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As we all know, aspirin doesn't actually thin the blood, as it has been explained to me, it makes it "slippery". Slippery blood doesn't stick to itself hence this helps prevent internal blood clots (or allows blood to pass more easily around an existing clot). I also understand that having your blood too "slippery" can lead to the body attempting to counteract that and making it too "sticky".

Anyhow, my question regarding that is this, how does aspirin work? How does it make the blood "slippery"? (If there is a more medically correct term for "slippery" and "sticky", I'm all ears).

P.S. I paid the Mayo Clinic's website a visit before coming here, the information about aspirin's mechanism wasn't particularly helpful to me.

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    $\begingroup$ Aspirin doesn't make blood slippery (like lubricant's might allow machinery to work.) Blood clots require thrombocytes (aka platelets) and blood proteins to form. Too many platelets and clotting is more likely; not enough (or inactivation of some of the platelets) and clots don't form as easily. Anything that activates platelets (as described below) can result in a clot. Aspirin inhibits that. $\endgroup$
    – anongoodnurse
    Aug 31, 2016 at 16:14

2 Answers 2

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Aspirine irreversibly inhibits the enzyme cyclooxygenase. This enzyme facilitates the reaction from arachidonic acid to prostaglandin G2/H2. The further reaction leads to the generation of Thromboxane A2 which is important for the activation and aggregation of platelets. See the figure (from here) for an overview:

enter image description here

Thromboxane A2 usually stimulates the activation of new platelets and increases their aggregation, with a shortage of this compound these activations are not possible and the coagulation of blood is reduced.

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Aspirin inhibits COX in the endothelium which is required for prostacyclin (PGI2) production. PGI2 is an anti aggregant and vasodilator . Aspirin also inhibits thromboxaneA2 ( TXA2) production in the platelets. TXA2 is a platelets aggregant and vasoconstrictor hence antagonist of PGI2. So aspirin decrease both PGI2 and TXA2 production but endothelium cells can reproduce new COX inside them hence can quickly come over the inhibition of aspirin while platelets can't reproduce new COX so once they are inhibited then they can come over this inhibition only when new platelets are produced in the bone marrow so it takes too much time . So what aspirin does it that it shifts the PGI2-TXA2 equilibria towards PGI2 so reduce platelets aggregation. Hemostasis , Harper 31st edition.

https://www.webofpharma.com/2021/02/harpers-illustrated-biochemistry-31st.html?m=1

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    $\begingroup$ Can you add sources to this answer as well to allow others to background read on your material? $\endgroup$
    – AliceD ♦
    May 7, 2021 at 13:24
  • $\begingroup$ Yupp now I added my resource: hemostasis chapter form Harper 31st edition $\endgroup$
    – Rahul Dhillon
    May 7, 2021 at 16:07
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    $\begingroup$ Please do not upload book pages. This is a copyright violation and not tolerable. $\endgroup$
    – Chris ♦
    May 7, 2021 at 16:11
  • $\begingroup$ Ohhk ,,I apologise $\endgroup$
    – Rahul Dhillon
    May 7, 2021 at 16:17
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    $\begingroup$ Thanks for all your efforts ro improve your post. Kudos. Can you please add a weblink to the book you cite? $\endgroup$
    – AliceD ♦
    May 8, 2021 at 19:11

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