EFFECT OF PRALIDOXIME ADMINISTRATION DURING CARDIOPULMONARY RESUSCITATION ON BRAIN TISSUE OXYGEN TENSION AFTER RESTORATION OF SPONTANEOUS CIRCULATION IN A SWINE MODEL OF CARDIAC ARREST
Keywords:
Brain Tissue oxygen ● pralidoxime ● cardiac arrestAbstract
Purpose: Previous studies suggested that epinephrine reduced brain tissue O2 tension (PbtO2) after restoration of spontaneous circulation (ROSC) via α1-adrenoceptor stimulation. Another previous study reported that pralidoxime had α1-adrenoceptor inhibitory action together with non-adrenergic vasopressor action. We sought to investigate the effects of pralidoxime administered during cardiopulmonary resuscitation (CPR) as a sole vasopressor on PbtO2 after ROSC. We hypothesized that pralidoxime administration would lead to a comparable ROSC rate and higher PbtO2 after ROSC when compared to epinephrine administration.
Methods: After 7 min of ventricular fibrillation, 24 pigs randomly received either pralidoxime or epinephrine during cardiopulmonary resuscitation (CPR). Cerebral measurements, including PbtO2, were measured from the parietal cortices during the 60min post-ROSC period.
Results: Coronary perfusion pressure (CPP) during CPR was significantly higher in the epinephrine group than in the pralidoxime group (P = 0.012). All animals in the epinephrine group achieved ROSC, while 7 (58.3%) did in the pralidoxime group (P = 0.037). The areas under the curves for PbtO2 during the post-ROSC period did not differ between the two groups.
Conclusions: Pralidoxime alone was significantly inferior to epinephrine in increasing CPP and achieving ROSC. In addition, pralidoxime administration did not improve PbtO2 during the post-resuscitation period as compared with epinephrine.
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