[Results of December joint plenum of Russian Scientific Society of pathophysiology and Scientific Council on general pathology and Pathophysiology. New areas of research in the pathophysiology].

Contains information on the joint plenum of Russian scientific society of pathophysiology and Scientific Council on General Pathology and Pathophysiology, held 17-18 December 2014 in Moscow at the FSBSI "Institute of General Pathology and Pathophysiology".

[Respiratory movements of the facial musculature and respiration resistance]. / Dykhatel'nye dvizheniia litsevoi muskulatury i soprotivlenie dykhaniiu.

Experiments were made on tracheotomized anesthetized rabbits. After trachea occlusion the increase in the nostril discharges becomes more remarkable than that in the diaphragm discharges. In the tracheotomized animals, the air passes into the lungs through the trachea. Nevertheless the respiratory movements of the facial muscles are of importance in the compensation of abnormalities caused by the increased respiratory resistance. Prevention of the respiratory movements of the face muscles results in a drastic increase in the inspiratory discharges of the diaphragm.

[Biological significance of physiologic hypoxemia]. / O biologicheskom znachenii fiziologicheskoi gipoksemii.

Preliminary inhalation of oxygen in conscious rabbits prevents increased respiratory muscle activity caused by airway occlusion. This is accounted for by hyperoxia that removes physiological hypoxemia and therefore depresses the sensitivity of the respiratory center which is needed to perform the reflex caused by airway occlusion. This also explains that hyperoxia prevents respiratory discomfort caused by temporary stoppage of artificial respiration in persons with respiratory paralysis.

[Mechanism of rhythmic breathing during hypocapnia]. / O mekhanizme ritmicheskogo dykhaniia pri gipokapnii.

It has been established that passive hyperventilation does not evoke apnoea if the excitability of the respiratory center is preliminarily increased. Comparison of the experimental results with the literature data suggests that rhythmical respiration during hyperventilation hypocapnia is consequent on the increased sensitivity of the respiratory center to CO2 as a result of the development of hypocapnia.

Why do patients with respiratory muscle paralysis require artificial hyperventilation?

The primary reason for the need of hyperventilation in patients with respiratory paralysis is the insufficiency of the inhibitory Hering-Breuer reflex. The artificial distension of the lungs with normal tidal volume cannot inhibit the respiratory centre in contrast to the normal state.

Hyperventilation and inhibitory synapses.

Injection of a subconvulsive dose of strychnine (which blocked the inhibitory synapses) increases respiratory muscle activity evoked by stimulation of a sciatic nerve as well as by inhalation of hypercapnic gas mixture. Thus the inhibitory synapses prevent an excessive hyperventilation.

[Hyperventilation and inhibitory synapses]. / Giperventiliatsiia i tormoznye sinapsy.

Injection of subconvulsive doses of strychnine blocking the inhibitory synapses significantly increases the reflex activity of the respiratory muscle evoked by stimulation of the sciatic nerve as well as by inhalation of hypercapnic gas mixture. Thus the inhibitory synapses prevent the extreme hypocapnia evoked by hyperventilation.

[Representation of the phrenic nerve in the cerebral cortex]. / Predstavitel'stvo diafragmal'nogo nerva v kore bol'shikh polusharii.

Electrical stimulation of the phrenic nerve gives rise to early (with latency of 8--12 msec) and late (with latency of 30--40 msec) surface-positive potentials in the contralateral sensory-motor cortex of cats. The early potentials occur only in two discrete areas of the rostral part of the posterior sigmoid gyrus: just rostromedial to the post-cruciate dimple and at the lateral tip of the cruciate sulcus. In contrast to the early potentials, the late ones can be recorded not only from the whole surface of the posterior sigmoid gyrus but also from the anterior sigmoid gyrus. The early potentials presumably appear on stimulation of group I muscle afferents. It is possible that impulses reaching the cerebral cortex from the phrenic nerve participate in provocation of the sensation of breathlessness.

[Extravagal respiratory reflex from pulmonary nociceptors]. / Ekstravagal'nyi dykhatel'nyi refleks s notsitseptorov legkikh.

A restricted damage of the lung parenchyma before vagotomy evokes an increase of inspiratory discharges of the diaphragm and an increase of the rate of respiration. Similar damage in vagotomized animals evokes only an increase of inspiratory discharges. The rate of respiration does not alter at all or changes insignificantly. An increase of the depth of respiration evoked by the lung nociceptors innervated by the extravagal afferents is of great importance because the lung ventilation is best provided by deep respiration. Probably not only the afferent fibers of the vagus nerves, but also the extravagal lung afferents must be taken into consideration in analysis of the relationship between the rate and depth of lung ventilation, particularly under pathological conditions.

[Relative stability of the central mechanisms that determine the depth and frequency of respiration]. / Otnositel'naia ustoichivost' tsentral'nykh mekhanizmov, opredeliaiushchikh glubinu i chastotu dykhaniia.

Not only an intensified respiration, but also an increase in inspiratory discharges can be caused by hypercapnia in vagotomized cats. With the deepening of anesthesia an increase of the inspiratory discharges persists, whereas an increased frequency of respiration disappears. This testifies to the presence of two different central mechanisms for the regulation of the rate and depth of respiration; the first is subject to the suprabulbar influences more than the second.

Muscular respiratory receptors in self-regulation of normal breathing in man.

In man, in the process of evolution the proprioceptive reflexes from the chest muscle during apnea become weak. Probably the impulses from the respiratory stretch receptors do not take part in self-regulation of eupnea.