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Artificial hyperventilation normalizes haemodynamics and arterial oxygen content in hypoxic rats

BACKGROUND: Although humans are capable of enduring critically low levels of oxygen, many hypoxaemic patients die despite aggressive therapies. Mimicking the physiological hyperventilation necessary to survive extreme hypoxic conditions could minimize the derangements caused by acute hypoxic-hypoxia...

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Detalles Bibliográficos
Autores principales: de Villalobos, Diego, Laserna, Andres, Fowler, Cosmo, Cuenca, John A., Martin, Peyton, Guindani, Michele, Dong, Wenli, Gutstein, Howard B., Price, Kristen J., Nates, Joseph L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10165328/
https://www.ncbi.nlm.nih.gov/pubmed/34284554
http://dx.doi.org/10.5114/ait.2021.106562
Descripción
Sumario:BACKGROUND: Although humans are capable of enduring critically low levels of oxygen, many hypoxaemic patients die despite aggressive therapies. Mimicking the physiological hyperventilation necessary to survive extreme hypoxic conditions could minimize the derangements caused by acute hypoxic-hypoxia. The objective of this study was to measure the haemodynamic-biochemical response to artificially induced hyperventilation in hypoxic rats. METHODS: Twenty-four deeply anaesthetized and mechanically ventilated rats were allocated to 3 groups: control (n = 5, FiO(2) = 1); hypoxic spontaneously hyperventilating (n = 10, FiO(2) = 0.08); and hypoxic artificially induced hyperventilation (n = 9, targeting PaCO(2) = 10 mm Hg, FiO(2) = 0.08). We compared the spontaneously and artificially hyperventilating groups. P-values < 0.01 were considered statistically significant. Mean arterial pressure (MAP) and serum chemistry were measured for 180 minutes. RESULTS: The control group remained stable throughout the experiment. The hypoxic groups developed profound hypotension after the decrease in FiO(2). However, the arti-ficially induced hyperventilated rats recovered their MAP to levels higher than the spontaneously hyperventilating group (117.1 ± 17.2 vs. 68.1 ± 16.0, P = 0.0048). In regard to the biochemical derangements, even though the serum lactate and PaO(2) were not different among the hypoxic groups, the artificially hyperventilated group achieved significantly higher SaO(2) (94.3 ± 3.6 vs. 58.6 ± 9.6, P = 0.005), pH (7.87 ± 0.04 vs. 7.50 ± 0.13, P = 0.005), and CaO(2) (17.7 ± 2.6 vs. 10.2 ± 1.3, P = 0.005) at 180 minutes. CONCLUSIONS: Artificially induced hyperventilation led to the correction of arterial oxygen content, severe serum chemistry, and haemodynamic derangements. These findings may represent a novel rescue manoeuvre and serve as a bridge to a permanent form of support, but should be further studied before being translated to the clinical setting.