I’m healthy and so are my friends; I’m not seeking medical advice, just curious.
Atrial fibrillation and deep-vein thrombosis are two (unrelated) conditions in which blood does not circulate properly, and tends to form dangerous clots as a result. In A-fib, blood is not pumped cleanly through the heart due to irregular contractions; in DVT, blood flows too slowly for too long a time due to physical inactivity (e.g. sitting in economy class for a trans-Pacific flight).
So why does blood form clots in these situations? Is there some scenario where the clotting of stagnant blood inside the body is useful, and these cases are merely unfortunate side effects of that otherwise useful response?
It’s an interesting question but, of course, the only answer can be a teleological one.
My guess is that it’s a result of the fact that around the area of an injury or wound, any blood that’s leaked out or spilled out of injured vessels becomes motionless. After all, once blood has left the circulation, how can it move? So, in other words, static blood corresponds to a site of bleeding (or more accurately ‘extravasation’) and thus it makes sense for clots to form.
Wild guess from someone who doesn’t know to keep his mouth shut: Clotting of stagnant blood inside the body is useful in forming black-and-blue marks. Without this feature, such injuries would hemorrage. That would be bad.
Wouldn’t exposure to air be a better/safer mechanism to trigger clotting?
In a stagnant triggered clotting system, if you have a large enough wound or close enough to major artery, without external pressure, blood would continue to flow out and never clot.
Stagnant blood tends to clot because… the veins are no longer flowing and producing nitric oxide. This is a neccessary is small component of blood and inhibits the platelet formation into a clot. When this happens, the platelet receptors can lock together. They then start procuding chemicals to speed healing and attract new cell growth.
They can’t be air-triggered, because it also has to happen within the body. otherwise, any internal bleeding would be fatal, probably including bruises.
OK, but by what mechanism does absence of blood flow affect nitric oxide formation?
I’m not disagreeing with you, but I’m not sure I understand what you’re getting at. Isn’t the bottom line that stasis leads to clot formation because stasis is a pretty good indicator that there’s been injury to a blood vessel (and in the absence of clot formation in that area, the injured vessel would continue to leak blood).
You’re talking two different levels of explanation. One is the ‘how’ (the chemical mechanism by which the clotting is triggered). One is the ‘why’ (what the selective advantage is to having the mechanism, such that it was fixed into the species’ genes).
In this case, it appears the ‘why’ is that it’s evolutionarily advantageous to have a mechanism that forms clots in stagnant blood, as this limits internal bleeding. The ‘how’, according to smiling bandit is that veins produce nitric oxide which prevents clotting; in the absence of nitric oxide, blood clots happen.
OK, so lack of NO starts the clotting process; this nicely explains why blood clots in hemorrhages (either internal or external). But if the blood is still inside the blood vessels - regardless of whether it’s flowing along nicely or not - isn’t it still being bathed in NO from the vessel walls?
Hey - the thing about normal blood flow is that it doesn’t allow the NO to build up - the flow carries it away and it can be metabolised elsewhere etc. With stagnant flow nothing is taking the NO away, so it biulds up and this is what allows it to promote clot formation - hope this helps
The extrinsic pathway is triggered when there is damage to a blood vessel. “Tissue Factor” from the damaged endothelium attracts soluble clotting factors in the blood and triggers a coagulation cascade, resulting in platelet activation and a fibrin clot.
The intrinsic pathway is triggered when clotting factors come into contact with collagen - again, a cascade of activated clotting factors will result in activated platelets and a fibrin clot.
NO is involved in platelet activation (in that it inhibits it), but it’s not the only player. Damage to the endothelium and the exposure of Von Willebrand factor is also extremely important.
I’m trying to find a cite for it but I’m in a rush and may need to come back later, but in DVT you have pools of stagnant blood hanging out at the venous valves. You’re stressing the endothelium by keeping it stretched out, and you’re also creating a place where platelets and clotting factors are all hanging out together and bumping into each other, increasing the chances of some clotting happening. NO probably plays some role here, but it’s far from the only cause.