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Biomedical subjects

S I Frankshteĭn

Publications and source records attributed to S I Frankshteĭn.

At least 19 recordsLinked to original sources
PubMed1986

[Effect of cerebral hypoxia and hyperventilation hypocapnia on the epileptiform activity of the cerebral cortex of the cat].

Influence of cerebral hypoxia and hyperventilatory hypocapnia on the ECoG and focal epileptiform activity of the cerebral cortex induced with local application of strychnine was studied in cats with transection of spinal cord at C1. Although both hypoxia and hypocapnia produced synchronization of the cerebral cortex electrical activity, i.e. exerted the same effects on the ECoG, their influence on cortical excitability was quite different: hypoxia suppressed the epileptiform activity whereas hypocapnia facilitated it.

Animals↗
PubMed1986

[Mechanism of hyperventilation in exertion (an uncommon factor)].

Electrical stimulation of the corticospinal tract increases the excitability of the phrenic motoneurons directly. As a result the responses of these motoneurons to the impulses from the respiratory centre are facilitated. Until now there were attempts to explain exercise hyperpnea by increasing the activity of the respiratory centre. The experiments permit to suppose that the hyperpnea may be produced by facilitatory action of the corticospinal tract on the respiratory motoneurons, i.e. independently from the respiratory centre.

Animals↗
PubMed1985

[Mechanism of the protopathic nature of visceral pains].

Experiments on decerebrated cats and rabbits have shown that local nociceptive stimulation (mechanical pressure and burns) of internal organs causes no reflex responses of the motor system. It is suggested that internal organs are either absolutely devoid of or lack specific nociceptors. Insufficiency of inhibitory mechanisms may account for protopathic nature of visceral pain.

Abdomen↗
PubMed1982

[Respiratory movements of the facial musculature and respiration resistance].

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.

Airway Resistance↗
PubMed1981

[Biological significance of physiologic hypoxemia].

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.

Animals↗
PubMed1980

[Mechanism of rhythmic breathing during hypocapnia].

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.

Animals↗
PubMed1980

[Role of the pyramidal tract in the mechanism of dyspnea and hyperventilation].

Hypoxia evoked by mechanical asphyxia first of all disturbs the generation of potentials in pyramidal tract neurons. Hypoxic work, therefore, causes inadequate contraction of somatic muscles, a difficulty in work performance and respiratory discomfort. Concurrently, the disturbance of the pyramidal tract disinhibits the respiratory center of the brain stem with a result of excessive hyperventilation during hypoxic work.

Afferent Pathways↗
PubMed1979

[Hyperventilation and inhibitory synapses].

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.

Animals↗
PubMed1978

[Relative stability of the central mechanisms that determine the depth and frequency of respiration].

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.

Animals↗
PubMed1978

[Representation of the phrenic nerve in the cerebral cortex].

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.

Animals↗
PubMed1975

[Nature of rhythmic discharges in ventral spinal cord roots].

Rhythmic "locomotor discharges" recorded in the ventral spinal roots by Perret et al proved to increase during asphyxia and disappeared during apnea. Thus, rhythmic discharges in the ventral spinal roots depended on irradiation from the respiratory centre and could not confirm the fact of existence of a special "locomotor pacemaker".

Animals↗