22.19:
Vascular Spasm
Hemostasis begins with a vascular spasm, also known as the vascular phase. It starts immediately after any damage to a blood vessel, causing a sudden reduction in its diameter to minimize blood loss.
After an injury, the damaged smooth muscles in the walls of the blood vessel induce a local myogenic spasm.
This muscle contraction initiates the process of vasoconstriction, which is facilitated by the endothelial cells.
These cells lining the inner surface of the blood vessels release various substances like adenosine diphosphate, tissue factor, prostacyclin, and peptide hormones such as endothelins.
These act as local vasoconstrictors, stimulating smooth muscle contraction and reducing the lumen diameter.
Additionally, the exposed endothelial cell membranes become slightly sticky and can act as temporary sealants to hold the opposite ends of the cut.
Together, these mechanisms make the spasm effectively constrict the blood vessel and limit blood flow from the wound for about 20-30 mins.
The vascular phase prepares the injury site for platelet adhesion, setting the stage for the subsequent phases of hemostasis.
22.19:
Vascular Spasm
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for about 30 minutes. The spasm response becomes more efficient with more extensive tissue damage, particularly in smaller blood vessels. This response is vital as a severely constricted artery can significantly reduce blood flow and promote healing.
During this phase, the endothelium changes at the injury site. Endothelial cells contract, exposing the underlying basement membrane to the bloodstream. They release chemicals such as ADP, tissue factor, prostacyclin, and peptide hormones known as endothelins. These local hormones enhance smooth muscle contraction and promote vascular spasms. They also stimulate the division of endothelial cells, smooth muscle cells, and fibroblasts to accelerate the repair process. Additionally, endothelial plasma membranes become sticky, sealing off tears in small arteries or veins and preventing blood flow along damaged capillaries. This stickiness also facilitates platelet attachment during the subsequent platelet phase.