Purpose
To evaluate the effects of controlled decompression and rapid decompression,
explore the potential mechanism, provide the theoretical basis for the
clinical application, and explore the new cell death method in intracranial
hypertension.
Methods
Acute intracranial hypertension was triggered in rabbits by epidural balloon
compression. New Zealand white rabbits were randomly put into the sham
group, the controlled decompression group, and the rapid decompression
group. Brain water content, etc., was used to evaluate early brain injury.
Western blotting and double immunofluorescence staining were used to detect
necroptosis and apoptosis.
Results
Brain edema, neurological dysfunction, and brain injury appeared after
traumatic brain injury (TBI). Compared with rapid decompression, brain water
content was significantly decreased, neurological scores were improved by
controlled decompression treatment. Terminal deoxynucleotidyl transferase
dUTP nick end labeling (TUNEL) staining and Nissl staining showed neuron
death decreased in the controlled decompression group. Compared with rapid
decompression, it was also found that apoptosis-related protein caspase-3/
tumor necrosis factor (TNF)-a was reduced markedly in the brain cortex and
serum, and the expression levels of necroptosis-related protein,
receptor-interacting protein 1 (RIP1)/receptor-interacting protein 1 (RIP3)
reduced significantly in the controlled decompression group.
Conclusions
Controlled decompression can effectively reduce neuronal damage and cerebral
edema after craniocerebral injury and, thus, protect the brain tissue by
alleviating necroptosis and apoptosis.