Gas preparation with anti-hypoxia effect and application thereof

Abstract

The invention discloses a gas preparation with an anti-hypoxia effect and application of the gas preparation, the gas preparation is obtained by taking normal-pressure air as diluent gas, introducing a small amount of NO and CO2 into the diluent gas to respectively reach corresponding final concentrations, the concentration of the NO is 10-30 ppm, and the concentration of the CO2 is 400-700 ppm. The gas preparation can effectively relieve hypoxia symptoms, and is quick in response, good in effect, wide in applicable crowd and free of side effects. Animal experiments prove that after the NO gas and the CO2 gas are mixed, lipid peroxidation caused by oxidative stress can be inhibited, and the activity of an antioxidant enzyme system of an organism is maintained, so that the NO gas and the CO2 gas are proved to have an anti-hypoxia effect after being mixed.

Description

Technical Field

[0001] The invention relates to a gas preparation with anti-hypoxia effect and application thereof. Background Art

[0002] Hypoxia refers to a condition in which the oxygen content in the environment drops below normal, resulting in a lack of adequate oxygen supply to various tissues and organs in the body. Oxygen plays a vital role in the life activities of humans and most animals. It is an indispensable resource for cellular respiration and supports normal metabolism and cell function. Therefore, hypoxia can cause a range of health problems, ranging from mild dizziness and fatigue to more serious symptoms such as increased heart stress, impaired brain function, and even, in extreme cases, permanent brain damage or death.

[0003] Currently, there are no specific drugs that can directly treat hypoxia in clinical practice. Other methods are mainly used to relieve the symptoms of hypoxia, such as physical oxygen production, chemical oxygen production, and liquid oxygen treatment. Physical oxygen production can only provide additional oxygen supplementation and cannot directly improve pulmonary blood flow or gas exchange processes. Higher concentrations of oxygen may be required, and long-term use may cause oxygen poisoning. Chemical oxygen production is usually used to provide oxygen for a short period of time. Its effect is short-lived and cannot maintain an efficient oxygen supply for a long time. Liquid oxygen provides additional oxygen, but cannot directly enhance respiratory drive or improve oxygen exchange efficiency. Therefore, it is necessary to find a simpler, non-toxic, and easy-to-implement treatment method. Summary of the Invention

[0004] In view of the above technical problems existing in the prior art, the purpose of this application is to provide a gas preparation with anti-hypoxia effect and its application. The gas formulation of the present invention can quickly relieve hypoxia symptoms with minimal side effects and obvious effects.

[0005] The technical solution adopted in the present invention is as follows:

[0006] A gas preparation with an anti-hypoxia effect, wherein the NO concentration of the gas preparation is 10-30 ppm and the CO2 concentration is 400-700 ppm under normal pressure.

[0007] Furthermore, the gas preparation has a NO concentration of 20 ppm±2 ppm and a CO2 concentration of 500 ppm±20 ppm at normal pressure.

[0008] Furthermore, the gas preparation of the present invention is prepared by using atmospheric pressure air as the diluent gas, into which a small amount of NO and CO2 are introduced to achieve corresponding final concentrations.

[0009] The present invention also provides the use of the gas preparation in anti-hypoxia. When used, the gas preparation of the present invention is filled into the nasal cavity or oral cavity of a human body.

[0010] According to the application of the present invention, the mixture of NO gas and CO2 gas in the gas preparation can prolong the survival time of an individual in an oxygen-deficient environment, such as in a closed environment or under conditions caused by poisoning.

[0011] According to the application of the present invention, in an oxygen-deficient environment, the NO gas and CO2 gas mixture can increase SOD activity and reduce MDA content.

[0012] According to the application of the present invention, in an oxygen-deficient environment, the NO gas and CO2 gas mixture can improve T-AOC capacity, GSH-Px activity and CAT activity.

[0013] According to the application of the present invention, in an oxygen-deficient environment, the NO gas and CO2 gas mixture can reduce LDH activity and increase ATP content.

[0014] The present invention has found that the NO gas and CO2 gas mixture in the gas preparation can inhibit lipid peroxidation caused by oxidative stress, maintain the activity of the body's antioxidant enzyme system, and thus improve the body's hypoxia tolerance.

