Hepatic arterial complications in pediatric segmental liver transplantations from living donors: assessment with color Doppler ultrasonography.

To investigate the clinical utility of color Doppler ultrasonography in detecting hepatic arterial complications in pediatric living-related liver transplantation, we studied peak systolic velocity (Vp) and pulsatility index (PI) intrahepatic artery during and after surgery in 122 transplants. Six cases with hepatic artery thrombosis were detected by Doppler studies. In 2 cases with dampened waveforms at intraoperative flowmetry (Vp < or = 23 and PI < or = 0.6), thrombosis occurred soon after surgery. A further 2 cases had a rapid decrease in Vp and PI values postoperatively, leading to absence of arterial signals. Follow-up Doppler studies suspected collateral formation after thrombosis in 2 survivors. Normal Doppler waveforms were obtained in all of the 116 cases without arterial complications. Among them, 6 cases had absent signals or dampened waveforms at initial intraoperative flowmetry (Vp < or = 30 and PI < or = 0.9), and maneuvers such as re-reanastomosis of the artery improved flow signals with an increase in Vp and PI values. Serial intra- and post-operative Doppler examinations are useful for early detection of arterial complications.

Kinetic analysis of impaired work-cost performance in jaundiced rabbit liver.

Impairment of energy metabolism was studied in jaundiced rabbit liver by kinetic analysis of energy transfer function. Free cytosolic ADP (ADPf), as calculated from the measured components of the glyceraldehyde-3-phosphate dehydrogenase and 3-phosphoglycerate kinase/lactate dehydrogenase reactions, decreased from the control value of 48.1 to 37.0 microM at 24 h after bile duct ligation. The maximal velocity (Vmax) of ATP synthesis, as measured by state 3 respiration of isolated mitochondria, decreased from the control value of 62.1 to 38.3 nmol ATP synthesized per min per mg mitochondrial protein, while the Michaelis constant for ADP (Km) decreased from the control value of 19.2 to 12.8 microM. ATP synthesis velocity in vivo }v: Vmax/[1 + (Km/[ADPf])], as calculated by Vmax, Km and ADPf, decreased from the control value of 44.4 to 28.5 nmol ATP synthesized per min per mg mitochondrial protein. Delta v/delta ADPf(delta v/delta ADPf: Vmax.Km/(Km + [ADPf])2), which indicates work-cost performance of the liver, decreased from the control value of 0.263 to 0.198. Biochemical output of the liver, as measured by hippurate synthesis from benzoate, decreased from the control value of 98.4 to 32.7 mg/h. These results indicate that synergistic decreases in ADPf, Vmax, v and delta v/delta ADPf take place in the course of deterioration of mitochondrial ATP synthesis and work output in jaundiced liver.