104
BRIAN POOLE
acids into liver following partial hepatectomy: one at 9 hr and another at
28 hr. The first peak is much smaller and reportedly is not associated with
protein accumulation (Busanny-Caspari and Deimel, 1963). The increased
rate of liver incorporation of isotopically labeled amino acids after partial
hepatectomy can also be demonstrated in a cell-free system prepared from
liver (von der Decken and Hultin, 1958; Hultin and von der Decken,
1957).
The DNA polymerase system (Bollum and Potter, 1959) and DNA
synthesis are elevated between 12 and 24 hr after hepatectomy, but mitotic
activity increases several hours later (Cater et al, 1956). The temporal
dissociation of these two processes would be expected in view of similar
observations by Walker (1952) and others on cells in tissue culture. Weinbren and Woodward (1964) reported that the peak of incorporation of P
32
into rat liver DNA occurs 24 hr later after 82% hepatectomy than it does
after 67% hepatectomy. Butler and Cohn (1963) reported that the ratio of
synthesis of histone to synthesis of other protein increases 12 hr after
hepatectomy. The normal diurnal cycle of mitotic activity in liver has very
high peaks for a number of days after hepatectomy (Bade and Echave
Llanos, 1963; Russo and Echave Llanos, 1964). Within the first day after
partial hepatectomy, mitoses are more frequent in periportal areas, but
after 1 day this pattern disappears (R. D. Harkness, 1952). There is an
increase in polyploidy in the hypertrophying liver (Laquerriere and Laumonier, 1963). Littoral cells have their peak proliferative response later
than do parenchymal cells (Edwards and Koch, 1964). The process of
collagen formation lags behind cellular proliferation, but probably catches
up after a couple of months (Harkness and Harkness, 1954).
The biochemical composition of liver undergoes dramatic changes during
hypertrophy. By 2 hr after partial hepatectomy, liver glycogen is almost
completely depleted; by 24 hr it is restored (Bogetti and Mazzocco, 1941).
Immediately after partial hepatectomy the phospholipid content of the
remnant drops, and the neutral lipid content rises until the remnant contains almost as much fat as the whole resting liver (rat—Bogetti and
Mazzocco, 1939; mouse—Tsuboi et al, 1954). Some enzyme systems are
reduced in hypertrophying liver (Novikoff and Potter, 1948). There is an
immediate increase in the free lysine content of liver, with a threefold peak
6 hr after partial hepatectomy, followed by a decline to normal levels by
16 hr (Fujioka et al, 1963). Conflicting reports concerning the pattern of
change in water content in the liver remnant after partial hepatectomy
(Bogetti and Mazzocco, 1939; Higgins and Anderson, 1931) are probably
a consequence of the diurnal cycle of liver water content reported by
Russo and Echave Llanos (1964). Aterman (1952) has reported the appearance of glycogen-free, fat-free vacuoles in liver cells 5 min after partial
BRIAN POOLE
acids into liver following partial hepatectomy: one at 9 hr and another at
28 hr. The first peak is much smaller and reportedly is not associated with
protein accumulation (Busanny-Caspari and Deimel, 1963). The increased
rate of liver incorporation of isotopically labeled amino acids after partial
hepatectomy can also be demonstrated in a cell-free system prepared from
liver (von der Decken and Hultin, 1958; Hultin and von der Decken,
1957).
The DNA polymerase system (Bollum and Potter, 1959) and DNA
synthesis are elevated between 12 and 24 hr after hepatectomy, but mitotic
activity increases several hours later (Cater et al, 1956). The temporal
dissociation of these two processes would be expected in view of similar
observations by Walker (1952) and others on cells in tissue culture. Weinbren and Woodward (1964) reported that the peak of incorporation of P
32
into rat liver DNA occurs 24 hr later after 82% hepatectomy than it does
after 67% hepatectomy. Butler and Cohn (1963) reported that the ratio of
synthesis of histone to synthesis of other protein increases 12 hr after
hepatectomy. The normal diurnal cycle of mitotic activity in liver has very
high peaks for a number of days after hepatectomy (Bade and Echave
Llanos, 1963; Russo and Echave Llanos, 1964). Within the first day after
partial hepatectomy, mitoses are more frequent in periportal areas, but
after 1 day this pattern disappears (R. D. Harkness, 1952). There is an
increase in polyploidy in the hypertrophying liver (Laquerriere and Laumonier, 1963). Littoral cells have their peak proliferative response later
than do parenchymal cells (Edwards and Koch, 1964). The process of
collagen formation lags behind cellular proliferation, but probably catches
up after a couple of months (Harkness and Harkness, 1954).
The biochemical composition of liver undergoes dramatic changes during
hypertrophy. By 2 hr after partial hepatectomy, liver glycogen is almost
completely depleted; by 24 hr it is restored (Bogetti and Mazzocco, 1941).
Immediately after partial hepatectomy the phospholipid content of the
remnant drops, and the neutral lipid content rises until the remnant contains almost as much fat as the whole resting liver (rat—Bogetti and
Mazzocco, 1939; mouse—Tsuboi et al, 1954). Some enzyme systems are
reduced in hypertrophying liver (Novikoff and Potter, 1948). There is an
immediate increase in the free lysine content of liver, with a threefold peak
6 hr after partial hepatectomy, followed by a decline to normal levels by
16 hr (Fujioka et al, 1963). Conflicting reports concerning the pattern of
change in water content in the liver remnant after partial hepatectomy
(Bogetti and Mazzocco, 1939; Higgins and Anderson, 1931) are probably
a consequence of the diurnal cycle of liver water content reported by
Russo and Echave Llanos (1964). Aterman (1952) has reported the appearance of glycogen-free, fat-free vacuoles in liver cells 5 min after partial