ARTERIAL KETONE-BODY RATIO AND ADENOSINE-TRIPHOSPHATE CONCENTRATION IN HEPATIC ISCHEMIA AND REPERFUSION

Citation
K. Hanazaki et al., ARTERIAL KETONE-BODY RATIO AND ADENOSINE-TRIPHOSPHATE CONCENTRATION IN HEPATIC ISCHEMIA AND REPERFUSION, Hepato-gastroenterology, 45(23), 1998, pp. 1816-1820
Citations number
18
Categorie Soggetti
Gastroenterology & Hepatology",Surgery
Journal title
ISSN journal
01726390
Volume
45
Issue
23
Year of publication
1998
Pages
1816 - 1820
Database
ISI
SICI code
0172-6390(1998)45:23<1816:AKRAAC>2.0.ZU;2-D
Abstract
BACKGROUND/AIMS: The arterial ketone body ratio (AKBR) and the cellula r adenosine triphosphate (ATP) concentration have been proposed as ind icators of liver function. However, recent studies of the utility of t he AKBR as a biochemical marker have been called into question. Furthe rmore, there is no practical data defining the relationship between AT P concentration and ischemia-reperfusion (IR) changes during liver sur gery. METHODOLOGY: The relationship of the AKBR and arterial ATP conce ntration to IR during hepatectomy was investigated. In 20 patients who underwent hepatectomy, arterial acetoacetate, beta-hydroxybutyrate, a nd ATP concentrations were measured. The ratio of acetoacetate to beta -hydroxybutyrate (AKBR) was calculated before and after vascular occlu sion. RESULTS: The AKBR 15 minutes after clamping was lower than the p reclamping values in all of the patients. It increased after unclampin g, returning toward the preclamping levels. An AKBR of less than 0.5 p rior to clamping did not correlate with preoperative hepatocellular fu nction. An AKBR of less than 0.7 throughout IR was not a consistent ri sk factor for postoperative complications and Liver dysfunction. The a rterial. ATP concentration did not correlate with the changes during I R or with preoperative hepatocellular function. CONCLUSIONS: Although the AKBR changed during IR as a general indicator of cellular activity , the absolute value of the AKBR was not an accurate predictor of live r function. The arterial ATP concentration also was not a suitable cli nical biochemical marker of hepatic function.