→ alveoli paru → darah → diangkut ke jar → sel
( metabolisme sel ) → diangkut dg arah berlawanan
contract. These plates become progressively less exten-
sive in the later generations of bronchi and are gone in
the bronchioles, which usually have diameters less than
1.5 millimeters. The bronchioles are not prevented from
collapsing by the rigidity of their walls. Instead, they are
kept expanded mainly by the same transpulmonary
pressures that expand the alveoli. That is, as the alveoli
enlarge, the bronchioles also enlarge, but not as much.
Muscular Wall of the Bronchi and Bronchioles and Its Control.
all areas of the trachea and bronchi not occupied by car-
tilage plates, the walls are composed mainly of smooth
muscle. Also, the walls of the bronchioles are almost
entirely smooth muscle, with the exception of the most
terminal bronchiole, called the respiratory bronchiole,
which is mainly pulmonary epithelium and underlying
ﬁbrous tissue plus a few smooth muscle ﬁbers. Many
obstructive diseases of the lung result from narrowing
of the smaller bronchi and larger bronchioles, often
because of excessive contraction of the smooth muscle
Resistance to Airﬂow in the Bronchial Tree.
air ﬂows through the respiratory
passageways so easily that less than 1 centimeter of
water pressure gradient from the alveoli to the atmos-
phere is sufﬁcient to cause enough airﬂow for quiet
breathing. The greatest amount of resistance to airﬂow
occurs not in the minute air passages of the terminal
bronchioles but in some of the larger bronchioles and
bronchi near the trachea. The reason for this high resist-
ance is that there are relatively few of these larger
bronchi in comparison with the approximately 65,000
parallel terminal bronchioles, through each of which
only a minute amount of air must pass.
Yet in disease conditions, the smaller bronchioles
often play a far greater role in determining airﬂow
resistance because of their small size and because they
are easily occluded by (1) muscle contraction in their
walls, (2) edema occurring in the walls, or (3) mucus col-
lecting in the lumens of the bronchioles.
Nervous and Local Control of the Bronchiolar Musculature—
“Sympathetic” Dilation of the Bronchioles.
Direct control of
the bronchioles by sympathetic nerve ﬁbers is relatively
weak because few of these ﬁbers penetrate to the
central portions of the lung. However, the bronchial tree
is very much exposed to norepinephrine and epineph-
released into the blood by sympathetic stimulation
of the adrenal gland medullae. Both these hormones—
especially epinephrine, because of its greater stimula-
tion of beta-adrenergic receptors—cause dilation of the
Parasympathetic Constriction of the Bronchioles.
parasympathetic nerve ﬁbers derived from the vagus
nerves penetrate the lung parenchyma. These nerves
secrete acetylcholine and, when activated, cause mild
to moderate constriction of the bronchioles. When a
disease process such as asthma has already caused some
bronchiolar constriction, superimposed parasympa-
thetic nervous stimulation often worsens the condition.
When this occurs, administration of drugs that block the
effects of acetylcholine, such as atropine, can sometimes
relax the respiratory passages enough to relieve the
Sometimes the parasympathetic nerves are also acti-
vated by reﬂexes that originate in the lungs. Most of
these begin with irritation of the epithelial membrane
of the respiratory passageways themselves, initiated by
noxious gases, dust, cigarette smoke, or bronchial infec-
tion. Also, a bronchiolar constrictor reﬂex often occurs
when microemboli occlude small pulmonary arteries.
Local Secretory Factors Often Cause Bronchiolar Constriction.
Several substances formed in the lungs themselves are