Haemorrhagic
shock (HS) and fluid
resuscitation can lead to increased
reactive oxygen species (ROS), contributing to ischaemia-
reperfusion injury and organ damage.
Ubiquinol is a potent
antioxidant that decreases ROS. This study examined the effects of
ubiquinol administered with fluid
resuscitation following controlled HS. Adult male Sprague-Dawley rats were randomly assigned to treatment [
ubiquinol, 1 mg (100 g
body weight)(-1)] or control groups. Rats were subjected to 60 min of HS by removing 40% of the total blood volume to a mean arterial pressure ∼45-55 mmHg. The animals were resuscitated with blood and
lactated Ringer solution, with or without
ubiquinol, and monitored for 120 min. At the end of the experiments, the rats were killed and the lungs, diaphragm, heart and kidneys harvested. Leucocytes were analysed for mitochondrial
superoxide at baseline, end of
shock and 120 min following fluid
resuscitation using
MitoSOX Red. Diaphragms were examined for
hydrogen peroxide using
dihydrofluorescein diacetate and confocal microscopy. The apoptosis in lungs, diaphragm, heart and kidneys was measured using fluorescence microscopy with
acridine orange and
ethidium bromide. Leucocyte mitochondrial
superoxide levels were significantly lower in rats that received
ubiquinol than in the control animals. Production of
hydrogen peroxide and apoptosis were significantly reduced in the organs of rats treated with
ubiquinol. These findings suggest that
ubiquinol, administered with fluid
resuscitation after HS, attenuates ROS production and apoptosis. Thus,
ubiquinol is a potent
antioxidant that may be used as a potential treatment to reduce organ injury following haemorrhagic events.