[0015] The present invention has found that the NO gas and CO2 gas mixture in the gas preparation can optimize the cell metabolic pathway and improve the efficiency of ATP synthesis, thereby enhancing the body's energy supply capacity in an oxygen-deficient environment and maintaining the stability of organ function.

[0016] The present invention also provides application of the gas preparation in resisting sodium nitrite poisoning.

[0017] The present invention also provides application of the gas preparation in acute cerebral ischemic hypoxia.

[0018] Compared with the prior art, the present invention has the following beneficial effects:

[0019] 1) In the gas preparation described herein, NO improves pulmonary blood flow distribution by dilating pulmonary blood vessels, while CO2 enhances oxygen exchange by promoting respiratory drive. This combined NO and CO2 mixture not only increases oxygen uptake efficiency but also directly improves pulmonary gas exchange and hemodynamics, making it particularly suitable for alleviating symptoms of hypoxia or altitude sickness. It also has minimal side effects, a rapid response, and a significant effect.

[0020] 2) The gas preparation described herein can effectively alleviate symptoms of hypoxia with rapid response, excellent efficacy, broad applicability, and no side effects. Animal experiments have demonstrated that a mixture of NO and CO₂ can inhibit lipid peroxidation caused by oxidative stress and maintain the activity of antioxidant enzymes, demonstrating the anti-hypoxic effect of a NO and CO₂ mixture.

[0021] 3) The gas preparation described in this invention can effectively alleviate the symptoms of hypoxia with rapid response, good efficacy, broad applicability, and no side effects. Animal experiments have demonstrated that a mixture of NO and CO₂ can optimize cellular metabolic pathways and increase ATP synthesis efficiency, thereby enhancing the body's energy supply capacity in hypoxic environments and maintaining stable organ function, thus demonstrating the anti-hypoxic effect of a NO and CO₂ mixture. BRIEF DESCRIPTION OF THE DRAWINGS

[0022] Figure 1 The effect of different contents of NO gas and CO2 gas mixture on the survival time of mice under normobaric hypoxia (x±s, n=10);

[0023] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P < 0.01;

[0024] Figure 2 The effect of different contents of NO gas and CO2 gas mixture on the survival time of mice poisoned by sodium nitrite (x±s, n=10);

[0025] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P < 0.01;

[0026] Figure 3 The effect of different contents of NO gas and CO2 gas mixture on the survival time of mice with acute cerebral ischemia and hypoxia (x±s, n=10);

[0027] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P < 0.01;

[0028] Figure 4 Effects of different NO and CO2 gas mixtures on SOD activity in lung tissue of normobaric hypoxic mice (x±s, n=10);

[0029] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P < 0.01;

[0030] Figure 5Effects of different NO and CO2 gas mixtures on MDA content in lung tissue of normobaric hypoxic mice (x±s, n=10);

[0031] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P < 0.01;

[0032] Figure 6 Effects of different NO and CO2 gas mixtures on T-AOC capacity in the brain tissue of normobaric hypoxic mice (x±s, n=10);

[0033] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P < 0.01;

[0034] Figure 7 Effects of different NO and CO2 gas mixtures on GSH-Px activity in brain tissue of normobaric hypoxic mice (x±s, n=10);

[0035] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P < 0.01;

[0036] Figure 8 Effects of different NO and CO2 gas mixtures on CAT activity in brain tissue of normobaric hypoxic mice (x±s, n=10);

[0037] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P<0.01.

[0038] Figure 9 Effects of different NO and CO2 gas mixtures on LDH activity in brain tissue of normobaric hypoxic mice (x±s, n=10);

[0039] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P<0.01.

[0040] Figure 10Effects of different NO and CO2 gas mixtures on ATP content in brain tissue of normobaric hypoxic mice (x±s, n=10);

[0041] Compared with the Control group, *P<0.05, **P<0.01; compared with the 20ppm NO group, # P<0.05, ## P<0.01. DETAILED DESCRIPTION

[0042] The present invention will be further described below with reference to specific embodiments, but the protection scope of the present invention is not limited thereto.

