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Abstract
Objectives: Excessive oxygen (O2) administration may have a negative impact on tissue perfusion by inducing vasoconstriction and oxidative stress. We aimed to evaluate the effects of different inhaled oxygen fractions (FiO2) on macro-hemodynamics and microvascular perfusion in a rat model.Methods: Isoflurane-anesthetised spontaneously breathing male Wistar rats were equipped with arterial (carotid artery) and venous (jugular vein) catheters and tracheotomy, and randomized into three groups: normoxia (FiO2 21%, n = 6), hyperoxia (FiO2 100%, n = 6) and mild hypoxia (FiO2 15%, n = 6). Euvolemia was maintained by infusing Lactate Ringer solution at 10 ml/kg/h. At hourly intervals for 4 h we collected measurements of: mean arterial pressure (MAP); stroke volume index (SVI), heart rate (HR), respiratory rate (by means of echocardiography); arterial and venous blood gases; microvascular density, and flow quality (by means of sidestream dark field videomicroscopy on the hindlimb skeletal muscle).Results: MAP and systemic vascular resistance index increased with hyperoxia and decreased with mild hypoxia (p < 0.001 in both cases, two-way analysis of variance). Hyperoxia induced a reduction in SVI, while this was increased in mild hypoxia (p = 0.002). The HR increased under hyperoxia (p < 0.05 vs. normoxia at 3 h). Cardiax index, as well as systemic O2 delivery, did not significantly vary in the three groups (p = 0.546 and p = 0.691, respectively). At 4 h, microvascular vessel surface (i.e., the percentage of tissue surface occupied by vessels) decreased by 29 ± 4% in the hyperoxia group and increased by 19 ± 7 % in mild hypoxia group (p < 0.001). Total vessel density and perfused vessel density showed similar tendencies (p = 0.003 and p = 0.005, respectively). Parameters of flow quality (microvascular flow index, percentage of perfused vessels, and flow heterogeneity index) remained stable and similar in the three groups.Conclusions: Hyperoxia induces vasoconstriction and reduction in skeletal muscle microvascular density, while mild hypoxia has an opposite effect.
Highlights
Supplemental oxygen (O2) is one of the most frequently applied therapies in clinical medicine and usually represents a life-saving intervention in patients with hypoxemia due to respiratory failure
mean arterial pressure (MAP) transiently increased after 1 h of hyperoxia and was stably reduced under mild hypoxia (Table 2) with a maximum decrease of 35 ± 6% at 3 h (p < 0.01 vs. normoxia, Figure 1)
The SVI decreased with hyperoxia as compared to baseline, while it tended to increase under mild hypoxia (Figure 1 and Table 2)
Summary
Supplemental oxygen (O2) is one of the most frequently applied therapies in clinical medicine and usually represents a life-saving intervention in patients with hypoxemia due to respiratory failure. Since clinicians often tolerate supranormal PaO2 values as perceived as a safety buffer against hypoxemia, many critically ill patients in Intensive Care Units (ICUs) are at risk of being exposed to excessive O2 administration [1]. Short term hyperoxia induced a reduction in sublingual microvascular density and flow [3]: this may lead to a paradoxical net reduction in regional O2 delivery to the cells. The use of a more restrictive O2 therapy, with precise control of arterial oxygenation, was able to improve survival in critically ill patients [7]
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