Hemostasis and Blood Coagulation
Hemostasis means prevention
of blood loss.
Whenever a vessel is severed or ruptured, hemostasis is achieved by several mechanisms:
(1) vascular constriction;
(2) formation of a platelet plug;
(3) formation of a blood clot as a result of blood coagulation; and
(4) eventual growth of brous tissue into the blood clot to close the hole in the vessel permanently
VASCULAR CONSTRICTION
Immediately after a blood vessel has been cut or ruptured, the trauma to the vessel wall causes
smooth muscle in the wall to contract; this instantaneously reduces the
ow of blood from the ruptured vessel.
The contraction results from the following:
(1) local myogenic spasm;
(2) local autacoid factors from the traumatized tissues, vascular endothelium, and blood platelets;
and
(3) nervous re exes.
The nervous re exes are initiated by pain nerve impulses or other sensory impulses that originate
from the traumatized vessel or nearby tissues.
Even more vasoconstriction probably results from local myogenic contraction of the blood vessels
initiated by direct damage to the vascular wall.
And, for the smaller vessels, the platelets are responsible for much of the vasoconstriction by
releasing a vasoconstrictor substance, thromboxane A2.
The more severely a vessel is traumatized, the greater the degree of vascular spasm.
The spasm can last for many minutes or even hours, during which time the processes of platelet
plugging and blood coagulation can take place.
FORMATION OF THE PLATELET PLUG
If the cut in the blood vessel is very small— many
very small vascular holes develop throughout the body each day— the cut is often
sealed by a platelet plug rather than by a blood clot.
To understand this process, it is important to know the nature of platelets themselves.
Physical and Chemical Characteristics Platelets
(also called thrombocytes) are minute discs 1 to 4 micrometers in diameter.
They are formed in the bone marrow from megakaryocytes, which are extremely large
hematopoietic cells in the marrow;
The megakaryocytes fragment into the minute platelets in the bone marrow or soon after entering
the blood, especially as they squeeze through capillaries.
The normal concentration of platelets in the blood is between 150,000 and 450,000/µl.
Platelets have many functional characteristics of whole cells, even though they do not have nuclei
and cannot reproduce.
In their cytoplasm are the following:
(1) actin and myosin molecules, which are
contractile proteins similar to those found in muscle cells, and still another
contractile protein, thrombosthenin, that can cause the platelets to contract;
(2) residuals of both the endoplasmic reticulum and Golgi apparatus that
synthesize various enzymes and especially store large quantities of calcium ions;
(3) mitochondria and enzyme systems that are
capable of forming adenosine triphosphate (ATP) and adenosine diphosphate
(ADP);
(4) enzyme systems that
synthesize prostaglandins, which are local hormones that cause many vascular and other local
tissue reactions;
(5) an important protein called brin-stabilizing factor, which is in
relation to blood coagulation; and
fl fl fl fi fi
, (6) a growth factor that causes vascular endothelial cells, vascular smooth muscle cells, and
broblasts to multiply and grow, thus causing cellular
growth that eventually helps repair damaged vascular walls.
On the platelet cell membrane surface is a coat of glycoproteins that repulses adherence to
normal endothelium and yet causes adherence to injured areas of the vessel wall,
especially to injured endothelial cells and even more so to any exposed collagen from deep within
the vessel wall.
In addition, the platelet membrane contains large amounts of phospholipids that activate multiple
stages in the blood-clotting process.
Thus, the platelet is an active structure. It has a
half-life in the blood of only 8 to 12 days, so over several weeks its functional processes run out; it
is then eliminated from the circulation mainly by the tissue macrophage system.
More than half of the platelets are removed by macrophages in the spleen, where the blood
passes through a latticework of tight trabeculae.
Mechanism of Platelet Plug Formation
Platelet repair of vascular openings is based on several important functions of the platelet.
When platelets come in contact with a damaged vascular surface, especially with collagen bers
in the vascular wall, the rapidly change their own characteristics drastically.