[0043] Example 1:

[0044] By establishing different hypoxia models, the effects of NO gas and CO2 gas mixture on the survival time of mice in different hypoxia models were observed. The anti-hypoxic effect of NO gas and CO2 gas mixture on mice in hypoxic environment was preliminarily evaluated from the overall level of mice, and the anti-hypoxic effect of NO gas and CO2 gas mixture was investigated.

[0045] (1) Experimental groups and methods

[0046] 1.1 Experimental animals

[0047] 150 SPF KM mice (purchased from Shanghai Slake Laboratory Animal Co., Ltd.) weighing approximately 36-40 g were used.

[0048] 1.2 Experimental Grouping

[0049] The raised mice were randomly divided into Control group, 20ppm NO group, 20ppm NO+CO2 group, 40ppm NO+CO2 group, and 60ppm NO+CO2 group, with 30 mice in each group.

[0050] The mice in the 20 ppm NO group were cultured in a culture chamber with an oxygen concentration of air at normal pressure and a NO gas concentration of 20 ppm. That is, the atmosphere in the culture chamber was a mixed gas formed by introducing NO gas with a final concentration of 20 ppm into normal pressure air.

[0051] Mice in the 20ppm NO+CO2 group were cultured in a culture chamber with an oxygen concentration of normal pressure air, a NO gas concentration of 20ppm, and a CO2 gas concentration of 500ppm. That is, the atmosphere in the culture chamber was composed of normal pressure air with the introduction of NO gas with a final concentration of 20ppm and an additional small amount of CO2 gas, so that the final concentration of the CO2 component in the mixed gas was 500ppm.

[0052] Mice in the 40ppm NO+CO2 group were placed in a chamber containing atmospheric air at atmospheric pressure, 40ppm NO, and 500ppm CO2. Specifically, the chamber atmosphere consisted of atmospheric air with a final concentration of 40ppm NO and a small amount of CO2 introduced into the mixture, resulting in a final CO2 concentration of 500ppm.

[0053] Mice in the 60ppm NO+CO2 group were placed in a chamber containing atmospheric air at atmospheric pressure, 60ppm NO, and 500ppm CO2. Specifically, the chamber atmosphere consisted of atmospheric air with a final concentration of 60ppm NO and a small amount of CO2 introduced into the mixture, resulting in a final CO2 concentration of 500ppm.

[0054] All four groups of mice were cultured in the chamber for 7 consecutive days, 8 hours per day. The mice in the control group were raised in a normal environment, that is, in an atmosphere of normal pressure.

[0055] 1.3 Experimental methods

[0056] One hour after the last ventilation culture, 10 mice from each group were randomly selected and placed in 250-mL wide-mouth bottles. Filter paper and 5 g of soda lime were placed in the bottles to absorb moisture and carbon dioxide. The bottle caps were tightened to ensure an airtight seal. The time was immediately counted. The cessation of the last respiratory cessation of the mouse (the mouse suddenly went limp after struggling and twitching, and the chest no longer rose and fell) was considered the sign of death. The survival time of the mice in normal pressure, airtight hypoxia was observed and recorded.

[0057] One hour after the last aeration culture, 10 mice were randomly selected from each group for a sodium nitrite poisoning survival experiment. Each mouse was intraperitoneally injected with 220 mg / kg / body weight of sodium nitrite solution. The mice were immediately timed and death was marked by respiratory arrest. Survival time was then recorded.

[0058] One hour after the last ventilation culture, 10 mice were randomly selected from each group for acute cerebral ischemia-hypoxia experiment. The head of each mouse was quickly cut off with scissors, and the time of open mouth breathing after decapitation was recorded.

[0059] (2) Conclusion

[0060] 2.1 Analysis of atmospheric pressure closed hypoxia experiment

[0061] Ten mice were randomly selected from each group for the closed hypoxia experiment, and the hypoxia model of each mouse was established. The survival time of the mice under hypoxia was analyzed by monitoring the anti-hypoxia time (Table 1). The results of the effects of different NO gas and CO2 gas mixtures on the survival time of mice under normal pressure hypoxia can be found in Figure 1 .

