CHAPTER 7 • ORGAN BLOOD FLOW
175
during respiration (see Chapter 5) alter the
transmural pressure that distends the vessels.
For example, during normal inspiration, the
fall in intrapleural pressure increases vascular
transmural pressure, which distends extra-
alveolar vessels (i.e., pulmonary arteries and
veins),
decreases resistance,
and increases
regional flow. The opposite occurs during a
forced expiration, particularly against a high
resistance (e.g., Valsalva maneuver). Vessels
associated with the alveoli are compressed
as the alveoli fill with air and enlarge during
inspiration. With very deep inspirations, this
capillary compression can cause an increase
in overall pulmonary resistance.
The primary purpose of the pulmonary cir-
culation is to perfuse alveoli for the exchange
of blood gases. Gas exchange depends, in part,
on diffusion distances and the surface area
available for exchange. The capillary-alveolar
arrangement is such that diffusion distances
are minimized and surface area is maximized.
Pulmonary capillaries differ from their sys-
temic counterparts in that they form thin
interconnecting sheets around and between
adjacent alveoli, which greatly increase their
surface area and reduce diffusion distances.
Unlike other organs, alveolar or arterial
hypoxia
causes
pulmonary
vasoconstric-
tion. The mechanism is not known; however,
evidence suggests that endothelin, reactive
oxygen
species,
and
intracellular
calcium
mobilization may be involved. This hypoxic
vasoconstriction,
especially
in
response
to regional variations in ventilation, helps
to
maintain
normal
ventilation-perfusion
ratios in the lung. Maintenance of normal
ventilation-perfusion
ratios
is
important
because high blood flow to hypoxic regions,
for example, would decrease the overall oxy-
gen content of the blood leaving the lungs.
Sympathetic adrenergic nerves innervate the
pulmonary vasculature, although their activation
has relatively weak effects on pulmonary vascu-
lar resistance and pulmonary artery pressure.
Summary of Special Circulations
Perfusion
pressure
and
vascular
resistance
determine blood flow in organs. Under normal
circumstances, the perfusion pressure remains
fairly constant owing to baroreceptor mecha-
nisms. Therefore, the primary means by which
blood flow changes within an organ is by
changes in vascular resistance, which is influ-
enced by extrinsic factors (e.g., sympathetic
nerves and hormones) and intrinsic factors
(e.g., tissue metabolites and endothelial-derived
substances). Basal vascular tone is determined
by the net effect of the extrinsic and intrinsic
factors acting on the vasculature. Resistance
can either increase or decrease from the basal
state by alterations in the relative contribu-
tion of extrinsic and intrinsic factors. Table 7-2
summarizes the relative importance of sympa-
thetic and metabolic control mechanisms and
the intrinsic autoregulatory capacity of several
major organ vascular beds.
TABLE 7-2
COMPARISON OF VASCULAR CONTROL MECHANISMS IN DIFFERENT
VASCULAR BEDS
C IR C U L A T O R Y B ED
| S Y M P A T H E T IC C O N T R O L
| m e t a b o l ic c o n t r o l
| a u t o r e g u l a t io n
C oronary
+1
+++
+++
Cerebral
+
+++
+++
Skeletal m uscle
+ +
+++
++
Cutaneous
+ + +
+
+
Intestinal
+ + +
++
++
Renal
+ +
+
+++
P ulm onary
+
+2
NA
+, weak; ++, moderate; +++, strong.
NA, not applicable because pressure is the dependent variable instead of flow as in other organs.
Sym pathetic vasoconstriction in the coronaries is overridden by metabolic vasodilation during sympathetic activation of the heart.
2Hypoxia causes vasoconstriction, the opposite of all other organs.
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