Utility of hepatic phosphorus-31 magnetic resonance spectroscopy in the healthy and diseased liver.

摘要

Adenosine triphosphate (ATP) and other high-energy molecules play a central role in the functional and morphological integrity of cells. During periods when energy levels are low the viability of cells may be compromised as demands may exceed supply. Ultimately these events may result in organ dysfunction. As such, disturbances in cellular energy metabolism have been implicated in the pathogenesis in a variety of diseases. In vivo phosphorus-31 magnetic resonance spectroscopy (31P MRS) is a non-invasive method that permits direct assessment of energy levels of tissues in situ. The principal aim of the present study was to determine whether differences in energy status of the liver, as determined by 31P MRS, could assess the extent of underlying liver disease.; Partial hepatectomies (PHx) were first employed in rats to determine whether changes in hepatic energy levels in healthy rats reflected the amount of residual liver parenchyma remaining after resection. Following 40%, 70% and 90% PHx hepatic energy levels, as reflected by ATP and ATP/Pi, decreased in proportion to the extent of resection with significantly lower ATP levels occurring following 70% and 90% PHx.; Various animal models of acute and chronic liver disease also displayed reduced energy levels with increasing severity of disease. During acute liver failure lower ATP levels were observed when more than 50% of the liver lobule was destroyed. Similar results were evident in rats subjected to parenchymal and cholestatic forms of chronic liver disease as reductions in hepatic ATP levels were only detected once extensive fibrosis or cirrhosis was established.; Patients with hepatitis C induced chronic liver disease also possessed lower hepatic ATP levels than healthy control subjects. However, these reductions did not occur until decompensated cirrhosis developed.; Taken together, the results from animal and human studies suggest that: (1) reduced hepatocyte numbers, (2) increased energy expenditure due to increased regenerative activity and functional demands, and (3) a decreased capacity to produce energy, all contribute to the reduction of hepatic ATP in advanced liver disease. The results also support the hypothesis that diminished energy reserves within the liver play a central role in the pathogenesis of hepatic dysfunction during liver disease.