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The ventilatory response to isocapnic hypoxia was studied using rebreathing techniques in anesthetized and tracheostomized rats both in supine and in head-down tilt position (HDT-30 degrees). Hypoxic responses were calculated by the slope of ventilation against end tidal P(A)O2. The end-tidal P(A)CO2 was kept constant by varying expired gas flow through a CO2-absorbing bypass. The rebreathing was continued until P(A)O2 had fallen to between 70 +/- 3 and 50 +/- 2 mm Hg. The obtained results demonstrated that the maximal minute lung ventilation was 269 +/- 30 % during rebreathing test in supine position and 117 +/- 21% in the head-down tilt. It was also shown that the slopes of the relationship between minute ventilation and the decrease of end tidal P(A)O2 was 3-fold greater in supine than in HDT. The body position seems to affect the ventilatory response to isocapnic progressive hypoxia. In general, it may be a result of hemodynamic conditions alteration which increased respiratory resistive loads, changed the functional condition of carotid hemoreceptors and baroreceptor activity that modulate ventilatory response to chemoreceptor stimulation.

The role of lung receptors in respiratory control during acute head-down tilt (AHDT, -30 degrees) was investigated in anesthetized, tracheostomized rats. The results show that AHDT increased the mechanical respiratory load, slowed inspiratory flow, reduced the end expiratory lung volume, tidal volume and minute ventilation. On the other hand, during AHDT a significant rise in inspiratory swings of oesophageal pressure was recorded indicated a compensatory increase in inspiratory muscle contraction force. These effects were reduced after transaction of the vagus nerve. It was also shown that respiratory response on added mechanical load was reduced during AHDT as compared with the value in horizontal position. This deference disappeared after vagotomy. The data obtained suggested that afferent information from lung receptors take part in compensation of respiratory effects of AHDT. The cause of reduction in respiratory response to loading during AHDT involves weakness of lung reflexes evoked by volume changes.

The focus was placed on the physiological mechanisms of correction of the blood redistribution during the head-down tilt (HDT) with a discrete or complex use of the methods of negative pressure respiration (NPR) and lower body negative pressure (LBNP). It was evidenced that rise in the intracranial hydrostatic pressure in HDT (-6 degrees) can be compensated by NPR within a range of -10 to -15 cm of water column causing decrease in the intrasternal pressure from -5.04 to -7.74 cm w.c. Bioimpedance and ultrasonic investigations led to the conclusion that the decreased transpulmonary pressure is responsible for blood outflow from the intracranial venous system till the level adequate to the horizontal position of the body. The results were verified in experiments with unconscious cats: pressure in the exterior jugular vein and v. cava superior during HDT (-30 degrees) with NRP at -5 cm w.c. decreased by 3.2. and 4.3. w.c., respectively. Experiments with human subjects also demonstrated that the complex use of NPR and LBNP produces an additive hemodynamic effect and can be considered a new method for correcting the adverse consequences of redistribution of the local blood volumes toward the head end.

Abdominal and thoracic functional reserves of respiration and level of their involvement in spontaneous breathing were investigated in 10 male volunteers aged 20 to 22 put in horizontal head-down (-7 degrees and -30 degrees) or orthostatic (+70 degrees) position. The thoracic-abdominal functional reserves of respiration dependent on the spatial positioning of the body were found to be the factor that determines magnitude of contribution of the thorax and diaphragm in the breathing volume.

In anaesthetised cats, antiorthostatic posture of the body with an inclination angle of 30 degrees increased pressure in the vena cava superior and in jugular vein. The rest of the cardio-respiratory parameters were changed insignificantly. Physical and physiological mechanisms of the blood regional redistribution in alteration of the body gravitation orientation, are discussed.

To improve methods of offsetting the hemodynamic shifts in microgravity, applicability of breathing at negative pressure (BNP, pressure relief by -5.0 cm of water column) during inspiration and expiration was assessed in acute experiments with unconscious cats tilted head-down (-30 degrees). Direct measurement of pressure in v. cava superior and v. jugularis externa using a catheter revealed a concurrent significant (p < 0.05) growth of the parameter which should be considered a sign of impeded venous outflow from the craniocervical vessels. BNP added to the sucking effect of the thoracic cavity (the siphoning effect) and led to more massive venous outflow from cephalic vessels as evidenced by pressure drop in the jugular vein and v. cava superior to the values determined in the basic horizontal position. However, BNP did not significantly alter arterial hemodynamics, respiration pattern or gas exchange. Data of the investigation attest effectiveness of this method of moderating blood flow to the cat's head during HDT and possibility to apply it in the zero-g environment.

