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   <subfield code="a">Conversion of mitochondrial redox state toward oxidation by prostacyclin in 70%-hepatectomized rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Taisuke Morimoto, Kazue Ozawa, Wolf Isselhard]</subfield>
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   <subfield code="a">Summary: Arterial blood ketone body ratio (KBR) and hepatic mitochondrial phosphorylation rate (PR) were investigated in partially (70%) hepatectomized rats treated with 100 μg/kg body weight prostacyclin (PGI2) analogue i.p. after operation and every 12 h thereafter up to 72h. Sampling was performed at 12, 24, 48, and 72 h after operation. In sham-operated rats, KBR significantly increased from the preoperative values of 0.34±0.03 and 0.38±0.03, to 0.55±0.03 and 0.58±0.02 at 12 h in the groups with and without PGI2 treatment, respectively (P&lt;0.001). KBR returned to the preoperative levels after 24 h in the PGI2-treated group, while it tended to be in the lower normal range in the untreated group. In the hepatectomized rats, KBR significantly decreased in the untreated group compared with the preoperative values and the values in the sham-operated group. It returned to the preoperative range within 72h. In the PGI2-treated group, KBR increased significantly, to values above 0.54, after a 24-h delay and was maintained at those levels for 72h. Concentrations of total ketone bodies (TKB) in the untreated groups remained in the upper range of preoperative values (above 200 nmol/ml) in the sham-operated rats and decreased significantly in the hepatectomized group (234 to 126 nmol/ml). TKB in the treated groups tended to decrease only in the sham-operated group (205 to 166 nmol/ml), and was massively reduced in the hepatectomized group (167 to 81 nmol/ml). PR was significantly enhanced after hepatectomy until 48h both in the groups with and without PGI2 treatment, but the degree of enhancement in PR was lower in the group with treatment than the one without treatment during the period of mitochondrial enhancement. It is suggested that PGI2 may convert the mitochondrial redox state toward oxidation accompanied by a suppression of ketogenesis and may activate the tricarboxylic acid (TCA) cycle. It is also suggested that PGI2 treatment may make it less necessary for mitochondria in the remnant liver to be enhanced to compensate the metabolic overload on the remnant liver and that PGI2 treatment may have a promoting effect on liver regeneration after hepatectomy.</subfield>
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   <subfield code="a">Partial hepatectomy</subfield>
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   <subfield code="a">Arterial blood ketone body ratio</subfield>
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