Recovery of liver cell mass following hepatectomy requires a metabolic comp
romise between differentiated function and organ regrowth. Clinical experie
nce has shown that hepatic failure after resection is more common when the
organ is diseased. We have evaluated intracellular hepatic biochemistry in
patients with normal and cirrhotic livers undergoing partial hepatectomy, u
sing 31-phosphorus magnetic resonance spectroscopy (P-31 MRS). Eighteen pat
ients were studied, half with normal liver architecture (normal group, n =
9) and half with cirrhotic parenchyma (cirrhosis group, n = 9). Magnetic re
sonance examinations were performed preoperatively and on postoperative day
s 2, 4, 6, 14, and 28. Hepatic volume (estimated by magnetic resonance imag
ing [MRI]) and blood chemistries were measured at the same intervals. Follo
wing a comparable reduction in parenchymal volume, the cirrhotic group demo
nstrated a more sustained fall in adenosine triphosphate (ATP) energy state
. Disturbance of membrane phospholipid metabolism and duration of acute-pha
se reaction were more marked when the liver was diseased. The pattern of de
rangement of hepatic function, however, was similar in the two groups. Over
all, the recovery process was less efficient in the cirrhotic organ, and cu
lminated in a diminished rate and extent of the regenerative response. Thes
e outcomes indicate that liver regeneration after partial hepatectomy invol
ves modulation of hepatic energy economy in response to changing work deman
ds. The efficiency of this process is influenced by the histopathologic sta
te of the organ, and in turn governs the physiologic reserve. These finding
s may explain the mechanism of posthepatectomy liver failure, and offer a r
ational basis for the assessment of novel hepatic support strategies.