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BIOC63H3 Chapter Notes -Thromboxane A2, Endothelium, Blood Vessel

Biological Sciences
Course Code
Ivana Stehlik

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The Cardiovascular System
The Blood : Hemostasis
__ Hemostasis refers to the stoppage of blood. When blood vessels are damaged or
ruptured, the hemostatic response must be quick, localized to the region of
damage, and carefully controlled.
__ Three basic mechanisms reduce blood loss: 1) vascular spasm, 2) platelet plug
formation and 3) blood clotting (coagulation). These mechanisms are useful for
preventing hemorrhage (loss of blood) in smaller blood vessels, but extensive
hemorrhage in larger vessels usually requires medical/veterinary intervention.
Vascular Spasm
__ When arteries or arterioles are damaged, the circularly arranged smooth muscle in
their walls contracts immediately. This is called vascular spasm. It reduces blood
loss for several hours, during which time the other hemostatic mechanisms go into
operation. The spasm is probably caused by damage to the smooth muscle and
from reflexes initiated by pain receptors.
Platelet Plug Formation
__ In their unstimulated state, platelets are disc-shaped. Two types of granules are
present in the cytoplasm:
1. Alpha granules. These contain clotting factors and platelet-derived
growth factor (PDGF) which can cause proliferation of vascular
endothelial cells, vascular smooth muscle fibers, and fibroblasts to help
repair damaged blood vessel walls.
2. Dense granules. These contain ADP, ATP, Ca2+ and serotonin. Also
present are enzymes that produce thromboxane A2, a prostaglandin;
fibrin-stabilizing factor, which helps to strengthen a blood clot; lysosomes;
some mitochondria; membrane systems that take up and store calcium and
provide channels for release of the contents of granules; and glycogen.
__ Platelet plug formation occurs as follows (Figure 1):
1. In the first phase of platelet plug formation, platelets contact and stick to
parts of the damaged blood vessel such as collagen underlying the
damaged endothelium cells. This process is called platelet adhesion. This
requires participation of an endothelial cell secretion of a protein called
von Willebrand factor (VWF).

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Figure 1
2. Adhesion activates the platelets. This changes their characteristics
dramatically. They extend many projections that enable them to contact
one another, and then they begin to liberate the contents of their granules.
This phase is called the platelet release reaction. Liberated ADP and
thromboxane A2 play a major role by acting on nearby platelets to activate
them as well. Serotonin and thromboxane A2 function as vasoconstrictors,
causing contraction of the vascular smooth muscle, which decreases blood
flow through the injured vessel.

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3. The release of ADP also make other platelets in the area sticky. The
stickiness of the newly recruited and activated platelets causes them to
adhere to the originally activated platelets. This gathering of platelets is
called platelet aggregation. Eventually, the accumulation and attachment
of large numbers of platelets form a mass called a platelet plug.
__ A platelet plug is very effective in preventing blood loss in a small vessel. The
platelet plug is initially loose. It becomes quite tight when reinforced by fibrin
threads formed during clotting. A platelet plug can stop blood loss completely if
the hole in a blood vessel is small.
Clotting (Coagulation) Phase
__ If the blood vessel damage is so extensive that the platelet plug cannot stop the
bleeding , the complicated process of clotting the coagulation phase begins.
__ Clotting involves several substances known as clotting (coagulation) factors.
These include Ca2+, several inactive enzymes that are synthesized by hepatocytes
(liver cells) and released into the blood stream, and various molecules associated
with platelets or released by damaged tissues. Many are identified by Roman
numerals which indicate the order of their discovery. The various clotting factors
and their synonyms, sources and pathways of activation are listed in Table 1.
Extrinsic and Intrinsic Pathways (Figure 2)
__ Two partially independent pathways have been identified for the triggering of a
blood clot: 1) The extrinsic pathway which is a rapid clotting system activated
when blood vessels are ruptured and tissues are damaged. 2) the intrinsic pathway
is activated when the inner walls of blood vessels become damaged.
Stage 1, the formation of prothrombinase (prothrombin activator), is
initiated by either the extrinsic or the intrinsic pathway or both. Once
prothrombinase is formed, the steps involved in the next two stages of
clotting are the same for both the extrinsic and intrinsic pathways. The two
stages together are referred to as the common pathway.
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