Study On The Effect Of Hypertonic Saline Dextran On Cerebral Resuscitation After Sudden Cardiac Arrest In Rats

Object To explore the effect of Hypertonic saline dextran on brain tissue after cardiopulmonary resuscitation(CPR) and seek for the modus operandi of cerebral resuscitation.Method 40 Sprague-Dawley male rats were randomly divided into four groups (10 for each group) as normal group (group A), shame-operated group (group B), CPR control group (group C) and HSD-treated group (group D).Sudden cardiac arrest was induced on rats by asphyxia. At the onset of CPR, 4ml/kg HSD was injected intravenously in the rats of group D and 4ml/kg normal saline was injected intravenously in the rats of group C. The time for both sudden cardiac arrest and restoration of spontaneous circulation (ROSC) were recorded, and a continuous monitoring on the change of mean arterial pressure(MAP)and electrocardiogram was held in 1h after ROSC. Blood urea nitrogen, blood glucose and serum electrolyte of the rats in each group at 1h after ROSC were determined, and then the plasma osmotic pressure in each group was calculated. Neurodeficit score (NDS) was also recorded in 24h after ROSC. At 24h after ROSC, the venous blood was got to detcect the concentration of serum neurone specific enolase (NSE) in each group, and the rats were sacrificed to get the brain tissue and compare the expression of S100 in hippocampus, brain water content and the hippocampus histopathological damages of the rats in each group.Result The difference in the time for SCA and ROSC between group D and C was not significant (P>0.05). The change of electrocardiogram after ROSC between group D and C were similar. MAP in group D at 1min after ROSC increased (P<0.05) compared with group B, but much lower than those in group C (P<0.05), and MAP at the other time points in group D and C were both lower than those in group B (P<0.05),with no significant difference between group D and C(P>0.05). There was no significant difference in the serum urea nitrogen, electrolyte and osmotic pressure among all the groups (P>0.05). Blood glucose at 1h after ROSC in group D was not obviously different with group A and B(P>0.05), but that in group C was much higher than those in all the other groups (P<0.01). Serum NSE level at 24h after ROSC in group D was not significantly different with group C and D, which in group C was elevated obviously contrasted to group A and B (P<0.01), and that in group D was much lower than in group C (P<0.01). The expression of S100 in hippocampus at 24h after ROSC was higher in group D (P<0.01) and much higher in group C (P<0.01) than both in group A and B, and that in group D was extremely higher than the one in group C (P<0.01).There was no significant difference among group A,group B and group D in the brain water content (P>0.05),which were all much lower than that in group C (P<0.01). There were less severe cerebral histopathological damages and higher NDS (P<0.01) in group D compared with group C, but NDS at any time point after ROSC in both group C and D were significantly lower than those in group A and B(P<0.01).Conclusion HSD has no significant effect on serum electrolyte and osmotic pressure as well as the time for ROSC after CPR. But indeed, the use of HSD in experimental sudden cardiac arrest is associated with more stable MAP,better balance of blood glucose, better homeostatic equilibrium, lower expression of S100 in hippocampus, lower serum NSE level, less cerebral edema, less histopathological damages and better neurologic recovery after ROSC, and therefor play a role in protection of brain tissue after CPR.