Abstract <p>Severe sepsis (endotoxicosis), similar to cytokine storm,is aggravated by acute respiratory failure, hypotension, hypoxemiaand hypercapnia, which is the main cause of high mortality. Theaim of the work is to study the effectiveness of hypercapnic-hypoxictraining (HHT) for the relief of cardiorespiratory disorders andincreased tolerance to acute hypoxia in rats with LPS-induced endotoxicosis.The experiments were conducted on anesthetized male Wistar rats.Endotoxicosis was simulated by administration of LPS (<i>Escherchia coli</i>) 7 mg/kg. The assessmentof resistance to hypoxia was carried out by the rebreathing method(RM) with a gradual decrease in oxygen in the rebreather from 21%to the onset of apnea. 3 groups of animals were studied: I—control—NaCl,II—LPS, III—LPS+HHT. The following parameters were recorded: externalrespiration, mean blood pressure (APm.), saturation (SpO<sub>2</sub>),fraction of inhaled O<sub>2</sub> (FiO<sub>2</sub>)and CO<sub>2</sub> (FiCO<sub>2</sub>), timeof onset of apnea, the amount of spontaneous respiratory recovery(autoresuscitation) in the posthypoxic period. The LPS+HHT groupwas previously subjected to hypercapnic-hypoxic training. For thispurpose, the rebreather was filled with room air, the volume ofwhich was selected in such a way that during the breathing of the animalinto/out of the rebreather, FiO<sub>2</sub> decreasedto 11 ± 0.5% for 3 minutes, and FiCO<sub>2</sub> increasedto 5.0 ± 0.5%, after which the rat was switched to breathing air.The training regime consisted of 3 cycles: 3&#xa0;min—HHT, 5 min—normoxia.It was found that the maximum decrease in resistance to acute hypoxia wasobserved in rats with LPS, respiratory recovery after apnea wascarried out in 10%, HHT prevented a fatal decrease in SpO<sub>2</sub> andAPm, autoresuscitation occurred in 100% of cases. Based on the data obtained,it can be concluded that the combined effects of hypercapnia andhypoxia effectively contribute to increased tolerance to acute hypoxiain rats with LPS-induced endotoxemia.</p>

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The Effectiveness of Hypercapnic-Hypoxic Training to Increase Resistance to Acute Hypoxia in Rats with LPS-Induced Endotoxemia

  • Zh. A. Donina

摘要

Abstract

Severe sepsis (endotoxicosis), similar to cytokine storm,is aggravated by acute respiratory failure, hypotension, hypoxemiaand hypercapnia, which is the main cause of high mortality. Theaim of the work is to study the effectiveness of hypercapnic-hypoxictraining (HHT) for the relief of cardiorespiratory disorders andincreased tolerance to acute hypoxia in rats with LPS-induced endotoxicosis.The experiments were conducted on anesthetized male Wistar rats.Endotoxicosis was simulated by administration of LPS (Escherchia coli) 7 mg/kg. The assessmentof resistance to hypoxia was carried out by the rebreathing method(RM) with a gradual decrease in oxygen in the rebreather from 21%to the onset of apnea. 3 groups of animals were studied: I—control—NaCl,II—LPS, III—LPS+HHT. The following parameters were recorded: externalrespiration, mean blood pressure (APm.), saturation (SpO2),fraction of inhaled O2 (FiO2)and CO2 (FiCO2), timeof onset of apnea, the amount of spontaneous respiratory recovery(autoresuscitation) in the posthypoxic period. The LPS+HHT groupwas previously subjected to hypercapnic-hypoxic training. For thispurpose, the rebreather was filled with room air, the volume ofwhich was selected in such a way that during the breathing of the animalinto/out of the rebreather, FiO2 decreasedto 11 ± 0.5% for 3 minutes, and FiCO2 increasedto 5.0 ± 0.5%, after which the rat was switched to breathing air.The training regime consisted of 3 cycles: 3 min—HHT, 5 min—normoxia.It was found that the maximum decrease in resistance to acute hypoxia wasobserved in rats with LPS, respiratory recovery after apnea wascarried out in 10%, HHT prevented a fatal decrease in SpO2 andAPm, autoresuscitation occurred in 100% of cases. Based on the data obtained,it can be concluded that the combined effects of hypercapnia andhypoxia effectively contribute to increased tolerance to acute hypoxiain rats with LPS-induced endotoxemia.