title: Vasodilation and mechanism of action of propofol in porcine coronary artery.
abstract: BACKGROUND
  A decrease in myocardial perfusion pressure may reduce myocardial blood flow. However, it may not significantly affect myocardial perfusion when in presence of a concurrent coronary artery vasodilation. However, the effects of propofol in coronary arteries are not well determined. In this study, the effects of propofol on porcine coronary artery responses to vasoactive agents that operate through voltage- and receptor-mediated calcium mechanisms were investigated.
  
  
  METHODS
  Hearts of adult pigs (n = 103) were obtained from a slaughter house, and the left anterior descending coronary arteries were dissected. The arteries were cut into vessel rings and prepared with and without the endothelium organ chambers filled with buffered salt solution. The effect of propofol (10(-7), 10(-6), 10(-5), and 10(-4) M) on vascular smooth muscle contraction caused by intracellular Ca(2+)-influx through voltage- and receptor-mediated mechanism also was studied at a cellular level.
  
  
  RESULTS
  Propofol relaxed coronary rings that were contracted by KCl, norepinephrine (NE), serotonin (5-HT), or carbachol (CCh). The minimal concentrations of propofol that produced significant vasorelaxation ranged from 3.16 x 10(-7) M to 3.16 x 10(-6) M. Vasodilation was more pronounced in rings contracted by NE, 5-HT, and CCh than by KCl. Propofol (10(-5) M) attenuated coronary vasoconstriction in response to cumulative concentrations of KCl, NE, 5-HT, and acetylcholine. Maximal contractions produced by NE and 5-HT were inhibited to a greater degree than contractions produced by KCl. Propofol at concentrations of 10(-5) M and higher attenuated a contraction in response to CaCl2 in vascular rings depolarized by KCl, but concentrations of 10-M did not attenuate contractions. Vasoconstriction in response to calcium entry in the presence of NE (and nifedipine 10(-6) M) was attenuated by propofol at concentrations of 10(-6) M and higher. Caffeine-induced contraction, caused by intracellular calcium release, was attenuated only at 10(-4) M of propofol.
  
  
  CONCLUSIONS
  Propofol possesses vasodilator effect and attenuates the effects of vasoconstrictor agents in porcine coronary artery. Further, an antagonism of calcium channels may be responsible for these effects of propofol.
authors.affiliation: Center for Anesthesia Research, Cleveland Clinic Foundation, Ohio 44195-5286.
authors.forename: T
authors.initials: T
authors.lastname: Yamanoue
authors.forename: J M
authors.initials: JM
authors.lastname: Brum
authors.forename: F G
authors.initials: FG
authors.lastname: Estafanous
mesh_terms: D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000502:physiology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D015640:Ion Channel Gating; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D015742:Propofol / Q000494:pharmacology*; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D013552:Swine; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D015220:Calcium Channels; D002110:Caffeine; D002118:Calcium; D015742:Propofol