Hypertensive intracerebral hemorrhage (ICH) is commonly provoked by rupture of basal ganglia and thalamus supplying lenticulostriate arteries (LSAs). The purpose of this study was to identify regions within the LSAs that are prone to rupture. A two-dimensional mathematical model of the LSAs was created in order to identify the location of vascular rupture and a parallel-plate flow chamber was used to evaluate the role of shear stresses on endothelial cell damage. Areas within the LSAs that were prone to rupture were distal parts of the vessels supplying the basal ganglia and thalamus, those located in close proximity to the trunk of the middle cerebral artery (MCA), as well as the vessel wall at the bifurcation point of the LSAs. Furthermore, more severe endothelial cell damage was observed at the origin of the LSAs. This study identified susceptible sites of blood vessel rupture within the LSAs, which, in the future, could be used to anticipate and potentially prevent the occurrence of clinical hypertensive ICH.

Compared to the secondary brain injury after intracerebral haemorrhage (ICH), fewer reports focused on the mechanism of primary brain injury induced by mass effect. Here, the tandem mass tag (TMT) labeling proteomics method was used to study the mechanical damage of the mass effect after ICH. A total of 5390 proteins were identified, and 4593 proteins were quantified, included 80 up-regulated proteins (M/N Ratio > 1.2) and 30 down-regulated proteins (M/N Ratio > 1.2). Bioinformatics and enrichment analysis showed that the differentially expressed proteins were mainly involved in immune response, signal transmission, and oxidative phosphorylation. The mass effect affects the synthesis and metabolism of ATP by mechanically stretching and squeezing the brain tissue. Furthermore, the cell morphology and dendritic development of neurons were also significantly influenced by mass effect, which also cause neuronal damage through the formation of oxidative stress and oxygen-glucose deprivation, and activate the neuronal protection and defense mechanisms. Our results provide the relevant channels and key proteins of primary brain injury caused by mass effect after ICH, which offer a scientific basis for the understanding of ICH injury.