The Study Of Laminar Shear Stress Of Cerebral Blood Flow In Early Exercise Training After Ischemic Stroke

Background:Reports have shown that early exercise training is an effective way to promote the recovery of neurological function in ischemic stroke in lots of clinical practice and animal experiments, but the molecular mechanisms involved were not yet fully understood. The research was to study the functions and mechanism of early exercise training on cerebral blood flow from the hemodynamic aspects of it. Ischemic stroke is a disease caused by thrombosis or blood vessel blockage which lead to a series of adverse consequences of secondary cerebral infarction of vascular-dominated brain because of lacking of blood and nutrients.Therefore,studing exercise training on brain perfusion in vivo and vitro levels is improtant.Methods:In vivo, study the functions of early exercise rehabilitation on nerve function, infarct volume and perfusion amount of infarction area on ischemic stroke rats as follows:Stroke was induced in adult male Sprague-Dawley rats by middle cerebral artery occlusion for60min, and the animals were then randomly assigned to early exercise or non-excise groups, and early exercise treadmill training(12m/min,30min/day) was performed24hours after cerebral ischemia in all of the groups. Nerve functions were measured with the methods of Rogers, infarct volume was detected with TTC staining and blood flow velocity of cerebral ischemic region was detected with laser speckle imaging (LSI). In vitro, endothelial cells constituting the blood vessel wall are the direct and the main acceptor from the force of the blood flow. Rat brain microvascular endothelial cells (RBMECs) were cultured and oxygen glucose deprivation (OGD) was given to establish the ischemia model. LS(5±0.05dynes/cm2vs.0dynes/cm2) was offered by parallel-plate flow chamber. Nuclear shrinkage cracking, the decline of mitochondrial membrane potential,permeability changes of cell membrane and apoptosis were detected with PE Annexin V/7-AAD,JC-land Hoechst33258/PI. The associated proteins and genes such as TIE-2, Akt and Bcl-2were detected with Real-time PCR and western blot.Results:In vivo, the results showed that compared with the ischemic control group, early exercise intervention can increase blood flow perfusion of the infarcted brain areas, reduce infarct volume and improve motor function of the hemiplegic limb in the ischemic exercise group. In vitro, rBMECs apoptosis was reduced with a larger flow (shear force=1±0.05dynes/cm2). Cracking and condensation of the nucleus, permeability changes of cell membrane and reduced of mitochondrial membrane potential were reduced to play the protective role through expressions changes of Tie-2, Akt, and Bcl-2. Of course,the protection role of the shearing force is necessarily limited in a range. However,shear force about0.05dynes/cm2increased cell apoptosis.Conclusions:Our results provide novel evidence that early exercise training plays a neuroprotective role. The mechanism of the neuroprotective effect may be related to the blood flow perfusion promotion of the ischemic area and vascular endothelial apoptosis reduced. The molecular mechanisms involved is still need to study.