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Biomedical subjects

A M Gurvich

Publications and source records attributed to A M Gurvich.

At least 19 recordsLinked to original sources
PubMed1994

[The neurology of terminal states].

The paper gives a theoretical justification of CNS abnormality developing in patients who have a history of critical and terminal states, including clinical death. The most significant abnormality is that which is termed posthypoxic and/or postresuscitation encephalopathies whose nature has not been elucidated particularly at the cellular and molecular levels. It is emphasized that this involves brain abnormalities, which is a sequela of hypoxia or ischemia of systemic origin, rather than primary brain damages. In some patients who have sustained a severe hypoxic episode of any nature and recovered their psychoneurological status ever rapidly and rather fully, there may be an abrupt progressive deterioration of their neurological status in some days or months, which results in death or grave irreversible disability. It is concluded that not only do reparative and compensatory processes occur, but also there are phenomena of progressive degenerative changes in a primarily successfully resuscitated person or experimental animal in the central nervous system in the postresuscitation period. A classification of psychoneurological disorders in patients in the early postresuscitation period has been made and ways of their prevention or alleviation have been indicated.

Central Nervous System↗
PubMed1992

[Changes in the glial condition in different sections of the rat brain after stopping the systemic circulation].

The effect of ischemia on the expression of GFAP in astrocytes of cerebrum, hippocampus and cerebellum was studied on rat clinical death model. Cardiac arrest was induced by 10-or 15-min intrathoracic compression of the heart vascular bundle. Immunohistochemical staining showed that GFAP immunoreactivity significantly increased in the white matter, and GFAP-expressing astrocytes appeared in the gray matter. The reaction activity correlated with ischemia duration and phases of postresuscitation process. The obtained data are indicative of possible changes in the astrocytes condition in the absence of manifest lesions of neurons. This brings up the question of the role of glia homeostasis derangements in the formation of brain postresuscitation pathology.

Animals↗
PubMed1991

[Role of the neurogenic component in post-resuscitation disorders of cardiovascular regulation].

The reactivity of the cardiovascular system in the first 3 hours after 20-minute isolated compression ischemia of the brain was studied in experiments on dogs. Changes of baroreflex regulation in short-term clamping of the carotid arteries and in reduced pressure in the aorta as well as disorders of compensatory potentials of the circulatory system in acute blood loss were revealed. The fact that sympathicotonia increases was established. It is concluded that a search for methods for correction of posthypoxic disorders of neuroreflex regulation of the cardiovascular system is necessary.

Animals↗
PubMed1989

[Changes in the spreading depression wave in rats in the postresuscitation period].

Functional state of the rat brain cortex after a 10-minute arrest of blood circulation was studied by means of the spreading depression wave, the latter leading to significant energy expenditures and being accompanied by a transmitter output and changes in extra- and intracellular ion concentration. The changes in the spreading depression wave took place at different stages of the postresuscitation period (2 hours to 2 1/2 months), suggesting various pathological changes in functional state of the brain cortex induced by disturbances in neurological interrelationships.

Animals↗
PubMed1981

[Role of certain brain structures in the generation and spread of alpha-like activity in dogs peculiar to the early stages of the postresuscitation period].

The role played by the amygdaloid nucleus, caudate nucleus, thalamus and brain cortex in propagation throughout the brain of generalized limbic alpha-like activity recorded on the EEG in the early postresuscitation period was studied in experiments on dogs resuscitated after a 13-15-minute circulatory arrest. Destruction or pharmacological inhibition of both amygdaloid nuclei resulted in disappearance of alpha-like activity from all the test structures. Coherent analysis showed that the caudate nucleus and thalamus, in particular, take an active part in propagation of alpha-like waves of biopotentials from the amygdaloid nucleus to other brain structures.

Amygdala↗
PubMed1978

[Electrical activity of the cortex and subcortical structures during the development of hypoxia due to blood loss].

Previous experiments on dogs showed that in several cases, along with the development of hypoxia, polymorphous delta-waves changed into synchronous oscillations, also of delta range, the so-called standard slow complexes (SSC). The new experimental data showed discharges of neuronal pool during SSC to be present in the caudate nucleus, lateral and medial thalamus, hypothalamus, hypocampus, n. amygdale, and mesencephalic reticular formation. The most frequent neuronal pulse activity was connected with the second half of the SSC negative phase (P is less than 0.01). Discharge flashes of the neuronal pool during the SSC indicated that SSC reflected the physiological processes occurring in these structures.

Animals↗