the rat basilar arteries (BAs) to determine transduction efficacy. We also assessed intraarterial HO-1 activity as cGMP (cyclic guanosine 3′, 5′-cyclic monophosphate) accumulation in SAH and determined whether protein transduction of 11R-HO-1 quantified the therapeutic effect in a rat double-hemorrhage model of SAH. The BAs expressed significantly more HO-1 in the group injected with 11R-HO-1 (3.56±0.54 (11R-HO-1) versus control (saline)), and transduction of 11R-HO-1 resulted in higher activity (>3.25-fold) in rat BAs with SAH. Moreover, the results of the rat double-hemorrhage model showed that the 11R-HO-1 protein significantly attenuated CV after SAH (317.59±23.48 μm (11R-HO-1) versus 270.08±14.66 μm (11R-fused enhanced green fluorescent protein), 252.05±13.95 μm (saline), P<0.01).


2009 ◽  
Vol 46 (3) ◽  
pp. 430-440 ◽  
Author(s):  
Kalpana Velmurugan ◽  
Jawed Alam ◽  
Joe M. McCord ◽  
Subbiah Pugazhenthi

2012 ◽  
Vol 23 (2) ◽  
pp. 87-95 ◽  
Author(s):  
M. Wagner ◽  
P. Steinbeis ◽  
E. Güresir ◽  
E. Hattingen ◽  
R. du Mesnil de Rochemont ◽  
...  

2016 ◽  
Vol 9 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Pervinder Bhogal ◽  
Yince Loh ◽  
Patrick Brouwer ◽  
Tommy Andersson ◽  
Michael Söderman

ObjectiveTo report our preliminary experience with the use of stent retrievers to cause vasodilation in patients with delayed cerebral vasospasm secondary to subarachnoid hemorrhage.MethodsFour patients from two different high volume neurointerventional centers developed cerebral vasospasm following subarachnoid hemorrhage. In addition to standard techniques for the treatment of cerebral vasospasm, we used commercially available stent retrievers (Solitaire and Capture stent retrievers) to treat the vasospastic segment including M2, M1, A2, and A1. We evaluated the safety of this technique, degree of vasodilation, and longevity of the effect.ResultsStent retrievers can be used to safely achieve cerebral vasodilation in the setting of delayed cerebral vasospasm. The effect is long-lasting (>24 hours) and, in our initial experience, carries a low morbidity. We have not experienced any complications using this technique although we have noted that the radial force was not sufficient to cause vasodilation in some instances. The vasospasm did not return in the vessel segments treated with stent angioplasty in any of these cases. In two of our cases stent angioplasty resulted in the reversal of focal neurological symptoms.ConclusionsStent retrievers can provide long-lasting cerebral vasodilation in patients with delayed cerebral vasospasm.


Sign in / Sign up

Export Citation Format

Share Document