They begin to swell, they assume irregular forms with numerous irradiating pseudopods
protruding from their surfaces,
Their contractile proteins contract forcefully and cause the release of granules that contain
multiple active factors, and
They become sticky so that they adhere to collagen in the tissues and to a protein called von
Willebrand factor (vWF), which leaks into the traumatized tissue from the plasma.
The platelet surface glycoproteins bind to vWF in the exposed matrix below the damaged
endothelium.
The platelets then secrete increased quantities of ADP and platelet-activating factor (PAF), and
their enzymes form thromboxane A2.
Thromboxane is a vasoconstrictor and, along with ADP and PAF, acts on nearby platelets to
activate them as well;
the stickiness of these additional activated platelets causes them to adhere to the original
activated platelets.
Therefore, at the site of a puncture in a blood vessel wall, the damaged vascular wall activates
successively increasing numbers of platelets that attract more and more additional platelets, thus
forming a platelet plug.
This plug is loose at rst but is usually successful in blocking blood loss if the vascular opening is
small.
Then, during the subsequent process of blood coagulation, brin threads form. These threads
attach tightly to the platelets,
Thus constructing an unyielding plug.
Importance of Platelet Mechanism for Closing Vascular Holes.
The platelet-plugging mechanism is extremely important for closing minute ruptures in very small
blood vessels that occur many thousands of times daily.
Indeed, multiple small holes through the endothelial cells themselves are often closed by platelets
actually fusing with the endothelial cells to form additional endothelial cell membranes.
Literally thousands of small hemorrhagic areas develop each day under the skin (petechiae,
which appear as purple or red dots on the skin) and throughout the internal tissues of a person
who has few blood platelets.
This phenomenon does not occur in persons with normal numbers of platelets.
BLOOD COAGULATION IN THE RUPTURED VESSEL
The third mechanism for hemostasis is formation of the blood clot.
The clot begins to develop in 15 to 20 seconds if the trauma to the vascular wall is severe and
in 1 to 2 minutes if the trauma is minor.
fi
fi fi fi
Hemostasis means prevention
of blood loss.
Whenever a vessel is severed or ruptured, hemostasis is achieved by several mechanisms:
(1) vascular constriction;
(2) formation of a platelet plug;
(3) formation of a blood clot as a result of blood coagulation; and
(4) eventual growth of brous tissue into the blood clot to close the hole in the vessel permanently
VASCULAR CONSTRICTION
Immediately after a blood vessel has been cut or ruptured, the trauma to the vessel wall causes
smooth muscle in the wall to contract; this instantaneously reduces the
ow of blood from the ruptured vessel.
The contraction results from the following:
(1) local myogenic spasm;
(2) local autacoid factors from the traumatized tissues, vascular endothelium, and blood platelets;
and
(3) nervous re exes.
The nervous re exes are initiated by pain nerve impulses or other sensory impulses that originate
from the traumatized vessel or nearby tissues.
Even more vasoconstriction probably results from local myogenic contraction of the blood vessels
initiated by direct damage to the vascular wall.
And, for the smaller vessels, the platelets are responsible for much of the vasoconstriction by
releasing a vasoconstrictor substance, thromboxane A2.
The more severely a vessel is traumatized, the greater the degree of vascular spasm.
The spasm can last for many minutes or even hours, during which time the processes of platelet
plugging and blood coagulation can take place.
FORMATION OF THE PLATELET PLUG
If the cut in the blood vessel is very small— many
very small vascular holes develop throughout the body each day— the cut is often
sealed by a platelet plug rather than by a blood clot.
To understand this process, it is important to know the nature of platelets themselves.
Physical and Chemical Characteristics Platelets
(also called thrombocytes) are minute discs 1 to 4 micrometers in diameter.
They are formed in the bone marrow from megakaryocytes, which are extremely large
hematopoietic cells in the marrow;
The megakaryocytes fragment into the minute platelets in the bone marrow or soon after entering
the blood, especially as they squeeze through capillaries.
