Regulation of Organic Metabolism and Energy Balance
595
a role, too. In addition to their effects on temperature, IL-1
and the other peptides have many other effects (described in
Chapter 18) that enhance resistance to infection and promote
the healing of damaged tissue.
The story is even more complicated, however, because
in response to a rising temperature the hypothalamus and
other tissues release messengers that prevent excessive fever
or contribute to the resetting of body temperature when the
fever-causing stimulus is eliminated. Such messengers are
termed
endogenous cryogens.
One known endogenous
cryogen is vasopressin, which functions in this regard as a
neurotransmitter rather than as a hormone.
One would expect fever, which is such a consistent
feature of infection, to play some important protective role.
Most evidence suggests that this is the case. For example,
increased body temperature stimulates a large number of
the body’s defensive responses to infection. The likelihood
that fever is a benefi cial response raises important questions
about the use of aspirin and other drugs to suppress fever
during infection. It must be emphasized that these questions
apply to the usual modest fevers. There is no question that
an extremely high fever can be harmful, particularly in its
effects on the central nervous system, and must be vigorously
opposed with drugs and other forms of therapy.
To reiterate, fever is an increased body temperature
caused by an elevation of the thermal set point. When body
temperature is elevated for any other reason beyond a narrow
normal range, it is termed
hyperthermia
.
The most common
cause of hyperthermia in a typical person is exercise; the rise
in body temperature above set point is due to retention of
some of the internal heat generated by the exercising muscles.
As shown in
Figure 16–20
, heat production rises
immediately during the initial stage of exercise and exceeds
heat loss, causing heat storage in the body and a rise in the
core temperature. This rise in core temperature triggers
refl exes, via the central thermoreceptors, that cause increased
heat loss. As skin blood fl ow and sweating increase, the
discrepancy between heat production and heat loss starts to
diminish but does not disappear. Therefore, core temperature
continues to rise. Ultimately, core temperature will be high
enough to drive (via the central thermoreceptors) the heat-
loss refl exes at a rate such that heat loss once again equals heat
production. At this point, core temperature stabilizes at this
elevated value despite continued exercise.
Liver
Macrophages
Secrete
endogenous pyrogens
(IL–1, IL–6, ? others)
Firing of neural
receptors
Multiple organs
Macrophages
Secrete
endogenous pyrogens
(IL–1, IL–6, ? others)
Hypothalamus
Temperature setpoint
Plasma IL–1, IL–6, ? others
Skeletal muscles
Curl up,
put on clothes
and blankets
Shivering
Skin arterioles
Vasoconstriction
Vagus
nerve
Systemic
circulation
Body temperature
Heat retention
Heat production greater than heat loss
Heat production
Heat loss
Infection
Figure 16–19
Pathway by which infection causes fever (IL-1 = interleukin 1,
IL-6 = interleukin 6). The effector responses serve to
raise
body
temperature during an infection.
Heat
production
Heat loss
(reflexly increased)
Core temperature
Exercise period
Time
Temperature
Heat (calories/m)
Figure 16–20
Thermal changes during exercise. Heat loss is refl exly increased,
and when it once again equals heat production, core temperature
stabilizes.
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