Objective To investigate the effect of hypertonic saline (HS) on the permeability of blood-brain barrier in a rat model of intracerebral hemorrhage (ICH).Methods Sixty healthy male Sprague-Dawley rats, aged 8 weeks, weighing 260-300 g, were randomly divided into 4 groups (n=15 each) using a random number table: sham operation group (group S), sham operation+HS group (group HS) ,ICH group, and ICH+HS group.ICH was commonly induced in anesthetized rats by intraparenchymal injection of autologous blood 50 μ1.The equal volume of normal saline was given instead in group S.The neurologic deficits were scored on a five-point scale, and a score of 1-3 indicated successful establishment of the model.At 48 h after establishment of the model, the rats were sacrificed, and brains were removed for determination of brain water content, expression of occludin in brain tissues (by Western blot) , and Evans blue content.Results Compared with group S, the brain water content and Evans blue content were significantly increased, and the expression of occludin was down-regulated in ICH and ICH+HS groups, and no significant change was found in the indices mentioned above in group S+HS.Compared with group ICH,the brain water content and Evans blue content were significantly decreased, and the expression of occludin was up-regulated in group ICH +HS.Conclusion HS can inhibit increase in the permeability of bloodbrain barrier, and reduce the cerebral edema in a rat model of ICH.

To explore the time-dependent of p harmacodynamics of lidocain alkalified solution. Method: On 8:00 am and 8:00 pm, surface anaesthesia and subarachnoid anaesthesia were con ducted in rabbits and 76 cases of surgical patients receiving epidureal anaesthe sia were observed in therapy effect.Results: The results of animal experimental showed the anaesthesia potency and anaesthesia incubatory period were better on 8:00 am than 8:00 pm; the clinical observation also obtain ed asimilar result. Conclusion: These results showed that lidocain alkalified solution had time-dependent of pharmacodynamics.