[0062] The researchers found that compared with untreated normobaric hypoxic mice in the control group, mice in the 20ppm NO, 20ppm NO+CO2, 40ppm NO+CO2, and 60ppm NO+CO2 groups were able to prolong their survival time under normobaric hypoxia. The survival extension rates of the 20ppm NO, 20ppm NO+CO2, and 40ppm NO+CO2 groups were 33.27%, 45.43%, and 7.72%, respectively (p < 0.01). Furthermore, the survival extension rate of the 20ppm NO+CO2 group was significantly higher than that of the 20ppm NO group by 9.12% (p < 0.01). The survival extension rate of the 60ppm NO+CO2 group was 1.99% (p > 0.05). This indicates that a mixture of NO and CO2 can prolong survival time under normobaric hypoxia and has a certain ability to resist hypoxia.

[0063] Table 1 Effects of different NO and CO2 gas mixtures on the survival time of mice under normal pressure and hypoxia (x±s, n=10)

[0064]

[0065] Note: Compared with the Control group, * P<0.05, ** P<0.01; compared with 20ppm NO group, # P<0.05, ## P<0.01

[0066] 2.2 Analysis of sodium nitrite poisoning experiments

[0067] The results of the sodium nitrite poisoning experiment are summarized in Table 2. The results of the effects of different NO gas and CO2 gas mixtures on the survival time of mice poisoned by sodium nitrite can be found in Figure 2 .

[0068] The results showed that compared with the untreated control group, the survival time of mice in the 20ppm NO and 20ppm NO+CO2 groups was significantly prolonged under nitrite poisoning, with extension rates of 25.51% and 35.59%, respectively (p < 0.01). The survival extension rate of mice in the 20ppm NO+CO2 group was significantly higher than that of the 20ppm NO group by 8.03% (p < 0.01). The survival extension rate of mice in the 40ppm NO+CO2 group under nitrite poisoning was 9.18% (p < 0.05), and the survival extension rate of mice in the 60ppm NO+CO2 group under sodium nitrite poisoning was 1.99% (p > 0.05). This indicates that a mixture of NO gas and CO2 gas can prolong the survival time of mice suffering from sodium nitrite poisoning and hypoxia.

[0069] Table 2 Effects of different NO and CO2 gas mixtures on the survival time of mice poisoned by sodium nitrite (x±s, n=10)

[0070]

[0071] Note: Compared with the Control group, * P<0.05, ** P<0.01; compared with 20ppm NO group, # P<0.05, ## P<0.01

[0072] 2.3 Experimental analysis of acute cerebral ischemia and hypoxia

[0073] The results of the acute cerebral ischemia and hypoxia experiments are summarized in Table 3. The effects of different NO and CO2 gas mixtures on the survival time of mice with acute cerebral ischemia and hypoxia can be found in Table 3. Figure 3 .

[0074] Compared with the control group, the survival time of mice in the 20ppm NO group and 20ppm NO+CO2 group under acute cerebral ischemia and hypoxia was significantly prolonged, with extension rates of 11.19% and 20.65%, respectively (p < 0.01). The survival time of mice in the 40ppm NO+CO2 group under acute cerebral ischemia and hypoxia was extended by 5.71% (p < 0.05). The survival time of mice in the 60ppm NO+CO2 group under acute cerebral ischemia and hypoxia was extended by 2.62% (p > 0.05). Compared with the mice in the 20ppm NO group with acute cerebral ischemia and hypoxia, the survival rate of the mice in the 20ppm NO+CO2 group was significantly increased by 8.51% (p < 0.01). The survival time of the mice in the Control group and the 60ppm NO+CO2 group under acute cerebral ischemia and hypoxia was significantly decreased (p < 0.05). The experimental results show that inhalation of a mixture of NO and CO2 can prolong the survival time of mice with acute cerebral ischemia and hypoxia.

[0075] Table 3 Effects of different NO and CO2 gas mixtures on the survival time of mice with acute cerebral ischemia and hypoxia ( n=10)

[0076]

[0077] Note: Compared with the Control group, * P<0.05, ** P<0.01; compared with 20ppm NO group, # P<0.05, ## P<0.01

[0078] Example 2: Study on the effects of NO and CO2 gas mixture on oxidative stress in normobaric hypoxic mice

[0079] (1) Experimental groups and methods

[0080] 1.1 Experimental animals

[0081] A total of 50 SPF KM mice (purchased from Shanghai Slake Laboratory Animal Co., Ltd.) were used, weighing approximately 36-40 g.

