LIVER

(Hati, Hepar)
HATI ( HEPAR )
STROMA
Glissons capsule (connective tissue liver capsule)
Hilum (entering spot of portal vein, hepatic artery, right and left
hepatic ducts, lymphatic vessels)
LOBULUS HEPATICUS (LIVER LOBULE)
* polygonal shape, 0,7x2 mm in size
* portal space, corners of lobule, 3-6 per lobule
+ contains branch of portal vein, hepatic artery,
bile duct system, lymphatic vessels
* cellular plates of hepatocytes (liver cell cords)
* liver sinusoids (sinusoidal capillaries)
* space of Disse (subendothelial space)
* lining of liver sinusoid : reticular fibers, endothelial cells, Kupffers
cells (macrophages)
HATI (HEPAR)
(SAMBUNGAN)
BLOOD SUPPLY
* from portal vein 80 % of blood supply, 20 % from hepatic artery

PORTAL VEIN SYSTEM

* portal venules >> distributing veins >> inlet venules >>
sinusoids >> central (centrolobular) veins >> sublobular veins
>> hepatic veins

ARTERIAL SYSTEM
* hepatic artery >> interlobular arteries >> inlet arterioles >>
(end directly at various distances from portal space) >>
sinusoids
HATI (HEPAR)
(SAMBUNGAN)

HEPATOCYTES
polyhedral shape, 6 or more surfaces, 20-30 um in diam., eosinophilic,
mitochondria, sooth and rough ER (endoplasmic reticulum)
bile canaliculus, 1-2 um diam., lining with plasma membrane,
microvilli
one or two nuclei with one or two nucleoli
rough ER responsible for synthetizing of protein albumin, fibrinogen
smooth ER responsible for process of oxydation, methylation,
conjugation, detoxyfication
HATI (HEPAR)
(SAMBUNGAN)

BILIARY TRACT
* bile canaliculi >> bile ductules (Herrings canals) >>
bile ducts >> hepatic ducts >> cystic duct >>
common bile duct (ductus choledochus)

