Effects of Ubiquinol with Fluid Resuscitation following Hemorrhagic Shock
type: CreativeWork
description: Abstract Hemorrhagic shock (HS) and fluid resuscitation triggers ischemia-reperfusion injury in cells and increases the production of reactive oxygen species (ROS) which are known to activate the intrinsic pathway of apoptosis and contribute to organ dysfunction.1 Ubiquinol is a potent free radical scavenger which is produced endogenously and functions as part of the mitochondrial respiratory chain.2 No study has been conducted to investigate the effects of ubiquinol related to HS. The overall aim of this study was to examine the effects of ubiquinol on leukocyte mitochondria and in the lungs, diaphragm, heart and kidneys as a supplemental treatment for HS. A randomized experimental design was used for this study. Adult male Sprague-Dawley rats (n = 20) were anesthetized and HS was induced by withdrawing 40% of the rat's blood volume to maintain a mean arterial pressure of 45-55 mmHg for 60 minutes. Following HS the rats were resuscitated with blood and lactated Ringer's (LR) with or without ubiquinol (1 mg per 100 g of body weight). The rats were monitored for 120 minutes, the animals were euthanized and the organs harvested. Leukocyte mitochondria superoxide (O2*⁻) was measured by flow cytometry using MitoSOX Red, a mitochondrial-targeted variant of the fluorescent probe hydroethidine. Superoxide levels were measured at baseline, end of HS and 120 minutes following fluid resuscitation. Arterial blood values were also recorded at these times. At the end of experiment, diaphragms were evaluated for hydrogen peroxide (H2O2) using the fluorescent probe dihydrofluorescein-diacetate (Hfluor). The lungs, diaphragm, heart, and kidneys were examined for percent of apoptotic nuclear membrane damage using a differential dye uptake method with acridine orange and ethidium bromide. No significant differences were found between groups with regard to the volume of blood removed, hemodynamic status or arterial blood values (p 0.05). Ubiquinol decreased leukocyte mitochondrial pro…
abstract: Abstract Hemorrhagic shock (HS) and fluid resuscitation triggers ischemia-reperfusion injury in cells and increases the production of reactive oxygen species (ROS) which are known to activate the intrinsic pathway of apoptosis and contribute to organ dysfunction.1 Ubiquinol is a potent free radical scavenger which is produced endogenously and functions as part of the mitochondrial respiratory chain.2 No study has been conducted to investigate the effects of ubiquinol related to HS. The overall aim of this study was to examine the effects of ubiquinol on leukocyte mitochondria and in the lungs, diaphragm, heart and kidneys as a supplemental treatment for HS. A randomized experimental design was used for this study. Adult male Sprague-Dawley rats (n = 20) were anesthetized and HS was induced by withdrawing 40% of the rat's blood volume to maintain a mean arterial pressure of 45-55 mmHg for 60 minutes. Following HS the rats were resuscitated with blood and lactated Ringer's (LR) with or without ubiquinol (1 mg per 100 g of body weight). The rats were monitored for 120 minutes, the animals were euthanized and the organs harvested. Leukocyte mitochondria superoxide (O2*⁻) was measured by flow cytometry using MitoSOX Red, a mitochondrial-targeted variant of the fluorescent probe hydroethidine. Superoxide levels were measured at baseline, end of HS and 120 minutes following fluid resuscitation. Arterial blood values were also recorded at these times. At the end of experiment, diaphragms were evaluated for hydrogen peroxide (H2O2) using the fluorescent probe dihydrofluorescein-diacetate (Hfluor). The lungs, diaphragm, heart, and kidneys were examined for percent of apoptotic nuclear membrane damage using a differential dye uptake method with acridine orange and ethidium bromide. No significant differences were found between groups with regard to the volume of blood removed, hemodynamic status or arterial blood values (p 0.05). Ubiquinol decreased leukocyte mitochondrial pro…
author: Bennetts, Paul S.
language: en_US
keywords: Nursing, Physiology, Health sciences, Antioxidants, Apoptosis, Hemorrhage, Mitosox red, Multiple organ failure, Reactive oxygen species
date published: 2013-08-31
date modified: 2026-07-24T02:45:31Z
provider: University of Kansas
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Kansas

PropertyValue
property ID: Handle
value: http://hdl.handle.net/1808/14848