Brain enzyme changes as markers of brain damage in rat cardiac arrest model. Effects of corticosteroid therapy

Apneic asphyxia to cardiac arrest (CA) in rats of 10 min was reversed by cardiopulmonary resuscitation (CPR), and after controlled ventilation and controlled normotension for 20 min, was followed by decapitation and brain freezing, and determination of brain concentrations of cytosolic and lysosomal enzymes. Normal values came from a control group of 10 rats without CA. In 20 rats with CA brain cytosolic enzymes CK, LD, and ASAT decreased postarrest, while lysosomal enzyme changes were variable (Table D. Brain lactate increased 8–10-fold post-CA. To test the model, effect of methylprednisolone (MP) was studied. The 20 rats with CA were divided into 4 groups: Group I, received placebo pre-CA; Group II, MP 30 mg/kg i.v. pre-CA; Group III, placebo post-CA; and Group IV, MP post-CA. The post-CA MP Group IV was the only one without norepinephrine requirement and with return of EEG activity at 20 min. Brain CK, LD, and ASAT losses post-CA were not different between groups; and showed no differences between MP groups II and IV vs. placebo Groups I and III. When comparing both pre-CA Groups (I and II) with both post-CA Groups (III and IV), post-CA CK and ASAT levels were the same, but LD was higher in the post-CA treatment group. The lysosomal enzymes acid phosphatase, mannosidase, β-glucuronidase and hexosamidase showed variable concentration changes post-CA in the four groups, with a trend toward a lesser increase of some after MP or after post-treatment. Brain enzyme changes in our asphyxial CA rat model can serve as markers of brain damage. MP post-CA might enhance cardiovascular and EEG recovery, but does not seem to influence brain enzyme levels at 20 min post-CA.