Vasoconstriction is the narrowing of the blood vessels, which reduces blood loss during injury.
- Describe vascular spasms in hemostasis
- Vasoconstriction is the narrowing of the blood vessels, which increases blood pressure but can decrease blood flow and loss.
- Vasoconstriction is mediated by contraction of the smooth muscles lining a blood vessel.
- Vasoconstriction is caused by thromboxane A2 from activated platelets and injured epithelial cells, nervous system reflexes from pain, and direct injury to vascular smooth muscle.
- Vasopressins are drugs that may induce vasoconstriction and increase blood pressure.
- Vasonstriction only lasts for a few minutes during hemostasis. During inflammation that follows the injury, it is replaced by vasodilation as the healing process begins.
- endothelial cells: The endothelium comprises the thin layer of endothelial cells
that lines the interior surface of blood and lymphatic vessels, forming an interface between circulating blood or lymph in the lumen and the rest of the vessel wall.
- vascular: Of, pertaining to, or containing vessels that conduct or circulate fluids such as blood, lymph, or sap through the body of an animal or plant.
- inflammation: A process that occurs during injury and generally follows hemostasis in which vasoconstriction ends and vasodilation begins.
Vasoconstriction is the narrowing of the blood vessels resulting from contraction of the smooth muscle wall of the vessels, particularly in the large arteries and small arterioles. The process is the opposite of vasodilation, the dilation and expansion of blood vessels. During hemostasis, a brief spasm of vasoconstriction occurs, which slows blood flow into the injured area while the clot forms.
Vasoconstriction during hemostasis: Blood vessel experiencing vasoconstriction as its smooth muscle contracts while the blood clot forms.
Mechanisms of Vasoconstriction
The vasoconstriction response is triggered by factors such as a direct injury to vascular smooth muscle, signaling molecules released by injured endothelial cells and activated platelets (such as thromboxane A2), and nervous system reflexes initiated by local pain receptors. The spasm response becomes more effective as the amount of damage is increased. Vascular spasm is much more effective at slowing the flow of blood in smaller blood vessels. Vasoconstriction also causes an increase in blood pressure for affected blood vessels.
Smooth muscle in the vessel wall goes through intense contractions that constrict the vessel. If the vessels are small, spasms compress the inner walls together and may be able to stop the bleeding completely. If the vessels are medium to large-sized, the spasms slow down immediate outflow of blood, lessening the damage but still preparing the vessel for the later steps of hemostasis. The spasm response becomes stronger and lasts longer in more severe injuries. Vasoconstriction may be induced by drugs called vasopressins, which increase blood pressure and can help treat certain conditions.
Injury and Inflammation
During injury, vasoconstriction is brief, lasting only a few minutes while the platelet plug and coagulation cascade occur. This is because as tissues are damaged during an injury, inflammation occurs as a result of inflammatory mediator release from immune system cells (such as mast cells or NK cells) that receive cell stress cytokines from damaged enothelial cells or vasoactive amines (serotonin) that are secreted by activated platelets. During inflammation, vasodilation occur, along with increased vascular permeability and leukocyte chemotaxis, ending the spasm of vasoconstriction and hemostasis as wound healing begins.