 So, hemostasis will only happen if there is damage to your blood vessel. And don't like, of course, hopefully you don't want hemostasis, you don't want blood clots to form if there isn't damage, if there's not a reason to form the blood clot or the blood clot, however you would like to say it. Blood clot is, it's whole purpose is not to clog up other vessels that are doing their job. The whole purpose is to stop the bleeding if there is damage. So, you have to think through, dude, this whole thing starts with damage. And damaged blood vessel is different. I mean, all my Wendy-style blood vessels that I can't help, I got to draw blood vessels all the time in our blood vessels. And then we've got other layers. And in order for blood loss to happen, somehow we have to like, now think about this for a second. If your endothelium, if your blood vessel isn't damaged, then endothelium is the only thing that will be in contact with the blood itself. And endothelium is really smooth. If you remember looking at cow hearts in anatomy, you open up that cow heart and you cut through the myocardium, the thick cardiac muscle tissue. And all lining the inside of the heart is, it's almost this whitish, shiny-ish tissue. And it's, it's different. It's really smooth. You could like slip right on through that. You can see how blood is just going to flow right through that. There's very little friction there. If you break that open, you are going to be exposing stuff that you wouldn't, that blood wouldn't otherwise be exposed to. That stimulates some responses. So one of the responses upon damage is that the vessel itself, the damaged vessel experiences a myogenic response. What is that? We've talked about this. We've seen a myogenic response in the past. It's when the smooth muscle in the vessel contracts. And what's the result of smooth muscle contraction in a blood vessel? Vasoconstriction. This happens because damaged blood vessel cells produce chemicals that say, dude, let's, let's, let's contract. Let's constrict, let's vasoconstrict, and it's automatic. And the bigger the blood vessel, the more vasoconstriction that happens because of this mechanism. In addition, you end up with the damaged tissue. In addition to the smooth muscle response to contract, the damaged tissue produces chemicals that increase vasoconstriction. So they just contribute to the whole process. And then damaged tissue has an effect on platelets. And the platelets become activated, and we're going to talk about this in the next section. Platelets get activated, and when they get activated, they produce another vasoconstrictor called thromboxane A2. Thromboxane A2 is a vasoconstrictor produced by activated platelets. Platelets activate when damaged tissue sends out messages that say, oh, God, this is not good, we need some help over here. That's going to activate the platelets. We're going to talk about that in a second because that's how you form a platelet plug. The response, there actually is a nervous system role in this. The nervous system will send a message as a response to pain in your blood vessels. Damaged blood vessels probably don't feel so great. Sends the message to the nervous system, whoa, we got some damage here. The nervous system sends the message back. Let's vasoconstrict. Why? Cut off the blood loss. If you vasoconstrict, you're going to have less blood flow or throw through that vessel. And if you have less blood flow, you will have less blood loss. This is all fast, this is all immediate. But next, it's not the end of the story. We didn't even begin to form a clot. There's nothing clot-ish that's happening here except we have a tiny little preview that, you know what, the damage itself can activate the platelets and that is going to be the topic of our next section.