Cardiac arrest induces whole-body
ischemia, which causes damage to multiple organs. Understanding how each organ responds to
ischemia/reperfusion is important to develop better
resuscitation strategies. Because direct measurement of organ function is not practicable in most animal models, we attempt to use mitochondrial respiration to test efficacy of
resuscitation on the brain, heart, kidney, and liver following prolonged
cardiac arrest. Male Sprague-Dawley rats are subjected to
asphyxia-
induced cardiac arrest for 30 min or 45 min, or 30 min
cardiac arrest followed by 60 min
cardiopulmonary bypass resuscitation. Mitochondria are isolated from brain, heart, kidney, and liver tissues and examined for respiration activity. Following
cardiac arrest, a time-dependent decrease in state-3 respiration is observed in mitochondria from all four tissues. Following 60 min
resuscitation, the respiration activity of brain mitochondria varies greatly in different animals. The activity after
resuscitation remains the same in heart mitochondria and significantly increases in kidney and liver mitochondria. The result shows that inhibition of state-3 respiration is a good marker to evaluate the efficacy of
resuscitation for each organ. The resulting state-3 respiration of brain and heart mitochondria following
resuscitation reenforces the need for developing better strategies to resuscitate these critical organs following prolonged
cardiac arrest.