Lonnie Schneider, PhD
Assistant Professor
University of Utah, United States
Disclosure information not submitted.
Scott Youngquist, MD
Associate Professor
University of Utah Division of Emergency Medicine, United States
Disclosure information not submitted.
Austin Johnson, MD, PhD
Assistant Professor
University of Utah, United States
Disclosure information not submitted.
Guillaume Hoareau, DVM, PhD, DACVECC
Assistant Professor
University of Utah, United States
Disclosure information not submitted.
Title: Organ-specific mitochondrial function following hemorrhagic shock and REBOA: A pilot study.
INTRODUCTION/HYPOTHESIS: Non-compressible torso hemorrhage (NCTH) can lead to profound hemorrhagic shock and death. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an important bridging therapy for patients with NCTH. However, ischemia-reperfusion injury (IRI) is a major contributor to death, and novel treatments to reduce IRI are necessary. Mitochondrial injury from hemorrhagic shock is thought to be compounded by REBOA. We sought to map regional mitochondrial function within the heart and kidney.
We hypothesized that following hemorrhagic shock, REBOA would induce mitochondrial injury resulting in altered bioenergetics balance between the left and right ventricles as well as renal cortex and medulla.
Methods: Five Yorkshire pigs were anesthetized, instrumented, and underwent a splenectomy. Four animals underwent hemorrhagic shock by removal of 25% of the animal’s estimated blood volume into citrated blood collection bags. They then underwent 45 minutes of complete aortic occlusion (balloon positioned immediately superior to the diaphragm). Animals were then transfused with autologous blood and calcium, and the balloon was removed. In the final phase, pigs received critical care and algorithmic resuscitation with isotonic crystalloids and norepinephrine to maintain normotension. One animal remained under anesthesia with no hemorrhage or REBOA. After euthanasia, myocardial (left and right ventricles) and renal (cortex and medulla) tissue homogenate were placed in a high-resolution OROBOROS respirometer for quantification of reserve respiratory capacity.
Results: In animals that underwent hemorrhagic shock and REBOA, renal medulla had a three-fold higher overall mitochondrial function when compared to the cortex (N=4). There were no significant changes in mitochondrial function between the left and right ventricles. In the control animal, there was a 50% decrease in mitochondrial function in the left ventricle compared to the right ventricle.
Conclusions: We described for the first time the regional variability in mitochondrial function within the heart and kidneys after hemorrhagic shock and REBOA. A better understanding of subcellular complications of REBOA will open future therapeutic research avenues to mitigate ischemia-reperfusion in patients with NCTH.