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Haemorrhage (blood loss) is caused by rupture of the vessel wall. This exposes sub-endothelial collagen from within the blood vessel's wall, which attracts blood platelets. Platelets are cell fragments which circulate the bloodstream in an inactive form. Upon binding with the collagen they become activated, changing morphology (shape) and releasing Thromboxane A2 (TXA2) and prostaglandins, which are both chemotractants. These attract other platelets as well as causing vasoconstriction which cause the vessel to constrict. This is in order to maintain a constant blood pressure despite the blood volume decreasing. The platelets aggregate (clump together) and form bonds with each other and the vessel wall, forming a clot. This is initially bound by soluble fibrinogen (), which is then converted into an insoluble gel-like solib substance called Fibrin by Plasim, formed from inactive plasminogen in the plasma converted/activated by 'tissue plasminogen activator'. This fibrin is very stable. Once the clot is no longer needed, the fibrin is broken down by the fibrinolytic system. Hope this helps.

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14y ago
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12y ago

It increases respiratory rate, slows down arterial pressure in order to maintain homeostasis...

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Q: What are 2 physiological responses to hemoraging?
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