Change of Rho kinase activity in brain tissue in high altitude condition and its relationship with high altitude cerebral edema: experiment with rats

Abstract

To observe the change of Rho kinase activity in brain tissue in the high altitude condition and its relationship with blood brain barrier permeability and high altitude cerebral edema (HACE), and to explore the pathological mechanism of HACE. 30 Wistar rats were divided randomly into 3 equal groups, high altitude (HA) group put in low pressure cabin mimicking high altitude of 7000 m for 24 hr and then gradually exposed to higher pressure until the normal pressure, fasudil group undergoing intraperitoneal injection of fasudil hydrochloride 30 mg/kg, a Rho-associated coiled-coil-containing protein kinase (ROCK) inhibitor, and then treated as the HA group, and normal control group (HC group). Five rats from each were decapitated with their brains taken out. The ratio of dry brain weight and wet brain weight was calculated. Western blotting was used to detect the expression of ROCK. Another 5 rats from each groups underwent injection of sodium fluorescein into the caudal vein and then the rats were decapitated to examine the natrium (sodium) fluorescence index (NaFI) of the central brain slice so as to observe the blood brain barrier permeability. The ROCK activity in brain tissue, ratio of dry and wet brain weight and NaFI of the HA group were significantly higher than those of the HC group (all P<0.001), and ROCK activity in brain tissue, ratio of dry and wet brain weight and NaFI of the fasudil group were all significantly lower than those of the HA group (all P<0.001) and not significantly different from those of the HC group (all P>0.05). ROCK in brain tissue is activated in high altitude condition, which may play a key role in the development of HACE.