[0082] 1.2 Experimental Grouping

[0083] Mice were randomly divided into a control group, a 20 ppm NO group, a 20 ppm NO+CO2 group, a 40 ppm NO+CO2 group, and a 60 ppm NO+CO2 group, with 10 mice in each group. Mice in the 20 ppm NO group were cultured in a chamber containing 20 ppm NO at normal pressure; mice in the 20 ppm NO+CO2 group were cultured in a chamber containing 20 ppm NO at normal pressure; mice in the 40 ppm NO+CO2 group were cultured in a chamber containing 40 ppm NO at normal pressure; and mice in the 60 ppm NO+CO2 group were cultured in a chamber containing 500 ppm CO2 at normal pressure. All four groups of mice were cultured in the chambers for 7 consecutive days, 8 hours per day. The control group was housed in a normal environment.

[0084] 1.3 Experimental methods

[0085] After the five groups of mice completed the closed hypoxia experiment, the brain tissue of each group of mice was taken to measure the MDA content, T-AOC capacity, GSH-Px activity, CAT activity, and SOD activity in the brain tissue of each mouse.

[0086] (2) Results

[0087] like Figure 4 As shown in the figure, compared with the control group, the SOD activity in the brain tissue of mice in the 20ppm NO group, 20ppm NO+CO2 group, 40ppm NO+CO2 group, and 60ppm NO+CO2 group increased after normobaric hypoxia. Among them, the SOD activity in the brain tissue of mice in the 20ppm NO+CO2 group increased significantly after normobaric hypoxia (p < 0.01), and the corresponding SOD activity increased by 13.82%. Figure 5 As shown in the results, the MAD content in the brain tissue of mice in the 20ppm NO group, 20ppm NO+CO2 group, 40ppm NO+CO2 group and 60ppm NO+CO2 group decreased after normobaric hypoxia. Compared with the Control group, the MAD content in the brain tissue of mice in the 20ppm NO group and 20ppm NO+CO2 group decreased extremely significantly (p < 0.01).

[0088] like Figure 6As shown, compared with the Control group that did not receive any treatment, the T-AOC capacity in the brain tissue of mice in the 20ppm NO group, 20ppm NO+CO2 group, 40ppm NO+CO2 group and 60ppm NO+CO2 group was significantly improved after normobaric hypoxia (p < 0.01), and the corresponding T-AOC capacity increased by 47.32%, 85.93%, 56.72% and 43.15%, respectively. Compared with the 20ppm NO group, the T-AOC capacity in the brain tissue of normobaric hypoxic mice in the 20ppm NO+CO2 group was significantly improved (p < 0.01), specifically increased by 26.21%. Figure 7 As shown, compared with the Control group without any treatment, the GSH-Px activity in the brain tissue of mice in the 20ppm NO group, 20ppm NO+CO2 group, 40ppm NO+CO2 group and 60ppm NO+CO2 group increased by 37.96%, 60.53%, 45.95% and 5.57%, respectively. Among them, the GSH-Px activity in the brain tissue of mice in the 20ppm NO+CO2 group and 40ppm NO+CO2 group increased extremely significantly (p < 0.01).

[0089] like Figure 8 As shown in the results, compared with the CAT activity of the Control group mice that did not receive any treatment, the CAT activity of the 20ppm NO group, 20ppm NO+CO2 group, 40ppm NO+CO2 group and 60ppm NO+CO2 group were all higher than that of the Control group, increasing by 27.49%, 41.01%, 11.93% and 8.84% respectively. Among them, the CAT activity in the brain tissue of the mice in the 20ppm NO+CO2 group was extremely significantly increased (p < 0.01).

[0090] The above experiment found that the mixture of NO gas and CO2 gas has an anti-hypoxia effect, which can improve the body's ability to resist oxidative stress by enhancing the activity of T-AOC, CAT, SOD, and GSH-PX in the body and reducing the content of MDA in the body, thereby enhancing the body's anti-hypoxia ability.

