Deans' stroke musings: Nicotine Accelerates Atherosclerosis in Apolipoprotein E–Deficient Mice by Activating α7 Nicotinic Acetylcholine Receptor on Mast Cells

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, December 22, 2016

Nicotine Accelerates Atherosclerosis in Apolipoprotein E–Deficient Mice by Activating α7 Nicotinic Acetylcholine Receptor on Mast Cells

You will need to have your doctor analyze the good points of nicotine for recovery and prevention of dementia. Regardless of what my doctor says, for my next stroke I'm doing nicotine patches.

Nicotine Holds Promise for Stronger Stroke Recovery

Nicotine Patch Appears To Help Mild Cognitive Loss

http://atvb.ahajournals.org/content/37/1/53?etoc=

, , Wei Zhu, Yinchuan Xu, , Lianlian Zhu, Fan Yang, Ling Zhang, Xianbao Liu, Zhiwei Zhong, Jing Zhao, , , Hong Yu, Xinyang Hu, ,

https://doi.org/10.1161/ATVBAHA.116.307264

Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:53-65

Originally published November 10, 2016

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Abstract

Objective—Cigarette smoking is an independent risk factor for atherosclerosis. Nicotine, the addictive component of cigarettes, induces mast cell (MC) release and contributes to atherogenesis. The purpose of this study was to determine whether nicotine accelerates atherosclerosis through MC-mediated mechanisms and whether MC stabilizer prevents this pathological process.

Approach and Results—Nicotine administration increased the size of atherosclerotic lesions in apolipoprotein E–deficient (Apoe^−/−) mice fed a fat-enriched diet. This was accompanied by enhanced intraplaque macrophage content and lipid deposition but reduced collagen and smooth muscle cell contents. MC deficiency in Apoe^−/− mice (Apoe^−/−Kit^W-sh/W-sh) diminished nicotine-induced atherosclerosis. Nicotine activated bone marrow–derived MCs in vitro, which was inhibited by a MC stabilizer disodium cromoglycate or a nonselective nicotinic acetylcholine receptor blocker mecamylamine. Further investigation revealed that α7 nicotinic acetylcholine receptor was a target for nicotine activation in MCs. Nicotine did not change atherosclerotic lesion size of Apoe^−/−Kit^W-sh/W-sh mice reconstituted with MCs from Apoe^−/−α7nAChR^−/− animals.

Conclusions—Activation of α7 nicotinic acetylcholine receptor on MCs is a mechanism by which nicotine enhances atherosclerosis.