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Biomedical subjects

G Mchedlishvili

Publications and source records attributed to G Mchedlishvili.

12 recordsLinked to original sources

Cerebral microcirculation: heterogeneity of pial arterial network controlling microcirculation of cerebral cortex.

Analysis of the functional behaviour of pial arterial ramifications feeding small areas of the cerebral cortex of rabbits uncovered well-defined heterogeneity of vascular responses during development of functional hyperemia. In the network of the smaller pial arteries, under 100 microns in diameter, the most active segments, the sphincters of offshoots of smaller arterial branches from larger trunks and the precortical arteries just before their penetration as the radial arteries into the cerebral cortex, have been discovered. The frequency of their dilatation was found to be higher, the latent periods of the vascular responses significantly shorter, and the degree of vasodilatation greater than of the adjacent arterial segments. An abundant amount of cholinergic nerve plexuses (containing the cholinesterase) was found in the walls of these active vascular segments, and microapplication of atropine resulted in a considerable decrease of their dilatation. These experimental results indicate the involvement of the cholinergic neurogenic mechanism in the functional vasodilatation, as distinct from the largely accepted effect of the humoral mechanism accomplished by diffusion of active vasodilatory substances from tissue elements to the walls of the feeding arterial branches.

Animals

Dynamic structure of blood flow in microvessels.

The present article summarizes the author's perennial research on the flow of red blood cells in microvessels, the major determinant of rheological properties of blood in the microcirculation. Two main patterns of blood flow structure in microvessels, in the smallest arteries and veins and in the capillaries are described. The red cell concentration (hematocrit) in the blood flowing in microvessels undergoes regular alterations with changes of blood flow rate and vessel diameter in the microvascular beds. Further, the red blood cell concentration and flow velocity gradients are found in the cross-section of microvessels that should considerably affect the blood rheological properties in the microcirculation. In addition, radial displacements and blood velocity fluctuations of red cells in the flow are discovered in the larger microvessels during ischemic decrease of blood flow rate. The main factor disturbing the normal blood flow structure, and hence the normal rheological properties of blood, is the intravascular aggregation of red blood cells, which is to be diagnosed and eliminated in patients with blood rheological disturbances.

Erythrocyte Aggregation

Mechanical properties of brain tissue related to oedema development in rabbits.

We studied the mechanical properties of the brain in anaesthetized rabbits by application of a standard external load to the exposed cerebral surface. The experimental model used allows one to eliminate potential circulatory factors. Brain oedema was produced by repeated episodes of ischaemia secondary to a decrease of the arterial blood pressure to zero. The development of brain oedema was assessed by an increase of the cerebral water content. In the course brain oedema development brain fluidity was found to steadily rise, while the brain compliance and the index of hysteresis decreased from the control value found at the onset of the experiment. Most important both, brain compliance and the index of hysteresis were already markedly elevated prior to the manifestation of brain oedema.

Animals

Pathogenetic role of circulatory factors in brain edema development.

Sufficient experimental evidence has been accumulated at present, proving that changes in cerebral blood circulation are largely involved in brain edema development. On the one hand, they might be an immediate cause of edema, e.g., a significant rise of the systemic arterial pressure surpassing the limits of cerebral blood flow autoregulation, or cerebral ischemia damaging brain tissue and the blood-brain barrier. On the other hand, circulatory changes, e.g., systemic arterial and venous pressure variations, as well as changes in cerebrovascular resistance or in the microcirculation of cerebral tissue, might be the factors which affect in different ways the development of edema of various etiologies. The effects of these circulatory changes may have dual implications, being either malignant, i.e., aggravating edema development, or compensatory, i.e., restricting or in some cases even eliminating brain edema. Knowledge of the circulatory changes is an essential tool in neurosurgical practice, providing for effective treatment of this severe pathological process in the brain.

Blood Pressure

Responses of the internal carotid artery to different endogenous vasoconstrictor substances.

In order to study the action of serotonin (5-HT), noradrenaline (NA), hypertensin (HT), prostaglandins A1, B1 and E2 (PGA1, PGB1 and PGE2) and vasopressin (VP), internal carotid arteries were isolated in situ from both cerebral and general circulation and perfused continuously with oxygenated Ringers' bicarbonate solution. The order of potencies of the vasoactive substances when administered intra-arterially was: 5-HT greater than HT greater than PGE2- greater than PGB1 greater than NA. The relative duration of the constrictor effects was: 5-HT less than PGA1-less than HT and PGE2 less than PGB1 and NA less than VP. The relaxation index of these substances on the vascular wall was: 5-HT less than PGE2 less than HT less than PGB1-less than NA less than PGA1 less than VP. Some of these substances, specifically PGB1, PGE2 and VP, frequently caused a residual constriction of the smooth muscle following their dilator effect. The role of these vasoactive substances in the development of vasospasm is discussed.

Angiotensinogen

Pathophysiological mechanisms of brain edema development: role of tissue factors.

In experiments carried out on adult rabbit "chest-head" preparations the volume changes of the exposed brain (BrV) were determined in repeated tests during a controlled increase of the systemic venous pressure (SVP) of about 13 mm Hg. The changes of both SVP and BrV were usually parallel at the onset of the experiments, but when the brains became preedematous hysteresis appeared in the plots of their relationships. The hysteresis increased gradually (sometimes with periods of partial decrease) thus indicating a delay in the draining of blood from the brain's venous system and in the removal of excess extracellular fluid from the cebral tissue. Evidence for water filtration through the capillary walls during increase of the SVP, and, thus, of brain intravascular pressure, was obtained by detecting the dynamics of [Na+] and [K+] in the extracellular fluid of the cerebral cortex by ion-selective electrodes. This process appeared reversible in normal brains while in the preedematous ones the excessive water filtration resulted in brain edema. The preedematous state of the brain is believed to be caused by changes of the mechanical properties of brain tissue and/or by changes in osmolarity.

Animals

Mechanisms of postischemic brain edema: contribution of circulatory factors.

Controlled cerebral ischemia was produced in rabbits by bilateral occlusion of the common carotid arteries and restriction of collateral blood flow by a decrease of the systemic arterial pressure to a desirable level (by hemorrhage into a pressurized reservior system). The following circulatory parameters were simultaneously monitored: systemic arterial pressure (SAP), pressure in the circle of Willis (Pcw), systemic venous pressure (SVP), and pressure in the sagittal venous sinus of brain (Pvs). The cerebral blood flow (CBF) was measured by means of the H2-clearance method, and the brain volume (BrV) changes were evaluated with a mechanical system of the sterotaxic device. It has been concluded that the pre-edematous changes in the brain tissue arise during deep ischemis but an important factor in the brain edema development is the recovery of the CBF with and increase of the intravascular pressure closely related to the brain blood volume augmentation. The latter may be pronouced because of diminution of the blood outflow from the brain when the SVP is increased. The compensation for the BrV increase (caused either by brain blood volume augmentation or by brain edema) is obtained by Pcw decrease probably due to resistance rise in the internal carotid and vertebral arteries. The brain edema may be additionally compensated by an active decrease of the systemic arterial pressure.

Animals