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Decreased cAMP Level and Decreased Downregulation of β-Adrenoceptor Expression in Therapeutic Hypothermia-Resuscitated Myocardium Are Associated With Improved Post-Resuscitation Myocardial Function.

Decreased cAMP Level and Decreased Downregulation of β-Adrenoceptor Expression in Therapeutic Hypothermia-Resuscitated Myocardium Are Associated With Improved Post-Resuscitation Myocardial Function.
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Wang W, Hua T, Li H, Wu X, Bradley J, Peberdy MA, Ornato JP, Tang W,


Wang W, Hua T, Li H, Wu X, Bradley J, Peberdy MA, Ornato JP, Tang W, (click to view)

Wang W, Hua T, Li H, Wu X, Bradley J, Peberdy MA, Ornato JP, Tang W,

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Journal of the American Heart Association 2018 03 237(6) pii e006573
Abstract
BACKGROUND
Epinephrine administered during cardiopulmonary resuscitation (CPR) is associated with severe post-resuscitation myocardial dysfunction. We previously demonstrated that therapeutic hypothermia reduced the severity of post-resuscitation myocardial dysfunction caused by epinephrine; however, the relationship between myocardial adrenoceptor expression and myocardial protective effects by hypothermia remains unclear.

METHODS AND RESULTS
Rats weighing between 450 and 550 g were randomized into 5 groups: (1) normothermic placebo, (2) normothermic epinephrine, (3) hypothermic placebo, (4) hypothermic epinephrine, and (5) sham (not subject to cardiac arrest and resuscitation). Ventricular fibrillation was induced and untreated for 8 minutes for all other groups. Hypothermia was initiated coincident with the start of CPR and maintained at 33±0.2°C for 4 hours. Placebo or epinephrine was administered 5 minutes after the start of CPR and 3 minutes before defibrillation. Post-resuscitation ejection fraction was measured hourly for 4 hours then hearts were harvested. Epinephrine increased coronary perfusion pressure during CPR (27±6 mm Hg versus 21±2 mm Hg<0.05). Post-resuscitation myocardial function was impaired in the normothermic epinephrine group compared with other groups. The concentration of myocardial cAMP doubled in the normothermic epinephrine group (655.06±447.63 μmol/L) compared with the hypothermic epinephrine group (302.51±97.98 μmol/L;<0.05). Myocardial β-adrenoceptor expression decreased with normothermia cardiac arrest but not with hypothermia regardless of epinephrine. CONCLUSIONS
Epinephrine, administered during normothermic CPR, increased the severity of post-resuscitation myocardial dysfunction. This adverse effect was inhibited by intra-arrest hypothermia resuscitation. Declined cAMP with more preserved β-adrenoceptors in hypothermia-resuscitated myocardium is associated with improved post-resuscitated myocardial function in vivo.

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