XXXX facilitates resuscitation from cardiac arrest and attenuates postresuscitation myocardial dysfunction.

@entity1707 @entity64 @entity26 @entity177 @entity2224 @entity7604 @entity204 @entity1002
BACKGROUND: @entity1002 with a low cardiac index after successful CPR contributes to early @entity204 attributable to @entity177 , and an effective treatment has not been identified. The purpose of this study was to investigate the use of @entity7604 , a selective phosphodiesterase III inhibitor, as treatment for @entity1002 after resuscitation. METHODS AND RESULTS: @entity2224 ( @entity2224 ) was induced electrically in 32 @entity1707 . After 5 minutes of @entity2224 , CPR was initiated and animals were randomized to receive either saline (control group, n=16) as a bolus and infusion or @entity7604 50 microg/kg as a bolus and then 0.5 microg/kg per min for 60 minutes (treatment group, n=16). After 2 minutes of CPR (total @entity2224 time, 7 minutes), countershocks were given. Coronary perfusion pressures during CPR were similar for the groups (24+/-2 versus 21+/-4 mm Hg). All animals were defibrillated; 6 of 16 control animals developed refractory postcountershock pulseless electrical activity compared with 0 of 16 treated animals (P=0.018). At 30 minutes after restoration of spontaneous circulation, @entity64 volume (16+/-3 versus 26+/-7 mL, P<0.01) and LV dp/dt (793+/-197 versus 1108+/-316 mm Hg/s, P<0.02) were higher in the treatment group. Similar differences were observed 60 minutes after restoration of spontaneous circulation. Significant differences in heart rates between groups were not observed, and peripheral vascular resistance was significantly greater in the control group 30 and 60 minutes after resuscitation. CONCLUSIONS: @entity7604 facilitates resuscitation from prolonged @entity2224 and attenuates @entity1002 after resuscitation without worsening major determinants of myocardial @entity26 demand.
