Hemostasis – Set of mechanisms which prevent bleeding on one side, and stop already existing bleeding on the other
side. Involves reaction of vessels, Action of platelets, and blood clotting.
Reaction of vessels - Vascular Spasm
Uninjured blood vessels have healthy endothelial cells that produce nitric oxide (NO) and Prostacyclin (PGI2) that
function as a natural anticoagulant to inhibit platelet activity and therefore keep the blood ‘thin’ and flowing.
Injured blood vessels will likely cause endothelial damage, leading to damage to the underlying tissue, where blood
may leak out and decrease blood volume, therefore, it is important to prevent this blood loss from occurring by
contracting or constricting blood vessels. This is done through 3 main mechanisms:
Endothelin:
Peptide secreted by injured endothelial cells that bind to receptors on smooth muscles and activate intracellular PIP2-
calcium mechanism which stimulates contraction of smooth muscles → triggering vessel vasoconstriction →
decreasing blood vessel diameter → preventing blood loss
Myogenic Mechanism:
Direct contact or injury to smooth muscle causing smooth muscle contraction.
Nociceptor Activation:
Inflammatory chemicals are released when there is inflammation (histamine, leukotrienes, prostaglandins, etc) which
stimulate the nociceptors (pain receptors) that will initiate pain, and the pain reflex induces vasoconstriction.
Vasoconstriction (depends on the severity of the injury)
• Serotonin (from dense granules of platelets)
• Endothelin
• Thromboxane A2
• Adrenaline/ Noradrenaline
• Fibrinopeptides
Vasodialators
NO, Histamine, Bradykinin
General structures of Platelets (Thrombocytes)
Origin Megakaryocytes of bone marrow under effect of colony stimulating factors – interleukins (IL-
(Thrombopoiesis) 1, IL-3, IL-6), and granulocytes and macrophages stimulating factor (GM-CSF)
Number 200 000 – 500 000 in µl (1/3 in lien, 2/3 in peripheral blood)
Shape Smooth, round discs, nucleus-free with no membrane organelles
Size 2 – 4 µm in diameter, 0,5 – 1 µm thickness, 4 – 8 fl volume
Life spam 9-12 days, biological half-life is about 4 days
Membrane Contains receptors for adhesion to certain surfaces (e.g. Collagen, von Willebrand factor
(vWF), Fibrinogen)
Structure
Granules Dense granules Non-protein substances: serotonin, ADP, Adenonucleotides
α-granules Protein substances: Clotting factors, Platelet derived growth factor (PDGF)
Glycocalyx 10-50 nm, mixture of proteins and mucopolysaccharides (clotting factors, ions, amino acids,
histamin, drugs)
Protection of organism Adhesion to collagen of vessel wall (by von Willebrand factor, vWF)
from blood loss: Aggregation to other platelets (by Fibrinogen)
Keep integrity of vessel wall and healing of the ruptured vessel (PDGF from α-granules)
FUNCTION
Immune function and inflammatory reactions (changes in permeability of capillaries, removal
of xenogenous substances, viruses, bacteria, etc.)
Carrier of many substances absorbed to platelet surface
side. Involves reaction of vessels, Action of platelets, and blood clotting.
Reaction of vessels - Vascular Spasm
Uninjured blood vessels have healthy endothelial cells that produce nitric oxide (NO) and Prostacyclin (PGI2) that
function as a natural anticoagulant to inhibit platelet activity and therefore keep the blood ‘thin’ and flowing.
Injured blood vessels will likely cause endothelial damage, leading to damage to the underlying tissue, where blood
may leak out and decrease blood volume, therefore, it is important to prevent this blood loss from occurring by
contracting or constricting blood vessels. This is done through 3 main mechanisms:
Endothelin:
Peptide secreted by injured endothelial cells that bind to receptors on smooth muscles and activate intracellular PIP2-
calcium mechanism which stimulates contraction of smooth muscles → triggering vessel vasoconstriction →
decreasing blood vessel diameter → preventing blood loss
Myogenic Mechanism:
Direct contact or injury to smooth muscle causing smooth muscle contraction.
Nociceptor Activation:
Inflammatory chemicals are released when there is inflammation (histamine, leukotrienes, prostaglandins, etc) which
stimulate the nociceptors (pain receptors) that will initiate pain, and the pain reflex induces vasoconstriction.
Vasoconstriction (depends on the severity of the injury)
• Serotonin (from dense granules of platelets)
• Endothelin
• Thromboxane A2
• Adrenaline/ Noradrenaline
• Fibrinopeptides
Vasodialators
NO, Histamine, Bradykinin
General structures of Platelets (Thrombocytes)
Origin Megakaryocytes of bone marrow under effect of colony stimulating factors – interleukins (IL-
(Thrombopoiesis) 1, IL-3, IL-6), and granulocytes and macrophages stimulating factor (GM-CSF)
Number 200 000 – 500 000 in µl (1/3 in lien, 2/3 in peripheral blood)
Shape Smooth, round discs, nucleus-free with no membrane organelles
Size 2 – 4 µm in diameter, 0,5 – 1 µm thickness, 4 – 8 fl volume
Life spam 9-12 days, biological half-life is about 4 days
Membrane Contains receptors for adhesion to certain surfaces (e.g. Collagen, von Willebrand factor
(vWF), Fibrinogen)
Structure
Granules Dense granules Non-protein substances: serotonin, ADP, Adenonucleotides
α-granules Protein substances: Clotting factors, Platelet derived growth factor (PDGF)
Glycocalyx 10-50 nm, mixture of proteins and mucopolysaccharides (clotting factors, ions, amino acids,
histamin, drugs)
Protection of organism Adhesion to collagen of vessel wall (by von Willebrand factor, vWF)
from blood loss: Aggregation to other platelets (by Fibrinogen)
Keep integrity of vessel wall and healing of the ruptured vessel (PDGF from α-granules)
FUNCTION
Immune function and inflammatory reactions (changes in permeability of capillaries, removal
of xenogenous substances, viruses, bacteria, etc.)
Carrier of many substances absorbed to platelet surface
