So this seems to solve 1 of 5 neuronal cascade of death issues. What the fuck is your hospital doing to solve the other 4? What research are they initiating? Or supporting?
Capillaries that don't open due to pericytes
The 5 causes of the neuronal cascade of death in the first week.
Targeted Myosin-2 Inhibition Improves Brain Regeneration After Stroke by Relaxing Hypoxia-Induced Vasoconstriction in Capillaries
Smooth muscle myosin-2 (SMM) is the key regulator of capillary blood flow in the brain
tissue. Pre-capillary contractile pericytes (smooth muscle cells, SMCs) block the
entrance of brain capillaries in answer to hypoxia during ischemic stroke. One of
the major obstacles in stroke therapies is that SMCs remain permanently contracted
even after removing the blood clot from large arteries, which hinders healthy blood
reperfusion of the infarcted brain regions. Thus, SMM could be an optimal target to
improve brain regeneration after clinical interventions. Therefore, we developed an
intra-arterial catheter mediated targeted administration of SMM inhibitors into the
ischemic brain regions and tested their effects on cerebral blood flow (CBF) after
transient middle cerebral artery occlusion (tMCAO) on rats. SPECT and MRI analyses
confirmed that different types of SMM inhibitors (e.g. MPH-222) could drastically
improve CBF in the ischemic brain areas. We also corroborated this vasodilatation
effect on ex vivo human arterioles, where SMM inhibitors could fully relax contracted
vessels even in the presence of upstream vasonstrictor signals. Moreover, MPH-222
could also induce neurite outgrowth in different types of neurons through its effect
on the non-muscle myosin-2 (NM2) isoforms. These results suggest that targeted, non-selective
myosin-2 inhibition is a conceptually new therapeutic way in stroke interventions,
which could be combined with current blood clot removing methods (thrombectomy and
thrombolysis).
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