title: Impaired β-adrenergic receptor signalling in post-resuscitation myocardial dysfunction.
abstract: OBJECTIVE
  Post-resuscitation myocardial dysfunction is a major cause of fatality in patients receiving successful cardiopulmonary resuscitation. The mechanism of post-resuscitation myocardial dysfunction is largely unknown, although is generally considered related to ischaemia occurring during cardiac arrest and resuscitation and/or reperfusion injury after restoration of circulation. A key mechanism responsible for reduced contractile reserves in chronic heart failure is impaired β-adrenergic receptor signalling. Thus, we hypothesised that β-adrenergic receptor signalling is markedly abnormal in the post-resuscitation period following cardiopulmonary resuscitation.
  
  
  METHODS
  Male landrace domestic pigs were randomised into a sham group (anaesthetised and instrumented, no ventricular fibrillation) or cardiopulmonary resuscitation (CPR) group (ventricular fibrillation) (n=8 per group). Haemodynamic and echocardiographic data were recorded. β-Adrenergic receptor signalling was assessed at 6h after the operation by measuring myocardial adenylate cyclase activity, β-adrenergic receptor density and β-adrenergic receptor kinase expression.
  
  
  RESULTS
  Left ventricular function in the CPR group was significantly decreased at 6 h after restoration of spontaneous circulation. Basal and isoproterenol-stimulated adenylate cyclase activity was blunted in the CPR group compared with the sham group. Total β-AR density was significantly decreased in CPR group compared with the sham group. Myocardial β-adrenergic receptor kinase expression was 2.03-fold greater in the CPR group than in the sham group.
  
  
  CONCLUSIONS
  β-Adrenergic receptor signalling is markedly impaired in the post-resuscitation period, which may be a mechanism of post-resuscitation myocardial dysfunction.
authors: Department of Emergency, Provincial Hospital Affiliated to Shandong University, Jinan, China.
authors: Xian-Fei
authors: XF
authors: Ji
authors: Shuo Wang
authors: Lin
authors: L
authors: Yang
authors: Chun-Sheng
authors: CS
authors: Li
mesh_terms: D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D016887:Cardiopulmonary Resuscitation; D004452:Echocardiography; D054768:G-Protein-Coupled Receptor Kinases / Q000378:metabolism*; D006323:Heart Arrest / Q000378:metabolism* / Q000503:physiopathology; D006439:Hemodynamics; D015151:Immunoblotting; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D010919:Placebos; D011869:Radioligand Assay; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D012151:Resuscitation; D015398:Signal Transduction; D013552:Swine; D014693:Ventricular Fibrillation / Q000378:metabolism*; D016277:Ventricular Function, Left; D051552:beta-Adrenergic Receptor Kinases / Q000378:metabolism*
chemical_list: D010919:Placebos; D011943:Receptors, Adrenergic, beta; D051552:beta-Adrenergic Receptor Kinases; D054768:G-Protein-Coupled Receptor Kinases; D000262:Adenylyl Cyclases