The normal concentration of platelets in the blood is between 150,000 and 450,000/µl.
Platelets have many functional characteristics of whole cells, even though they do not have nuclei
and cannot reproduce.
In their cytoplasm are the following:
(1) actin and myosin molecules, which are
contractile proteins similar to those found in muscle cells, and still another
contractile protein, thrombosthenin, that can cause the platelets to contract;
(2) residuals of both the endoplasmic reticulum and Golgi apparatus that
synthesize various enzymes and especially store large quantities of calcium ions;
(3) mitochondria and enzyme systems that are
capable of forming adenosine triphosphate (ATP) and adenosine diphosphate
(ADP);
(4) enzyme systems that
synthesize prostaglandins, which are local hormones that cause many vascular and other local
tissue reactions;
(5) an important protein called brin-stabilizing factor, which is in
relation to blood coagulation; and
fl fl fl fi fi
, (6) a growth factor that causes vascular endothelial cells, vascular smooth muscle cells, and
broblasts to multiply and grow, thus causing cellular
growth that eventually helps repair damaged vascular walls.
On the platelet cell membrane surface is a coat of glycoproteins that repulses adherence to
normal endothelium and yet causes adherence to injured areas of the vessel wall,
especially to injured endothelial cells and even more so to any exposed collagen from deep within
the vessel wall.
In addition, the platelet membrane contains large amounts of phospholipids that activate multiple
stages in the blood-clotting process.
Thus, the platelet is an active structure. It has a
half-life in the blood of only 8 to 12 days, so over several weeks its functional processes run out; it
is then eliminated from the circulation mainly by the tissue macrophage system.
More than half of the platelets are removed by macrophages in the spleen, where the blood
passes through a latticework of tight trabeculae.
Mechanism of Platelet Plug Formation
Platelet repair of vascular openings is based on several important functions of the platelet.
When platelets come in contact with a damaged vascular surface, especially with collagen bers
in the vascular wall, the rapidly change their own characteristics drastically.
They begin to swell, they assume irregular forms with numerous irradiating pseudopods
protruding from their surfaces,
Their contractile proteins contract forcefully and cause the release of granules that contain
multiple active factors, and
They become sticky so that they adhere to collagen in the tissues and to a protein called von
Willebrand factor (vWF), which leaks into the traumatized tissue from the plasma.
The platelet surface glycoproteins bind to vWF in the exposed matrix below the damaged
endothelium.
The platelets then secrete increased quantities of ADP and platelet-activating factor (PAF), and
their enzymes form thromboxane A2.
Thromboxane is a vasoconstrictor and, along with ADP and PAF, acts on nearby platelets to
activate them as well;
the stickiness of these additional activated platelets causes them to adhere to the original
activated platelets.
Therefore, at the site of a puncture in a blood vessel wall, the damaged vascular wall activates
successively increasing numbers of platelets that attract more and more additional platelets, thus
forming a platelet plug.
This plug is loose at rst but is usually successful in blocking blood loss if the vascular opening is
small.
Then, during the subsequent process of blood coagulation, brin threads form. These threads
attach tightly to the platelets,
Thus constructing an unyielding plug.
Importance of Platelet Mechanism for Closing Vascular Holes.
The platelet-plugging mechanism is extremely important for closing minute ruptures in very small
blood vessels that occur many thousands of times daily.
Indeed, multiple small holes through the endothelial cells themselves are often closed by platelets
actually fusing with the endothelial cells to form additional endothelial cell membranes.
Literally thousands of small hemorrhagic areas develop each day under the skin (petechiae,
which appear as purple or red dots on the skin) and throughout the internal tissues of a person
who has few blood platelets.
This phenomenon does not occur in persons with normal numbers of platelets.
BLOOD COAGULATION IN THE RUPTURED VESSEL
The third mechanism for hemostasis is formation of the blood clot.
The clot begins to develop in 15 to 20 seconds if the trauma to the vascular wall is severe and
in 1 to 2 minutes if the trauma is minor.
fi
fi fi fi
