Maintenance of the Body
Describe the process of hemostasis. List factors that limit
clot formation and prevent undesirable clotting.
Give examples of hemostatic disorders. Indicate the cause
of each condition.
Normally, blood ﬂows smoothly past the intact blood vessel lin-
ing (endothelium). But if a blood vessel wall breaks, a whole
series of reactions is set in motion to accomplish
sis), which stops the bleeding (
Without this plug-the-hole defensive reaction, we would quickly
bleed out our entire blood volume from even the smallest cuts.
Te hemostasis response is fast, localized, and carefully con-
trolled. It involves many
normally present in
plasma as well as several substances that are released by platelets
and injured tissue cells. During hemostasis, three steps occur in
plug formation, and
coagulation (blood clotting). Following
hemostasis, the clot retracts. It then dissolves as it is replaced by
ﬁbrous tissue that permanently prevents blood loss.
Step 1: Vascular Spasm
In the ﬁrst step, the damaged blood vessels respond to injury
by constricting (vasoconstriction) (Figure 17.13
that trigger this
include direct injury to vas-
cular smooth muscle, chemicals released by endothelial cells
and platelets, and reﬂexes initiated by local pain receptors.
Te spasm mechanism becomes more and more eﬃcient as
the amount of tissue damage increases, and is most eﬀective
in the smaller blood vessels. Te spasm response is valuable
because a strongly constricted artery can signiﬁcantly reduce
blood loss for 20–30 minutes, allowing time for the next two
steps, platelet plug formation and blood clotting, to occur.
Step 2: Platelet Plug Formation
In the second step, platelets play a key role in hemostasis by ag-
gregating (sticking together), forming a plug that temporarily
seals the break in the vessel wall (Figure 17.13
). Tey also
help orchestrate subsequent events that form a blood clot.
As a rule, platelets do not stick to each other or to the smooth
endothelial linings of blood vessels. Intact endothelial cells re-
lease nitric oxide and a prostaglandin called
). Both chemicals prevent platelet aggregation in undam-
aged tissue and restrict aggregation to the site of injury.
However, when the endothelium is damaged and the under-
lying collagen ﬁbers are exposed, platelets adhere tenaciously to
the collagen ﬁbers. A large plasma protein called
stabilizes bound platelets by forming a bridge between
collagen and platelets. Platelets swell, form spiked processes, be-
come stickier, and release chemical messengers including the
Adenosine diphosphate (ADP)
—a potent aggregating agent
that causes more platelets to stick to the area and release their
stamps and seeding the blood with platelets. Te plasma mem-
branes associated with each fragment quickly seal around the
cytoplasm to form the grainy, roughly disc-shaped platelets (see
±able 17.2), each with a diameter of 2–4 μm. Each microliter of
blood contains 150,000 to 400,000 tiny platelets.
Check Your Understanding
Which WBCs turn into macrophages in tissues? Which other
WBC is a voracious phagocyte?
Platelets are called “thrombocytes” in other animals. Which
term that you’ve just learned relates to this name? What
does this term mean?
Amos has leukemia. Even though his WBC count is
abnormally high, Amos is prone to severe infections,
bleeding, and anemia. Explain.
For answers, see Appendix H.
• Smooth muscle contracts,
• Injury to lining of vessel
exposes collagen Fbers;
• Platelets release chemicals
that make nearby platelets
sticky; platelet plug forms.
• ±ibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
Events of hemostasis.