title: Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade.
abstract: OBJECTIVE
  To determine whether beta-adrenergic blockade augments cocaine-induced coronary artery vasoconstriction.
  
  
  METHODS
  Randomized, double-blind, placebo-controlled trial.
  
  
  METHODS
  A cardiac catheterization laboratory in an urban teaching hospital.
  
  
  METHODS
  Thirty clinically stable patient volunteers referred for catheterization for evaluation of chest pain.
  
  
  METHODS
  Heart rate, arterial pressure, coronary sinus blood flow (by thermodilution), and epicardial left coronary arterial dimensions were measured before and 15 minutes after intranasal saline or cocaine administration (2 mg/kg body weight) and again after intracoronary propranolol administration (2 mg in 5 minutes).
  
  
  RESULTS
  No variables changed after saline administration. After cocaine administration, arterial pressure and rate-pressure product increased; coronary sinus blood flow fell (139 +/- 28 [mean +/- SE] to 120 +/- 20 mL/min); coronary vascular resistance (mean arterial pressure divided by coronary sinus blood flow) rose (0.87 +/- 0.10 to 1.05 +/- 0.10 mm Hg/mL.min); and coronary arterial diameters decreased by between 6% and 9% (P less than 0.05 for all variables). Subsequently, intracoronary propranolol administration caused no change in arterial pressure or rate-pressure product but further decreased coronary sinus blood flow (to 100 +/- 14 mL/min) and increased coronary vascular resistance (to 1.20 +/- 0.12 mm Hg/mL.min) (P less than 0.05 for both).
  
  
  CONCLUSIONS
  Cocaine-induced coronary vasoconstriction is potentiated by beta-adrenergic blockade. Beta-adrenergic blocking agents probably should be avoided in patients with cocaine-associated myocardial ischemia or infarction.
authors.affiliation: University of Texas Southwestern Medical Center, Parkland Memorial Hospital, Dallas.
authors.forename: R A
authors.initials: RA
authors.lastname: Lange
authors.forename: R G
authors.initials: RG
authors.lastname: Cigarroa
authors.forename: E D
authors.initials: ED
authors.lastname: Flores
authors.forename: W
authors.initials: W
authors.lastname: McBride
authors.forename: A S
authors.initials: AS
authors.lastname: Kim
authors.forename: P J
authors.initials: PJ
authors.lastname: Wells
authors.forename: J B
authors.initials: JB
authors.lastname: Bedotto
authors.forename: R S
authors.initials: RS
authors.lastname: Danziger
authors.forename: L D
authors.initials: LD
authors.lastname: Hillis
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000187:drug effects; D003042:Cocaine / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000503:physiopathology; D003331:Coronary Vessels / Q000187:drug effects*; D004311:Double-Blind Method; D004357:Drug Synergism; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology; D011897:Random Allocation; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D011433:Propranolol; D003042:Cocaine