[0091] Example 3: Study on the Effect of NO and CO2 Gas Mixture on Energy Metabolism in Normal Pressure Hypoxic Mice

[0092] (1) Experimental groups and methods

[0093] 1.1 Experimental animals

[0094] A total of 50 SPF KM mice (purchased from Shanghai Slake Laboratory Animal Co., Ltd.) were used, weighing approximately 36-40 g.

[0095] 1.2 Experimental Grouping

[0096] Mice were randomly divided into a control group, a 20 ppm NO group, a 20 ppm NO+CO2 group, a 40 ppm NO+CO2 group, and a 60 ppm NO+CO2 group, with 10 mice in each group. Mice in the 20 ppm NO group were cultured in a chamber containing 20 ppm NO at normal pressure; mice in the 20 ppm NO+CO2 group were cultured in a chamber containing 20 ppm NO at normal pressure; mice in the 40 ppm NO+CO2 group were cultured in a chamber containing 40 ppm NO at normal pressure; and mice in the 60 ppm NO+CO2 group were cultured in a chamber containing 500 ppm CO2 at normal pressure. All four groups of mice were cultured in the chambers for 7 consecutive days, 8 hours per day. The control group was housed in a normal environment.

[0097] 1.3 Experimental methods

[0098] After the five groups of mice completed the closed hypoxia experiment, the brain tissue of each group of mice was taken to measure the ATP content and LDH activity in the brain tissue of each mouse.

[0099] (2) Results

[0100] like Figure 9 As shown in the results, compared with the Control group, the LDH activities in the brain tissues of mice in the 20ppm NO group and the 20ppm NO+CO2 group decreased by 20.95% and 28.07%, respectively, with extremely significant differences (p < 0.01); while the LDH activities in the brain tissues of mice in the 40ppm NO+CO2 group and the 60ppm NO+CO2 group were significantly higher than those in the 20ppm NO group and close to those in the Control group (p < 0.01); Figure 10 As shown in the data, compared with the Control group, the ATP content in the brain tissue of mice in the 20ppm NO group and the 20ppm NO+CO2 group increased by 66.95% and 53.90%, respectively, and the differences were extremely significant (p < 0.01). However, the ATP content in the brain tissue of mice in the 40ppm NO+CO2 group and the 60ppm NO+CO2 group was significantly lower than that in the 20ppm NO group, and was close to that in the Control group (p < 0.01).

[0101] The above experiment found that the mixture of NO gas and CO2 gas has an anti-hypoxic effect. It can enhance the body's energy supply capacity in an oxygen-deficient environment and maintain the stability of organ function by reducing the activity of LDH in the body and increasing the content of ATP in the body.

[0102] The contents described in this specification are merely an enumeration of implementation forms of the inventive concept, and the protection scope of the present invention should not be considered as being limited to the specific forms described in the embodiments.

Claims

1. A gas preparation with anti-hypoxia effect, characterized in that The gas preparation has an NO concentration of 10-30 ppm and a CO2 concentration of 400-700 ppm under normal pressure.

2. A gas preparation with anti-hypoxia effect according to claim 1, characterized in that The gas preparation has a NO concentration of 20 ppm±2 ppm and a CO2 concentration of 500 ppm±20 ppm at normal pressure.

3. A gas preparation with anti-hypoxia effect according to claim 1, characterized in that The gas preparation is prepared by using atmospheric pressure air as a diluent gas, into which a small amount of NO and CO2 are introduced to achieve corresponding final concentrations.

4. Use of the gas preparation according to claim 1 in combating hypoxia.

5. The use of the gas preparation according to claim 4 in anti-hypoxia, characterized in that The gas preparation inhibits lipid peroxidation caused by oxidative stress and maintains the activity of the body's antioxidant enzyme system, thereby improving the body's hypoxia tolerance.

6. Use of the gas preparation according to claim 4 in anti-hypoxia, characterized in that The gas preparation improves the ATP synthesis efficiency by optimizing the cell metabolic pathway, thereby enhancing the body's energy supply capacity in an oxygen-deficient environment and maintaining the stability of organ functions.

7. Use of the gas preparation according to claim 1 in resisting sodium nitrite poisoning.

8. Use of the gas preparation according to claim 1 in acute cerebral ischemic hypoxia.

Images