Biomedical subjects

S Vlajkovic

Publications and source records attributed to S Vlajkovic.

5 recordsLinked to original sources

PubMed1990

Self-stimulation behavior: consequences upon immunity?

A variety of behavioral and emotional factors can affect the immune response by changing the brain immunoregulatory mechanisms, resulting in immunosuppression or immunopotentiation. This experiment deals with the effect of chronic self-stimulation behavior on the immune response and lymphoid tissue. Male rats were stereotaxically implanted with bipolar electrodes into the lateral hypothalamus and 7 days after surgery were screened for self-stimulation behavior. Lateral hypothalamus self-stimulating rats (LH-SS) were allowed to self-stimulate for 60 min/day for a period of 9 consecutive days: 5 days before and 4 days after immunization with 5 x 10(9) sheep red blood cells (SRBC). The animals were sacrificed and plaque-forming cell assay (PFC), microhaemmagglutination reaction with SRBC, and differential blood leucocyte counts were performed. The thymus, spleen, and inguinal lymph nodes were weighed and processed for histological examination. In the LH-SS group, an enhanced PFC response and increased anti-SRBC antibody titer were observed when compared to controls. The thymus and spleen of LH-SS rats were smaller in size in comparison with controls, but only with moderate changes in splenic cellular make-up. The relative number of lymphocytes was increased in peripheral blood of LH-SS rats when compared to intact animals. The results obtained suggest that chronic self-stimulation behavior can modulate some parameters of humoral immune response and affect the relative weight of lymphoid organs in the rat.

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PubMed1986

Magnetic resonance imaging of brain tissue displacement and brain tissue water contents during progressive brain compression. An experimental study in dogs.

Continuous recording of vital physiologic parameters and magnetic resonance imaging (MRI) was performed during continuous expansion of extradural rubber balloons in spontaneously ventilated anesthetized dogs. Initial physiologic changes appeared when the pontine cistern was compressed while respiratory arrest was regularly paralleled by marked tentorial and tonsillar herniation. Local increase in brain tissue water progressed during brain compression and was most marked in white matter of the brain. This was related to the regional decrease in cerebral perfusion pressure. The correlation between the morphologic and physiologic course of events during brain compression has a predictive value.

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PubMed1986

Magnetic resonance imaging of water intoxication. An experimental study in dogs.

Sequential magnetic resonance imaging (MRI) was performed to correlate signs of herniation and increase in local brain tissue water content with continuous changes in vital physiologic parameters during progressive water intoxication in anaesthetized dogs. The intracranial pressure increase ultimately resulted in respiratory and cardiac arrest. MRI concomitantly showed an increase in local brain water content starting and dominating in the cerebral cortex but progressing to all parts of the central nervous system. The late appearance of transtentorial pressure gradients and of brain herniation suggests that development of cerebral edema occurs in at least two stages, an intracellular osmotic edema appearing first, being followed by an ischemic edema related to a progressive decrease in local perfusion pressure.

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PubMed1986

Magnetic resonance imaging of cerebral compression and local brain tissue water content during continuous extradural bleeding. An experimental study in dogs.

Continuous recording of vital physiologic parameters and magnetic resonance imaging were performed during progressive extradural bleeding in spontaneously ventilated anesthetized dogs. The volume of the bleeding could exceed the intracranial volume by 500 per cent due to the formation of an extradural arteriovenous shunt. The rate of hematoma growth was dependent on the area of stripped dura. Midline shift, herniation and lateral ventricle compression occurred early, corresponding to changes in vital parameters. Local brain water increased non-linearly with white matter preceding gray matter. Water increase started first in the ipsilateral hemisphere followed by the contralateral hemisphere, brain stem and cerebellum. The correlation between local tissue water increase and local perfusion pressure supports the notion of an ischemic brain edema being formed during an extradural bleeding.

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PubMed1986

Evaluation of intracranial pressure rebound after evacuation of intracranial expanding lesions. An experimental study in dogs.

Sequential magnetic resonance imaging was used to follow brain displacement, signs of herniation and increase in local brain tissue water content during expansion and after evacuation of an extradural balloon in anesthetized, artificially ventilated dogs. A fatal intracranial pressure (ICP) rebound occurred if the cerebral perfusion pressure (CPP) was critically reduced to 20 mm Hg for more than half an hour. Despite reduction of brain displacement after balloon evacuation brain water content continued to increase. Compression of CSF outflow pathways and signs of herniation remained. CPP continuously fell to zero. ICP rebound is a grave situation significantly influenced by a large increase in brain tissue water.

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