Hepatic microsomal adenosine triphosphatase and mitochondrial function. Response to cold and warm ischemia
M. C. Townsend, M. D. Yokum and D. E. Fry
We investigated the response of mitochondrial function and microsomal
adenosine triphosphatase (ATPase) activity in rat liver tissue subjected to
in vitro ischemia at either 0 degree C to 4 degrees C or 37 degrees C for
30 to 60 minutes. Mitochondrial coupling, expressed as respiratory control
index, was preserved at up to 60 minutes' cold ischemia. However,
respiratory control index was decreased significantly from control by 30
minutes of warm ischemia. Both microsomal magnesium-activated ATPase and
sodium-potassium ATPase activity were significantly increased by 60 minutes
of warm ischemia yet were unaltered by 60 minutes of ischemia at 0 degree C
to 4 degrees C. Warm ischemia produces deleterious effects on
energy-generating (mitochondria) and energy-utilizing (ATPase) activity.
Hypothermia provides a significant prolongation of cellular viability in
ischemic tissue in terms of bioenergetic status. In addition to organ
procurement and transplantation, hypothermic cytoprotection may prove
valuable in areas such as shock, ischemia, and other clinical conditions of
compromised visceral perfusion.