Abstract
Background Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. In many settings of ischemia, vasodilation to increase perfusion is a suitable approach; yet in stroke it bears the risk of systemic hypotension, shunting of blood from the ischemic to healthy areas, increased infarcts and eventually reduced survival. One potentially innovative and mechanism-based approach are sGC activators, as they represent diseasespecific vasodilators that are potentiated under conditions of oxidative stress and have microvascular selectivity e.g. to unload the acutely failing heart.
Highlights
Ischemic stroke is the second leading cause of death worldwide
One potentially innovative and mechanism-based approach are sGC activators, as they represent diseasespecific vasodilators that are potentiated under conditions of oxidative stress and have microvascular selectivity e.g. to unload the acutely failing heart
Here we show that in the experimental stroke model of transient middle cerebral artery occlusion in the mouse, substantial oxidative stress leads to 100% mortality after one week
Summary
From 6th International Conference on cGMP: Generators, Effectors and Therapeutic Implications Erfurt, Germany. From 6th International Conference on cGMP: Generators, Effectors and Therapeutic Implications Erfurt, Germany. 28-30 June 2013
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