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Physiology of the Heart and Circulation / 341
In order to eject blood from the ventricle Structure and Function of Blood
Vessels
during systole, the pressure in the ventricle
VetBooks.ir must overcome the pressure in the vascular
system on the other side of the semilunar
valves. The load experienced by the ventri Microscopic Structure of Blood Vessels
cle during contraction is afterload, and A single layer of endothelium, a simple squa
the primary contributor to afterload is the mous epithelium, lines all vessels. Capillaries
mean system pressure. Together, preload are essentially endothelial tubes (Fig. 18‐8),
and afterload create the work that the heart but they differ notably among themselves in
must complete with each cardiac cycle. cell‐to‐cell junctions and the structure of
individual endothelial cells. Tight junctions
connect the endothelial cells of some capil
Cardiac Contractility and laries, and this forms a relatively impermea
Stroke Volume ble barrier to non–lipid‐soluble particles.
Other capillaries appear to be quite porous
The contraction force generated by indi because of openings in the endothelial cells
vidual myocardial cells can also be changed themselves, and these are found where high
by a mechanism that is independent of the rates of capillary exchange occur.
length to which cardiac muscle is stretched A wall with three layers, or tunics, char
prior to contraction. This phenomenon is a acterizes all types of veins and arteries.
change in cardiac contractility; it typically From innermost to outermost, these layers
results from the direct action on myocar are the tunica interna (intima), tunica
dial cells of a hormone, neurotransmitter, media, and tunica externa (adventitia)
or drug. Agents that can elicit changes in (Fig. 18‐8). The tunica interna consists of
cardiac contractility are inotropes. the lining endothelium, a subendothelial
Norepinephrine and epinephrine are layer primarily consisting of connective
positive inotropes, because both increase tissue, and in some cases, an internal elas-
cardiac contractility. Norepinephrine and tic membrane. The internal elastic mem
epinephrine both bind to β‐adrenergic brane consists of elastin and is especially
receptors on myocardial cells, and subse prominent in large arteries.
quent to this binding, both elicit increases The tunica media of all veins and arter
in the availability of intracellular calcium ies contains smooth muscle. Arteries have
in stimulated myocardial cells. The a much thicker tunica media than veins of
increased calcium, as well as other changes a corresponding size, and this characteristic
in intracellular metabolism brought about can be used to differentiate between the
by the β‐adrenergic receptor stimulation, two types of vessels.
promotes an increase in the force of con Elastic arteries are a special type whose
traction. Other inotropes use different tunica media contains concentric elastic
membrane receptors, but the intracellular laminae. The elastic properties of this type
events usually involve calcium availability of artery permit vascular expansion and
or the affinity of intracellular proteins for contraction during the various phases of
calcium. the cardiac cycle. The aorta is an elastic
An indicator of myocardial contractility artery that expands to increase its volume
in the intact heart is the percentage of the during ventricular systole and then
EDV that is ejected during ventricular sys rebounds during ventricular diastole to
tole (i.e., ejection fraction). A typical maintain relatively high arterial blood
value for ejection fraction in a resting ani pressure. Arteries whose tunicae mediae
mal is 40%. With sympathetic stimulation, consist primarily of smooth muscle are
this increases (Fig. 18‐7), while with muscular arteries. An external elastic
primary cardiac diseases it may reduce to membrane is the outermost layer of the
15 to 20%. tunica media, but it is often difficult to