title: Altered adrenergic receptor density in myocardial hibernation in humans: A possible mechanism of depressed myocardial function.
abstract: BACKGROUND
  Alterations in adrenergic receptor densities can potentially contribute to myocardial dysfunction. Their relevance to myocardial hibernation in humans is unknown.
  
  
  RESULTS
  Accordingly, 22 transmural myocardial biopsies were obtained in 11 patients with ischemic ventricular dysfunction during bypass surgery, guided by transesophageal echocardiography. Patients underwent dobutamine echocardiography (DE) and rest scintigraphic studies before revascularization and DE at 3 to 4 months. alpha- and ss-receptor density (ARD and BRD) and extent of fibrosis were quantified from the myocardial biopsies. Of the 22 segments, 16 had abnormal rest function and 6 were normal. Severely hypokinetic or akinetic segments showed a 2.4-fold increase in ARD with a concomitant 50% decrease in BRD compared with normal segments. An increase in ARD, a decrease in BRD to a lesser extent, and thus an increase in ARD/BRD ratio were seen in dysfunctional segments with contractile reserve compared with normal segments and were most pronounced in those without contractile reserve (P:<0.001). Similar findings were observed if recovery of function or scintigraphic uptake was analyzed as a marker for viability. No significant relation between either ARD or BRD and percent myocardial fibrosis was noted (r=0.37 and -0.39, respectively).
  
  
  CONCLUSIONS
  Thus, graded and reciprocal changes in alpha- and ss-adrenergic receptor densities occur in viable, hibernating myocardium and may account in part for the observed depression in resting myocardial function and preserved contractile reserve in this entity.
authors.affiliation: Department of Medicine, Section of Cardiology, Baylor College of Medicine, University of Texas Medical School, Houston 77030, USA.
authors.forename: K
authors.initials: K
authors.lastname: Shan
authors.forename: R J
authors.initials: RJ
authors.lastname: Bick
authors.forename: B J
authors.initials: BJ
authors.lastname: Poindexter
authors.forename: S F
authors.initials: SF
authors.lastname: Nagueh
authors.forename: S
authors.initials: S
authors.lastname: Shimoni
authors.forename: M S
authors.initials: MS
authors.lastname: Verani
authors.forename: F
authors.initials: F
authors.lastname: Keng
authors.forename: M J
authors.initials: MJ
authors.lastname: Reardon
authors.forename: G V
authors.initials: GV
authors.lastname: Letsou
authors.forename: J F
authors.initials: JF
authors.lastname: Howell
authors.forename: W A
authors.initials: WA
authors.lastname: Zoghbi
mesh_terms: D000368:Aged; D001706:Biopsy; D001026:Coronary Artery Bypass; D004280:Dobutamine; D004452:Echocardiography; D005260:Female; D005355:Fibrosis / Q000473:pathology; D006321:Heart / Q000000981:diagnostic imaging; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D017682:Myocardial Stunning / Q000378:metabolism* / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D011859:Radiography; D011877:Radionuclide Imaging; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D020127:Recovery of Function; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000209:etiology / Q000601:surgery
chemical_list: D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D004280:Dobutamine