blood flow may be reduced to <1% of cardiac
ouput, and during severe heat stress, skin blood
flow can approach 60% of the cardiac output.
If core temperature decreases, heat reten-
tion mechanisms are activated by the hypo-
thalamus, leading to increased sympathetic
adrenergic outflow to the skin. This decreases
cutaneous blood flow and reduces heat loss to
the environment. If core temperature begins to
rise (e.g., during physical exertion), heat loss
mechanisms are activated by the hypothala-
mus, which decrease sympathetic adrenergic
outflow to the skin. This reduces vasocon-
vasodilation and increased blood flow. Vaso-
dilation resulting from withdrawal of sympa-
thetic vasoconstrictor influences is referred
to as “passive vasodilation.” If core tempera-
ture continues to rise, then “active vasodila-
tion” results from sympathetic cholinergic
nerve activation and the neuronal co-release
of vasodilator substances such as vasoactive
intestinal polypeptide (VIP). There is also evi-
dence that substance P, histamine, prostaglan-
dins, and nitric oxide may contribute to active
vasodilation. Vasodilation enables more warm
blood to circulate in the subepidermal layer of
the skin so that more heat can be transferred
to the environment.
Local changes in skin temperature selec-
tively alter blood flow to the affected region.
For example, if a heat source is placed on a
small region of the skin on the back of the hand,
blood flow will increase only to the region that
is heated. This response appears to be medi-
ated by local axon reflexes and local formation
of nitric oxide instead of by changes in sympa-
thetic discharge mediated by the hypothalamic
ing produces vasoconstriction through local
mechanisms that involve sympathetic adrener-
gic nerves and locally stimulated norepineph-
rine release. If tissue is exposed to extreme
cold, a phenomenon called cold-induced vaso-
dilation may occur following an initial vaso-
constrictor response, especially if the exposed
body region is a hand, foot, or face. This phe-
nomenon causes light-colored skin to appear
red, and it explains the rosy cheeks, ears, and
nose a person may exhibit when exposed to
very cold air temperatures. With continued
exposure, alternating periods of dilation and
constriction may occur (“hunting response”).
The mechanism for cold-induced vasodilation
is not clear, but it probably involves changes in
local control of blood vessels.
Tissue injury from mechanical trauma, heat, or
chemicals releases paracrine substances such
as histamine and bradykinin, which increase
blood flow and cause localized edema by
increasing microvascular permeability. If the
skin is firmly stroked with a blunt object, the
skin initially blanches owing to localized vaso-
constriction. This is followed within a minute
by the formation of a red line that spreads away
from the site of injury (red flare); both the red
line and red flare are caused by an increase in
blood flow. Localized swelling (wheal forma-
tion) may then follow, caused by increased
microvascular permeability and leakage of fluid
into the interstitium. The red line, flare, and
wheal are called the triple response. Both par-
acrine hormones and local axon reflexes are
believed to be involved in the triple response.
The vasodilator neurotransmitter involved in
local axon reflexes has not been identified.
Splanchnic Circulation
The splanchnic circulation includes blood
flow to the gastrointestinal tract, spleen, pan-
creas, and liver. Blood flow to these combined
organs represents 20% to 25% of cardiac out-
put (see Table 7-1). Three major arteries aris-
ing from the abdominal aorta supply blood to
the stomach, intestine, spleen, and liver— the
celiac, superior mesenteric, and inferior mes-
enteric arteries.
The following focuses on
blood flow to the intestines and liver.
rior mesenteric artery supply blood to the
subsequent branches
travel through the mesentery that supports
the intestine. Small arterial branches enter
the outer muscular wall of the intestine and
divide into several smaller orders of arteries
and arterioles, most of which enter into the
previous page 182 Cardiovascular Physiology Concepts  2nd Edition read online next page 184 Cardiovascular Physiology Concepts  2nd Edition read online Home Toggle text on/off