Tibet is an area in China with a high incidence of
stroke, typically attributed to hypobaric
hypoxia. The present study aimed to observe the neuronal injury of
ischemic stroke after hypobaric
hypoxia and explore the mechanism by which
N-methyl-D-aspartate receptor (NMDAR) and its downstream pathways are involved. This study employed a hypobaric chamber to imitate high altitude at 4000 m. After
hypoxia, the
middle cerebral artery occlusion (MCAO) model was used to mimic
ischemic stroke. Behavioral tests and measurements of
infarct area were used to observe neuronal
injuries. The expression of NMDAR, Ca2+/
calmodulin-dependent protein kinase II (
CaMKII) and phosphorylated
CaMKII (
Threonine 286) (P-
CaMKII) was tested by western blot, and hematological tests were used to count the number of red blood cells (RBCs) and
hemoglobin. Compared with the plain+MCAO group, the neurological deficit scores and
infarct area of rats in the 4000 m + MCAO group were all decreased, and the
protein expression of NMDAR,
CaMKII and P-
CaMKII was reduced. Compared with the plain group, the numbers of RBCs,
hemoglobin and hematocrit were increased in the 4000 m group; compared with the 4000 m groups, the three indexes were increased in the 4000 m + MCAO groups. The neuronal
injuries after
hypoxia were not more serious than those in rats enduring
ischemia and reperfusion in plain. The underlying mechanisms were related to the decreased expression of NMDAR and
CaMKII; furthermore, the increased numbers of RBCs and
hemoglobin may be crucial mechanisms for the incidence and development of
ischemic stroke at high altitude.