Works on heart, how about brain? Effect of hyperkalemia on focal cerebral ischemia/reperfusion injury in rats

• Published in: European review for medical and pharmacological sciences Vol. 22; no. 9; p. 2839
• Main Authors: Qin, T, Li, N, Tan, X-F, Zheng, J-H, Tao, R, Chen, M-H
• Format: Journal Article
• Language: English
• Published: Italy 01.05.2018
• ISSN: 2284-0729
• DOI: 10.26355/eurrev_201805_14985

To investigate the effects of hyperkalemia on the brain after I/R in h transient middle cerebral artery occlusion (tMCAO) model. A total of 120 adult male SD rats were randomly assigned to four groups: (1) hyperkalemia 80 µg/g (HK80) group; (2) hyperkalemia 40 µg/g (HK40) group; (3) normal saline (NS) group; (4) sham (SH) group. The concentration of serum K+ was elevated in HK80 and HK40 groups. The transient middle cerebral artery occlusion (tMCAO) model was used to assess the effect of hyperkalemia on the brain after I/R. After 24 h reperfusion, the infarct volume and cell damage of rat's I/R brain tissue sections were analyzed. The concentration of K+, Ca2+ and calmodulin (CaM), the activity of Ca-ATPase, the expression of Western blot of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and Na+/Ca2+ exchanger 1 (NCX1), were also measured. After 24 h reperfusion, compared with NS group, the two-hyperkalemia groups (HK80 and HK40) were with less infarct volume and cell damage, higher concentration of K+ but lower Ca2+ and CaM compared with NS group. The activity of Ca-ATPase was also elevated, the expression of CaMK II and NCX1 were down-regulated in the two hyperkalemia groups. Hyperkalemia could also ameliorate the brain I/R injury by alleviating calcium overload inhibiting the activity of NCX1, lowering the concentration of Ca2+.