Page 781 - Fundamentals of anatomy physiology

768 Unit 4 Fluids and Transport blood pressure decreases. We can group these mechanisms as
and increases the amount of reabsorption. The result is a
decrease in the volume of interstitial fluid and an increase
in the circulating plasma volume. This process is known as
a recall of fluids.
If dehydration occurs, the plasma volume decreases due to
water loss, and the concentration of plasma proteins in-
creases. The increase in BCOP accelerates reabsorption and
a recall of fluids that delays the onset and severity of clini-
cal signs and symptoms.
If the CHP rises or the BCOP declines, fluid moves out of
the blood and builds up in peripheral tissues, a condition
called edema.
Checkpoint
5. Identify the factors that contribute to total peripheral
resistance.
6. In a healthy person, where is blood pressure greater:
at the aorta or at the inferior vena cava? Explain.
7. While standing in the hot sun, Sally begins to feel
light-headed and faints. Explain what happened.
8. Mike’s blood pressure is 125/70. What is his mean
arterial pressure?
See the blue Answers tab at the back of the book.
21-3 Cardiovascular regulatory
mechanisms involve autoregulation,
21 neural mechanisms, and endocrine
responses
Learning Outcome Describe the control mechanisms that regulate
blood flow and pressure in tissues, and explain how the activities of the
cardiac, vasomotor, and respiratory centers are coordinated to control
blood flow through the tissues.
Homeostatic mechanisms regulate cardiovascular activity to
ensure that blood flow through tissues, called tissue perfu-
sion, meets the demand for oxygen and nutrients. The factors
that affect tissue perfusion are (1) cardiac output, (2) periph-
eral resistance, and (3) blood pressure. We discussed cardiac
output in Chapter 20 (p. 737). We considered peripheral resis-
tance and blood pressure earlier in this chapter.
Most cells are relatively close to capillaries. When a group
of cells becomes active, the circulation to that region must in-
crease to bring the necessary oxygen and nutrients, and to carry
away the waste products and carbon dioxide they generate. The
purpose of cardiovascular regulation is to ensure that these
blood flow changes occur (1) at an appropriate time, (2) in the
right area, and (3) without drastically changing blood pressure
and blood flow to vital organs.
The regulatory mechanisms focus on controlling cardiac
output and blood pressure to restore adequate blood flow after
follows:
Autoregulation. Local factors change the pattern of blood
flow within capillary beds as precapillary sphincters open
and close in response to chemical changes in interstitial
fluids. This is an example of autoregulation at the tissue
level. Autoregulation causes immediate, localized homeo-
static adjustments. If autoregulation fails to normalize
conditions at the tissue level, neural mechanisms and
endocrine factors are activated.
Neural Mechanisms. Neural mechanisms respond to
changes in arterial pressure or blood gas levels sensed at
specific sites. When those changes occur, the cardiovascular
center of the autonomic nervous system adjusts cardiac
output and peripheral resistance to maintain blood pres-
sure and ensure adequate blood flow.
Endocrine Mechanisms. The endocrine system releases hor-
mones that enhance short-term adjustments and that direct
long-term changes in cardiovascular performance.
Now let’s see how each of these regulatory mechanisms
responds to inadequate perfusion of skeletal muscles. The regu-
latory relationships are diagrammed in Figure 21–12.
Autoregulation of Blood Flow within Tissues
Under normal resting conditions, cardiac output remains sta-
ble, and peripheral resistance within individual tissues is ad-
justed to control local blood flow.
Factors that promote the dilation of precapillary sphincters
are called vasodilators. Local vasodilators act at the tissue
level to accelerate blood flow through their tissue of origin.
Examples of local vasodilators include the following:
Decreased tissue oxygen levels or increased CO2 levels.
Lactic acid or other acids generated by tissue cells.
Nitric oxide (NO) released from endothelial cells.
Rising concentrations of potassium ions or hydrogen ions
in the interstitial fluid.
Chemicals released during local inflammation, including
histamine and NO. p. 170
Elevated local temperature.
These factors work by relaxing the smooth muscle cells of
the precapillary sphincters. All of them indicate that tissue con-
ditions are in some way abnormal. An increase in blood flow,
which brings oxygen, nutrients, and buffers, may be sufficient
to restore homeostasis.
As noted in Chapter 19, aggregating platelets and damaged
tissues produce compounds that stimulate precapillary sphinc-
ters to constrict. These compounds are local vasoconstrictors.
Examples include prostaglandins and thromboxanes released