European Journal of Cardio-Thoracic Surgery, Vol 10, 273-278, Copyright © 1996 by European Association for Cardio-thoracic Surgery
Influence of hepatic mitochondrial redox state on complement biosynthesis and activation during and after cardiopulmonary bypass operations
S Nomoto, Y Shimahara, K Kumada, Y Okamoto and T Ban
Department of Cardiovascular Surgery, Kyoto University Medical School, Japan.
We have proposed the hazardous phenomena associated with cardiopulmonary
bypass (CPB) are due to metabolic derangement by hepatic mitochondrial
dysfunction during and after CPB. On the contrary, complement activation
and consumption during CPB is reported to be related to the morbidity
associated with cardiac surgery. To determine the significance of the
hepatic mitochondrial function on the morbidity of cardiac surgery, we
measured the serum levels of complements (C3 and C4), activated complements
(C3a and C4a), and the arterial ketone body ratio (AKBR), which reflects
the hepatic mitochondrial redox state, in 30 patients undergoing CPB. The
AKBR, which was at a normal level preoperatively, dropped to a critical
level after the initiation of CPB and remained at a low level during the
CPB, returning to the preoperative level on the second postoperative
morning in a time dependent fashion. The patients group were assigned to
two groups according to their AKBR on the first postoperative morning.
Group I consisted of patients whose AKBR had recovered to above 0.7 on the
first postoperative morning (n = 16). Group II consisted of the rest of the
patients (n = 14). The serum complement concentration had considerably
decreased by the end of bypass, but recovered in a time- dependent fashion
after CPB. The group I patients (C3: 71% of its preoperative value, C4: 85%
of its preoperative value) recovered their complements more quickly than
the group II patients (C3: 56% of its preoperative value, C4: 54% of its
preoperative value). However, the serum C3a and C4a concentrations
increased by the end of bypass (C3a: 806% of its preoperative value, C4a:
341% of its preoperative value). The activated complements were
significantly higher in the group II patients (C3a: 124% of its
preoperative value, C4a: 236% of its preoperative value) than in the group
I patients (C3a: 75% of its preoperative value, C4a: 113% of its
preoperative value) on the first postoperative morning. It is suggested
that hepatic mitochondrial function is related to recovering the
complements and to reducing the activated complements after CPB.
