Artificial hypobiosis as a method of acute altitude illness negative impact reduction

Introduction. Critical stage of acute mountain (altitude) sickness, manifesting by loss of consciousness, convulsions, apnea and high risk of death, develops at altitudes above 8 km. Acute oxygen starvation of the central nervous system while significant hypobaric hypoxia is the main mechanism of critical stage of acute mountain sickness. Alpinists and professional guides, extreme athletes are the main risk group. It is proposed to reduce the level of metabolism (artificial hypobiosis induction) to prevent the negative impact of acute hypobaric hypoxia on central nervous system. The study aims to assess the efficiency of the metabolic rate reduction for the organism negative impact prevention while acute hypobaric hypoxia. Materials and methods. Study had 2 stages. The 1st - definition of the possibility of using artificial hypobiosis model. The 2nd - the model efficiency definition. Syrian hamsters 90-110 g weight were used in the study. 5 groups, 8 animals in each. Animals of two experimental groups (1 - on the 1st stage and 1 - is on the 2nd) had intramuscular injections of 1 g/kg Methyldopa (CAS Number 555-30-6). Animals control groups (1 - on the 1st stage and 2 - is on the 2nd) had 0,9% NaCl. Indirect calorimetry was performed on the 1st stage. Oxygen consumption and carbon dioxide elimination speed were measured in each animal group twice: before intramuscular injection and 3 hours after. Critical stage of acute mountain (altitude) sickness was performed on the 2nd stage. In 3 hours after intramuscular injection animals of each group had been placed in hypobaric chamber. 30 kPa underpressure for control group #1 animals and 20 kPa for control group #2 and experimental group animals, speed - 1,25 kPa/s. To avoid CO2 accumulation continuous chamber air flow was made. Continuous visual observation carried out. Consciousness, posture maintenance time, convulsive seizures, agonal breathing, and apnea were registered. Results. 1st stage. Experimental group animals’ mean base oxygen consumption speed was 4,04±0,3 ml/100 g/min, and 2,70±0,11 ml/100 g/min (p<0,01) after intramuscular injection., carbon dioxide elimination speed was 3,17±0,27 ml/100 g/min and 2,26±0,09 ml/100 g/min (p<0,01) respectively. Control group animals’ mean base oxygen consumption speed was 3,80±0,43 ml/100 g/min, and 3,88±0,37 ml/100 g/min after intramuscular injection, carbon dioxide elimination speed was 2,95±0,31 ml/100 g/min and 2,92±0,2 ml/100 g/min, respectively. 2nd stage. 20 kPa control group: since start of exposure the average animal posture maintenance time was 3±2 s, the first convulsion time - 20±3 s, the second convulsion - 56±5 s, agonal breath start - 52±9 s, apnea - 114±26 s. Consciousness absence in all animal was observed. Experimental group: none of the parameters is to register were observed. All animals had consciousness, actively restored their position, while chamber was tilted. The exposure lasted for 20 minutes. 30 kPa control group: 1 animal of 8 had convulsions on 56 s of 20-minute exposure. None of the parameters is to register were observed in other animals. All animals had consciousness, actively restored their position, while chamber was tilted. Conclusions. The effectiveness of lowering the metabolic rate for the prevention of loss of consciousness and the development of generalized convulsions in acute hypobaric hypoxia has been experimentally proven; in a state of artificial hypobiosis, the time of safe stay in a hypoxic environment increases by more than 20 times. Ethics. The study was carried out in accordance with the ethical principles of the Declaration of Helsinki. The Clinical Study Protocol was reviewed at a meeting of the local Ethics Committee FSBSI IRIOH.