Ita Kaiserman-Abramof, Ph.D.
Analysis of Functional Adaptations to Metabolic
Stress in Brain Tissues
The primary interest of
this laboratory is to closely assess and
substantiate, on an ultrastructural level, the
tissue responses to pathological changes
resulting from stroke and hypoxia in brain.
Cytotoxic edema causes metabolic and vascular
failure and it has detectable structural
characteristics which can be observed, analyzed,
and reconstructed at an ultrastructural level.
Two of the parameters which are likely to be
sensitive to metabolic and vascular failure are
endothelial cells and astrocytes, especially
those closer to capillaries.
The central nervous system
sequelae of cardiac arrest and resuscitation can
be understood as two distinct phenomena. The
first is the acute dysfunction or death of CNS
neurons which result in cardiovascular and
respiratory collapse leading to death of the
organism. The acute phase can limit
resuscitation from longer arrest and can also
occur up to three days after resuscitation
leading to secondary ischemic death. This
phenomenon is most likely occurring through
metabolic and functional failure of the
brainstem, since the ischemic pressor response
and apnea are known to be mediated by the
ventral medulla. The second phenomenon is that
of selective delayed neuronal degeneration. Some
event triggered during the ischemia, and set
into motion during the first few hours after
resuscitation, results 3 or 4 days later in
selective neuronal degeneration typified by the
CA1 neurons of the hippocampus. Electron
micrographs from rats perfused 5 minutes after
resuscitation from 10 minutes of cardiac arrest
show that the hippocampus capillaries exhibit
swelling of pericapillary astrocytes and
endothelial cells. However, neurons from CA1
hippocampal region are indistinguishable from
control neurons with intact mitochondria and no
swelling. In addition, the capillaries from the
brainstem exhibit damage to the endothelial
cells in the form of blebbing, but no swelling
of the pericapillary astrocytes.
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recovery of acute and chronic hyperglycemic rat
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