Abstract
Objective
The present study investigated the effect of controlled hypotension (CH) levels regulated
by nitroprusside on hippocampal CA1 neurons.
Materials and methods
All experimental rabbits were randomly divided into five groups to perform CH for
recording their vital signs and survived for a certain time. The arterial blood was
collected to measure the serum levels of interleukin 6 and tumor necrosis factor α
and then the brain tissues were perfused and sectioned to carry out hematoxylin–eosin
staining, TdT-mediated dUTP nick end labeling fluorescence, c-fos immunohistochemistry,
and ultrastructural observation of hippocampal neuronal mitochondria. All data were
analyzed with SPSS13.0 software, and P < 0.05 was indicated as statistically significant.
Results
Heart rate, mean arterial pressure, and the dosage of sodium nitroprusside were not
statistically significant between groups, but at T2, heart rate levels in groups II–IV
were lower than those in groups I and V. Simultaneously, interleukin 6 was remarkably
overexpressed in group II than in other groups at T2, whereas tumor necrosis factor
α was higher in groups I–III than in groups IV and V. At the light and electronic
microscopic levels, the CA1 regional neurons of group IV were more seriously damaged
and deranged compared with other groups so was the expression of c-fos. However, fluorescence
from TdT-mediated dUTP nick end labeling assay was more intensive in groups II–IV
than that in other groups. Results further showed that Flameng scores of mitochondria
were the highest in group IV, but they were not statistically significant among the
other groups.
Conclusions
The different levels of CH remarkably affected the functional activities of hippocampal
CA1 neurons; with the decrease of mean arterial pressure, neuronal apoptosis, and
c-fos expression was gradually increased and reached the peak in 45% of basic values
of blood pressure.
Keywords
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Article info
Publication history
Published online: September 25, 2012
Accepted:
September 4,
2012
Received in revised form:
August 30,
2012
Received:
April 16,
2012
Identification
Copyright
© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
