title: Does selective beta-1 blockade provide bone marrow protection after trauma/hemorrhagic shock?
abstract: BACKGROUND
  Previously, nonselective beta-blockade (BB) with propranolol demonstrated protection of the bone marrow (BM) after trauma and hemorrhagic shock (HS). Because selective beta-1 blockers are used commonly for their cardiac protection, the aim of this study was to more clearly define the role of specific beta adrenergic receptors in BM protection after trauma and HS.
  
  
  METHODS
  Male Sprague-Dawley rats underwent unilateral lung contusion (LC) followed by HS for 45 minutes. After resuscitation, animals were injected with a selective beta-blocker, atenolol (B1B), butoxamine (B2B), or SR59230A (B3B). Animals were killed at 3 hours or 7 days. Heart rate and blood pressure were measured throughout the study period. BM cellularity, growth of hematopoietic progenitor cells (HPCs) in BM, and hemoglobin levels (Hb) were assessed.
  
  
  RESULTS
  Treatment with a B2B or B3B after LCHS restored both BM cellularity and BM HPC colony growth at 3 hours and 7 days. In contrast, treatment with a B1B had no effect on BM cellularity or HPC growth but did decrease heart effectively rate throughout the study. Treatment with a B3B after LCHS increased Hb as compared with LCHS alone.
  
  
  CONCLUSIONS
  After trauma and HS, protection of BM for 7 days was seen with use of either a selective beta-2 or beta-3 blocker. Use of a selective beta-1 blocker was ineffective in protecting the BM despite a physiologic decrease in heart rate. Therefore, the protection of BM is via the beta-2 and beta-3 receptors and it is not via a direct cardiovascular effect.
authors.affiliation: Division of Trauma, Department of Surgery, UMDNJ-New Jersey Medical School, Newark, NJ, USA.
authors.forename: Latha V
authors.initials: LV
authors.lastname: Pasupuleti
authors.forename: Kristin M
authors.initials: KM
authors.lastname: Cook
authors.forename: Ziad C
authors.initials: ZC
authors.lastname: Sifri
authors.forename: Srinath
authors.initials: S
authors.lastname: Kotamarti
authors.forename: Gabriel M
authors.initials: GM
authors.lastname: Calderon
authors.forename: Walter D
authors.initials: WD
authors.lastname: Alzate
authors.forename: David H
authors.initials: DH
authors.lastname: Livingston
authors.forename: Alicia M
authors.initials: AM
authors.lastname: Mohr
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001853:Bone Marrow / Q000187:drug effects* / Q000473:pathology; D002078:Butoxamine / Q000494:pharmacology; D003288:Contusions / Q000150:complications*; D004195:Disease Models, Animal; D006412:Hematopoietic Stem Cells / Q000187:drug effects*; D055370:Lung Injury / Q000150:complications*; D008297:Male; D011412:Propanolamines / Q000494:pharmacology; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000188:drug therapy* / Q000209:etiology
chemical_list: C097869:3-(2-ethylphenoxy)-1-(1,2,3,4-tetrahydronaphth-1-ylamino)-2-propanol oxalate; D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D020011:Protective Agents; D002078:Butoxamine; D001262:Atenolol