Effect Of Hypertensive Reperfusion On Canine Cerebral Ischemic Injury After Cardiac Arrest And Resuscitation

Objective: The goal of our study was to compare measurements of cerebral arteriovenous oxygen content differences(oxygen utilization coefficients), brain lactic acid levels and creatine kinase(CK) activities , and ultrastructal changes of cerebral ischemic injury in dogs resuscitated under normotension vs. hypertension for 4h.Methods: In 12 dogs, the model of ventricular fibrillation of 8 min was used, reperfused with open cardiopulmonary resuscitation, and normal or high mean arterial prssure(MAP), and controlled ventilation to 4h. Animals were assigned to Group NT (normotensive reperfusion, i.e. MAP was about baseline levels before cardiac arrest, n=6) and Group HT(hypertensive reperfusion, i.e. MAP was elevated 10%-15% over baseline, n=6).Results: In Group NT, the cerebral arterio-venous O2 content difference was 7.6±1.8ml/dl before arrest; was low during reperfusion(transient hyperemia) and increased(worsened) significantly to 12.0±1.1ml/dl(p<0.01) at 240min after reperfusion. In Group HT, the cerebral arterio-venous O2 content difference was not different from that in Group NT before arrest, but it was significantly different(p<0.01) at 30 min after cardiac arrest, which decreased to 3.4±1.0ml/dl(p<0.01). These values were not significantly different in Group NT and HT thereafter. The cerebral venous(saggital sinus) PO2(PssO2) was about 36mmHg in two groups before arrest and decreased below baseline values, between 60min and 240min after arrest; the lowest mean values were 29.5 mmHg in Group NT and 30.0mmHg in Group HT. Lactic acid measurements in brain tissue were significantly lower in Group HT than those in Group NT, andCK activites in Group HT were not different from those in Group NT. Ultrastructure of cerebral ischemic injury in Group NT was sever and in Group HT was mild.Conclusions:1.After cardiac arrest, the downward and upward trends in cerebral venous O2 values and O2 utilization coefficients respective suggest the cerebral O2 uptake/delivery mismatching. 2.Hypertensive reperfusion improves the homogeneity of hyperemia early after cardiac arrest.3.Hypertensive reperfusion after arrest does not mitigate the mismatching between cerebral O2 uptake and delivery during the delayed hypoperfusion phase.4.Moderate hypertensive reperfusion can ameliorate cerebral ischemic injury and thus benefits cerebral resuscitaion.