Controlled decompression alleviates early brain injury in rabbit intracranial hypertension model by regulating apoptosis/necroptosis

Abstract

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.

Comparison of the effects of stepwise intracranial decompression and decompressive craniectomy in the treatment of severe traumatic brain injury: A randomized controlled trial

“…[ 13 ] In SID, through appropriate controlled stepwise decompression, it is possible to prevent or reduce the occurrence of delayed cerebral hematoma by avoiding the sudden disappearance of the tamponade effect, resulting in dural detachment, damage to reflux venous vessels, etc. [ 13 , 14 ] Meanwhile, Zhang et al [ 15 ] pointed out in their study that due to the segmented, multiple, and gradual mesh-like opening of the dura mater, the stepwise decrease in brain pressure can prevent significant displacement of brain tissue, thereby avoiding the occurrence of local cerebral hernia, and there is no rapid displacement of the brain tissue. It does not cause further deformation, distortion, or stretching of the cerebral blood vessels, thus preventing the occurrence of large-scale cerebral infarction.…”

“…After radial cutting of the dura mater, necrotic brain tissue and residual hematoma must be quickly removed to achieve internal decompression. [ 15 , 16 ] However, it is necessary to ensure that the dural incision is as far away from the lateral fissure blood vessels as possible and to carry out treatment operations in the lateral fissure area as carefully and gently as possible to avoid compression of the lateral fissure blood vessels caused by the dural incision. Effective protection should be provided to lateral fissure blood vessels to prevent blood reflux and reduce the risk of cerebral infarction and venous congestion.…”