This is an overview of investigations performed in actual and simulated flights to study the effects of microgravity and acceleration, space cabin and space suit artificial atmosphere on the respiratory function. The conceptual prediction of the effects that the space environment produces on the respiratory system suggests the following changes in respiration, gas exchange, and acid-base equilibrium: respiration biomechanics; gas diffusion and ventilation-perfusion ratios in the lungs; regulation of respiration and function of respiratory muscles; lung hydration and blood filling; respiratory changes in acid-base equilibrium and blood gases. Besides, the combined effect of microgravity, acceleration, low barometric pressure and modified gas composition may cause lung atelectases and concomitant disorders in pulmonary ventilation and gas exchange. These changes may have an adverse effect on the health condition and physical work capacity.

Time course variations in the ventilation and gas exchange functions of the lungs, gas composition and acid-base equilibrium of blood were investigated in 22 male test subjects, aged 27-49 years, who were kept in the head-down position (-8 degrees) and rocked in parallel swings. The subjects susceptible to motion sickness developed lung hyperventilation and concomitant alveolar-arterial hypocapnia and respiratory alkalosis which may potentiate a symptom-complex of vestibular disorders. To control hypocapnia, the subjects used a hypercapnic breathing mixture (4% CO2, 96% air). This eliminated the above changes in the gas composition and acid-base equilibrium of blood, and in 7 out of 10 subjects alleviated vestibular symptoms and elongated the time of motion tolerance. In addition, the prophylactic effect of hypercapnic exposure showed individual variations which seem to be associated with individual sensitivity of the respiratory center to hypercapnic stimulation.

The effect of accelerations of different value and duration combined with air or pure oxygen breathing on the pulmonary function was investigated in centrifugation experiments on six healthy male test subjects, aged 20--23. The dynamics of the emergence and back development of the respiratory syndrome induced by the combined effect of acceleration and pure oxygen breathing, its symptoms, spyrographic and roentgenologic components were studied. It was demonstrated that both the value and duration of acceleration played a certain role in the pathogenesis of functional disorders of the respiratory system and atelectasis; however, the time factor exerted the major effect on their development.

In 12 healthy male test subjects, aged 18--35, respiratory characteristics during talking at rest and when doing static exercises were studied by simultaneous recording of their pneumotachograms, integrated spirograms and transpulmonary intrathoracic pressures. By building pressure-volume curves for lungs and correcting them for transpulmonary pressure, variations in the pressure under the vocal cords when saying a standardized phrase were determined as related to the exercise level. The relationship between the rate and volume parameters of pulmonary ventilation and airway resistance during talking, on the one hand, and the level of exercises, on the other, was established.

The effect of gravitation +Gz (2-8 Gz, 5 min) combined with air or pure oxygen breathing on the lung volume and expiratory airway closure was studied in 9 subjects. It was demonstrated that lung atelectasis induced by oxygen breathing causes restriction of lung ventilation and obstruction of the peripheral airways. The authors discuss the effect of restrictive and obstructive disorders of lung ventilation on gas exchange and development of circulatory hypoxia during acceleration.

A study was performed on 8 healthy male subjects to investigate the effect of nonelastic resistance 6-40 GPa (the air flow velocity being 90 l/min) on the duration of proprioceptive reflexes of respiratory muscles, volume and velocity parameters of forced exhalation. Resistances of 15 and 25 GPa combined with a workload of 100-150 W increased the duration of proprioceptive reflexes from 0.18 +/- 0.015 to 0.29 +/- 0.012 sec and to 0.38 +/- 0.06 sec, respectively, which indicates fatigue of respiratory muscles. Resistance of 25 GPa reduced significantly (by 55%) the maximum volume velocity of forced exhalation and increased its duration by 31%, the exhalation volume decreasing insignificantly (by 6%). The major factor limiting man's tolerance to external respiration resistance is functional deficiency of proprioceptive regulation of respiration and strength and velocity of respiratory muscles.