Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,372 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Wednesday, September 12, 2018
Roles of Nicotine in the Development of Intracranial Aneurysm Rupture
You'll have to ask your doctor if the problem is the nicotine or the many thousands of unknown sustances in cigarettes. Because I'm going to get nicotine patches for my next stroke. Don't follow me, I'm not medically trained in stroke. Is your doctor? What proof does your doctor show you of the results they provide on recovering from stroke? Just listening to my doctor talk about my stroke it was incredibly obvious he knew absolutely nothing about stroke recovery.
34 posts on nicotine
which your doctor will know zilch about. Time for you to train your
doctor again. I'm going to do the nicotine patches for my next stroke
even though I have no clue on dosage.
Originally published10 Sep 2018Stroke. 2018;0:STROKEAHA.118.021706
Abstract
Background and Purpose—
Tobacco
cigarette smoking is considered to be a strong risk factor for
intracranial aneurysmal rupture. Nicotine is a major biologically active
constituent of tobacco products. Nicotine’s interactions with vascular
cell nicotinic acetylcholine receptors containing α7 subunits
(α7*-nAChR) are thought to promote local inflammation and sustained
angiogenesis. In this study, using a mouse intracranial aneurysm model,
we assessed potential contributions of nicotine exposure and activation
of α7*-nAChR to the development of aneurysmal rupture.
Methods—
Intracranial
aneurysms were induced by a combination of deoxycorticosterone-salt
induced hypertension and a single-dose elastase injection into
cerebrospinal fluid in mice.
Results—
Exposure
to nicotine or an α7*-nAChR–selective agonist significantly increased
aneurysm rupture rate. Coexposure to an α7*-nAChR antagonist abolished
nicotine’s deleterious effect. In addition, nicotine’s promotion of
aneurysm rupture was absent in smooth muscle cell–specific α7*-nAChR
subunit knockout mice but not in mice lacking α7*-nAChR on endothelial
cells or macrophages. Nicotine treatment increased the mRNA levels of
vascular endothelial growth factor, platelet-derived growth factor-B,
and inflammatory cytokines. α7*-nAChR antagonist reversed
nicotine-induced upregulation of these growth factors and cytokines.
Conclusions—
Our
findings indicate that nicotine exposure promotes aneurysmal rupture
through actions on vascular smooth muscle cell α7*-nAChR.
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