1. The alterations in hepatic energy metabolism in hypotension induced by the administration of trimetaphan camsylate (Arfonad) were investigated in comparison with those produced by hypotension resulting from massive haemorrhage by measuring the arterial ketone body ratio, which reflects the hepatic mitochondrial redox state, and other indices of hepatic energy metabolism together with simultaneous measurement of hepatic blood flow in dogs.
2. Mean arterial blood pressure was decreased from 130 mmHg to 60 mmHg by the continuous intravenous infusion of trimetaphan camsylate or by the use of Wiggers' shock model. In hypotension induced by trimetaphan camsylate, the arterial ketone body ratio, ATP and total adenine nucleotide concentrations and energy charge were maintained at near-control values throughout the experimental period. By contrast, the arterial ketone body ratio decreased from 1.04 ±0.09 to 0.29 ±0.06 at 3 h after haemorrhage in Wiggers' shock model (P <0.01). The ATP and total adenine nucleotide concentrations and energy charge also decreased significantly in this model (P <0.05). The difference in hepatic energy status was also shown by data from 31P nuclear magnetic resonance spectroscopy.
3. During hypotension, portal venous and total hepatic blood flows diminished significantly compared with the control values in each group (P <0.01). Although there was no significant difference in total hepatic flow between the two groups, the portal venous blood flow in hypotension induced by trimetaphan camsylate was significantly higher than that in Wiggers' shock model (P <0.05).
4. During hypotension induced by trimetaphan camsylate, the hepatic energy metabolism was well maintained at the mean arterial blood pressure value of 60 mmHg, but in haemorrhagic hypotension it was severely curtailed, although there was no significant difference in total hepatic blood flow between the two groups. It is conjectured that the portal venous blood flow contributes significantly to the maintenance of hepatic energy metabolism and hepatic tissue perfusion during hypotension induced by trimetaphan camsylate.