Coenzyme Q10: A New Treatment for Hemorrhagic Shock


Name: Janet Pierce

Rank: CAPT

Organization: The University of Kansas Medical Center

Performance Site: University of Kansas Medical Center, Kansas City, KS

Year Published: 2011

Abstract Status:


Military personnel treat hemorrhagic shock (HS) in the field and hospitals with fluid resuscitation and multiple drugs. The objective of this treatment is to normalize hemodynamic parameters and cell oxygenation. The significant loss of intravascular volume that occurs with HS results in insufficient blood flow to the tissues. This leads to hemodynamic instability, decreased oxygen delivery, cellular hypoxia, organ damage, and death. An increased production of reactive oxygen species (ROS) occurs with HS and resuscitation treatments. Oxidative stress is caused by an increase in ROS and results in microcirculation and organ damage. When endogenous antioxidants are not sufficient enough to appropriately scavenge, a more potent antioxidant such as Coenzyme Q10 (ubiquinone) could be used during HS to reduce oxidative stress. Using an in-vivo rat model, we obtained pilot data indicating HS and fluid replacement causes leukocyte mitochondrial and microcirculation damage. We are assuming that the mitochondrial release of ROS results in cellular apoptosis and microvascular damage. When we administered intravenous Coenzyme Q10 (CoQ10) we observed a reduction in lung and vascular injury. Our overall objective of this grant is to determine using a rat model if intravenous CoQ10 will reduce oxidative stress in the lungs, diaphragm and vascular endothelium. In AIM #1, we will examine the effect of CoQ10 in leukocytes, the lung, and the diaphragm as a treatment for HS. Following 1 hour of HS, we will administer intravenous CoQ10 and determine serum CoQ10 concentration, ROS in leukocyte mitochondria, and lung and diaphragm hydrogen peroxide and apoptosis. In AIM #2, we will examine the effect of CoQ10 in the microcirculation as a treatment for HS. We will determine leukocyte adherence, mast cell degranulation, vascular permeability, and microvascular ROS levels. CoQ10 has been used successfully as a treatment for cardiovascular disease, cancer and diabetes. We are hopeful that our results from this study will demonstrate that CoQ10 could be an adjunct treatment for HS that could be used to prevent the cellular damage that accompanies HS and resuscitative therapies.  

Relevance: Outcomes from these proposed studies related to CoQ10 will potentially expand treatment options for HS patients. Administering CoQ10 could reduce the cellular organ damage observed in war fighters experiencing HS and positively impact their survival rate. These AIMS clearly address several of the priorities mandated by TSNRP such as translating research into practice & health care of military personnel.


Final report is available on NTRL at: