Objective: To investigate the protective effects and mechanisms of NaomaiⅡ oral liquor( 脑脉Ⅱ号口服液 ) on brain injury induced by hypertensive intracerebral hemorrhage (HICH) in rats. Methods: Fifty eight male SpragueDawley rats were randomly divided into shamoperation, model and treatment group. HICH was induced in the model made by clipping renal blood vessels in both kidneys and injecting 2 μl normal saline containing 0 4 U bacterial collagenase into the right caudate nucleus. Shamoperated rats were subjected to the same surgical procedures in the model rats but only 2 μl normal saline was injected into the caudate nucleus. At 1 hour after anesthesia and resuscitation, by gastric tube 8 ml distilled water was given to the model group and 6 times of NaomaiⅡ oral liquor dosage for 70 kg adult were administered to the treatment group. At 4, 24, 48, and 72 hours after operation, neurological deficits were scored. At 72 hours after operation , histopathological changes in the brain were observed, and the size of hematoma, the contents of water, sodium, and Evans blue (EB) in the brain were measured, respectively.
Results: No hematoma and histological abnormalities were found in the brain, and no neurological deficits exhibited in the shamoperated rats. In rats of the model group , brain hematoma and obvious neurological deficits were seen; the contents of water, sodium and EB in the brain were markedly higher than those in the shamoperation group ( P <0 05 or P <0 01). In rats of treatment group, diameter of the hematoma was makedly reduced, neurological deficits scores were obviously decreased, the contents of water, sodium, and EB in brain were significantly attenuated ( P <0 05 or P <0 01), and the brain injury was much more alleviated in comparison with those in the model group. Conclusion: NaomaiⅡ oral liquor has protective effects on brain injury induced by HICH. It could improve absorption of hematoma , reduce permeability of bloodbrain barrier and attenuate brain edema.