GALLBLADDER
* can store 30-50 ml bile
* wall of gallbladder :
** tunica mucosa : + simple columnar epithelium
+ lamina propria
** tunica muscularis
** perimuscular connective tissue
** tunica serosa
 Figure 1611. Schematic
drawing of the structure of the
liver. The liver lobule in the
center is surrounded by the
portal space (dilated here for
clarity). Arteries, veins, and
bile ducts occupy the portal
spaces. Nerves, connective
tissue, and lymphatic vessels
are also present but are (again,
for clarity) not shown in this
illustration. In the lobule, note
the radial disposition of the
plates formed by hepatocytes;
the sinusoidal capillaries
separate the plates. The bile
canaliculi can be seen between
the hepatocytes. The
sublobular (intercalated) veins
drain blood from the lobules.
(Redrawn and reproduced,
with permission, from Bourne
G: An Introduction to
Functional Histology.
Churchill, 1953.)
Figure 1612. Three-dimensional aspect of the normal liver. In the upper center is
the central vein; in the lower center, the portal vein. Note the bile canaliculus, liver
plates, Herings canal, Kupffer cells, sinusoid, fat-storing cell, and sinusoid
endothelial cells. (Courtesy of M Muto.)
Figure 1613. Photomicrograph of the liver. A: A central (centrolobular) vein.
Note the liver plates that anastomose freely, limiting the space occupied by the
sinusoids. PT stain. Medium magnification. B: A portal space with its
characteristic small artery, vein, lymph vessel, and bile duct surrounded by
connective tissue. PT stain. Medium magnification. C: Collagen III reticular
fibers in the lobule, forming a scaffold for the hepatic tissue. Silver
impregnation. Medium magnification.
 Figure 1614. Scanning electron micrograph of the endothelial lining of a
sinusoidal capillary in rat liver, showing the grouped fenestrations in its wall.
At the borders, edges of cut hepatocytes are present, with their villi
protruding into spaces of Disse. x6500. (Courtesy of E Wisse.)
 Figure 1615.
Liver section
showing sinusoid
capillaries with
their endothelial
cells close to the
hepatocytes. The
thin slit between
the hepatocytes and
the endothelium is
the space of Disse.
Kupffer cells can
be seen inside the
sinusoid. PT stain.
High
magnification.
 Figure 1616. The heterogeneity of hepatocytes from the perilobular to the centrolobular regions. Cells in the
perilobular region are the first to alter the incoming blood and the first to be affected by it. Cells in the middle are
the next to respond to the blood, and those in the centrolobular region see portal vein blood that has already been
altered by cells in previous regions. For example, after feeding, peripheral lobular cells are the first to receive
incoming glucose and to store it as glycogen (shown on the figure as dots grouped in threes). Any glucose passing
these cells would probably be picked up by cells in the next region. In the fasting state, perilobular (peripheral)
cells would be the first to respond to glucose-poor blood by breaking down glycogen and releasing it as glucose.
In this event, the cells in intermediate and centrolobular regions would not respond to the fasting condition until
the glycogen in peripheral cells was depleted. This zonal arrangement would account for some of the differences
in the selective damage of hepatocytes caused by various noxious agents or disease conditions. (Courtesy of A
Brecht.)
 Figure 1617.
Scanning electron
micrograph of
branching bile
canaliculi in the liver.
Note the microvilli
lining the internal
surface. (Reproduced,
with permission, from
Motta P et al: The
Liver: An Atlas of
Scanning Electron
Microscopy. Igaku-
Shonin, 1978.)
 Figure 1618.
Ultrastructure of a
hepatocyte. RER,
rough endoplasmic
reticulum; SER,
smooth endoplasmic
reticulum. x10,000.
 Figure 1619. Electron micrograph of a bile canaliculus in rat liver. Note
the microvilli in its lumen and the junctional complexes (arrows) that seal
off this space from the remaining extracellular space. x54,000. (Courtesy of
SL Wissig.)
Figure 1620. The confluence of bile canaliculi and bile ductules, which
are lined by cuboidal epithelium. The ductules merge with bile ducts in the
portal spaces.
 Figure 1621. Electron micrograph of the liver. Note the two adjacent hepatocytes with a
bile canaliculus between them. The hepatocytes contain numerous mitochondria (M) and
smooth and rough endoplasmic reticulum. A prominent Golgi complex (G) is near the bile
canaliculus. The sinusoid is lined by endothelial cells with large open fenestrae. The space of
Disse (D) is occupied by numerous microvilli projecting from the hepatocytes. x9200.
(Courtesy of D Schmucker.)
 Figure 1622. Electron
micrograph of a hepatocyte.
In the cytoplasm, below the
nucleus, are mitochondria
(Mi), rough endoplasmic
reticulum (RER), glycogen
(GI), lysosomes (Ly), and
peroxisomes (P). x6600.
Figure 1623. Protein synthesis and
carbohydrate storage in the liver.
Carbohydrate is stored as glycogen,
usually associated with the smooth
endoplasmic reticulum (SER). When
glucose is needed, glycogen is
degraded. In several diseases,
glycogen degradation is depressed,
resulting in abnormal intracellular
accumulations of glycogen. Proteins
produced by hepatocytes are
synthesized in the rough endoplasmic
reticulum (RER), which explains why
hepatocyte lesions or starvation lead
to a decrease in the amounts of
albumin, fibrinogen, and prothrombin
in a patients blood. The impairment
of protein synthesis leads to several
complications, since most of these
proteins are carriers, important for the
bloods osmotic pressure and for
coagulation.
Figure 1624. Mechanism
of secretion of bile acids.
About 90% of bile acids are
derived from the intestinal
epithelium and transported
to the liver. The remaining
10% are synthesized in the
liver by the conjugation of
cholic acid with the amino
acids glycine and taurine.
This process occurs in the
smooth endoplasmic
reticulum (SER).
 Figure 1625. The secretion of
bilirubin. The water-insoluble form of
bilirubin is derived from the metabolism
of hemoglobin in macrophages.
Glucuronyltransferase activity in the
hepatocytes causes bilirubin to be
conjugated with glucuronide in the
smooth endoplasmic reticulum, forming
a water-soluble compound. When bile
secretion is blocked, the yellow bilirubin
or bilirubin glucuronide is not excreted;
it accumulates in the blood, and jaundice
results. Several defective processes in
the hepatocytes can cause diseases that
produce jaundice: a defect in the
capacity of the cell to trap and absorb
bilirubin (1), the inability of the cell to
conjugate bilirubin because of a
deficiency in glucuronyltransferase (2),
or problems in the transfer and excretion
of bilirubin glucuronide into the bile
canaliculi (3). One of the most frequent
causes of jaundice, howeverunrelated
to hepatocyte activityis the obstruction
of bile flow as a result of gallstones or
tumors of the pancreas.
Figure 1626. Section of human liver with cirrhosis induced by the local
inflammatory action of the eggs of a nematode (Schistosoma). Collagen
content was increased severalfold, resulting in circulatory disturbance.
Picrosirius stain and polarizing microscopy. Medium magnification.
 Figure 1627.
Photomicrograph
of a section of
gallbladder. Note
the lining of
columnar
epithelium and the
smooth muscle
layer (M). PT stain.
Low magnification.
 Figure 1628. Electron
micrograph of the
gallbladder of a guinea
pig. Note the microvilli
(MV) on the surface of the
cell and the secretory
granules (G) containing
mucus. Arrows indicate
the intercellular spaces.
These epithelial cells
transport sodium chloride
from the lumen to the
subjacent connective
tissue. Water follows
passively, causing the bile
to become concentrated.
x5600.
Reference :
Basic Histology
Text & Atlas

tenth edition, 2003

Junqueira, L C
Carneiro, J
Lange Medical Books McGraw-Hill
New York, USA