Abstract. The aims of the present study were to establish a model of embolic stroke in rabbits and to evaluate the efficacy and safety of intra-arterially administered tirofiban combined with urokinase thrombolysis. The middle cerebral artery occlusion model (MCAO) of embolic stroke was established in New Zealand rabbits via an autologous clot. The model rabbits were allocated at random into four groups: Tirofiban group (T group), urokinase group (UK group), tirofiban and urokinase group (T + UK group) and the control group (C group). The recanalization rate, relative-apparent diffusion coefficient (rADC) and neurological function deficit score (NFDS) values were compared among the four groups. The recanalization rate, rADC and NFDS values were improved in the T + UK group compared with the other groups. In summary, the intra-arterial administration of tirofiban combined with urokinase thrombolysis was a more effective intervention in an MCAO model compared with intra-arterial urokinase alone, and may promote reperfusion and reduce infarct volume.

Although hypertonic saline (HS) has been extensively applied to treat brain edema in the clinic, the precise mechanism underlying its function remains poorly understood. Therefore, the aim of the present study was to investigate the therapeutic mechanism of HS in brain edema in terms of aquaporins and inflammatory factors. In the present study, traumatic brain injury (TBI) was established in male adult Sprague-Dawley rats, which were continuously administered 10% HS by intravenous injection for 2 days. In addition, brain edema and brain water content were detected by MRI and wet/dry ratio analysis and histological examination, respectively. Immunohistochemical staining for albumin and western blotting for occludin, zonula occludens-1 and claudin-5 was performed to evaluate the integrity of the blood-brain barrier. Aquaporin 4 (AQP4) expression was also analyzed using western blotting and reverse transcription-quantitative PCR, whilst interleukin (IL)-1β and NF-κB levels were measured using ELISA. It was demonstrated that HS treatment significantly reduced brain edema in TBI rats and downregulated AQP4 expression in cerebral cortical tissues around the contusion site. In addition, IL-1β and NF-κB levels were found to be downregulated after 10% HS treatment. Therefore, results from the present study suggested that HS may protect against brain edema induced by TBI by modulating the expression levels of AQP4, NF-κB and IL-1β.