Examining the Sex Effect on Oxidative Stress during Simulated Hemorrhage Induced by Lower Body Negative Pressure




Luu, My-Loan
Park, Flora
Kay, Victoria
Sprick, Justin
Rosenburg, Alexander
Mallet, Robert T.
Rickards, Caroline


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Purpose Traumatic hemorrhage is one of the leading causes of death in both the military and civilian settings. Massive blood loss is known to elicit an increase in oxidative stress as a consequence of tissue ischemia and hypoxia. We have recently demonstrated that simulated hemorrhage via application of lower body negative pressure (LBNP) also elicits an increase in oxidative stress (indexed by circulating F2-isoprostanes). It is not clear, however, whether oxidative stress responses to stimulated hemorrhage are differentiated based on sex. The aim of this study was to assess sex differences in the oxidative stress response during simulated hemorrhage via application of pre-syncopal LBNP. Methods Fifteen healthy human subjects (11 M, 4 F) participated in a LBNP step protocol until presyncope (-15, -30, -45, -60, -70, -80, -90, -100 mmHg LBNP for 5-min each). Venous blood samples were collected at baseline and at presyncope then analyzed for F2-isoprostanes. Stroke volume and mean arterial pressure were obtained via finger photoplethysmography, while muscle oxygen saturation was measured via a near infrared spectroscopy device attached to the forearm. Time to reach presyncope was measured in seconds. Results The following results are only preliminary based on the small number of female subjects tested (N=4). There was no difference in tolerance to LBNP between males and females (Males: 1616 ± 132 s vs. Females: 1486 ± 216 s; P=0.63). F2-isoprostane concentrations were similar between the sexes at baseline (P=0.27), and there was no statistical difference in the % change in concentration with application of maximal LBNP (Males: 37.0 ± 15.4 % vs. Females: 5.0 ± 10.1; P=0.11). The decreases in stroke volume (Males: -52.4 ± 5.3 % vs. Females: -56.5 ± 5.5 %; P=0.50),mean arterial pressure (Males: -11.9 ± 3.4 % vs. Females: -14.6 ± 4.2 %; P=0.63), and muscle oxygen saturation (Males: -9.1± 1.7 % vs. Females: -9.4 ±2.3 %; P=0.91) were also similar between males and females. Conclusions These preliminary data indicate that there is no effect of sex on the oxidative stress response induced by application of simulated hemorrhage with maximal LBNP. This analysis is limited and inconclusive, however, as there were only 4 females and 11 males in this group of subjects. In our current study, we plan to recruit equal numbers of males and females to further explore whether biological sex plays a role in the oxidative stress response to blood loss injuries.