title: Vasodilator signals from the ischemic myocardium are transduced to the coronary vascular wall by pertussis toxin-sensitive G proteins: a new experimental method for the analysis of the interaction between the myocardium and coronary vessels.
abstract: OBJECTIVE
  We sought to detect cross-talk between the beating heart and coronary vascular bed during myocardial ischemia and to test the hypothesis that the cross-talk is mediated by pertussis toxin (PTX)-sensitive G proteins (G(PTX)) in vessels.
  
  
  BACKGROUND
  Coronary flow is closely related to the myocardial metabolic state, indicating the existence of a close interaction between cardiac muscle and coronary vascular beds. Experimental methods for the analysis of the interaction, however, have not been established.
  
  
  METHODS
  Coronary detector vessels (DVs) were isolated from rabbit hearts. One end of the vessel was cannulated to a micropipette, and the other end was ligated. After the DV was pressurized (60 cm H(2)O), it was gently placed on the myocardium, which was perfused by the left anterior descending coronary artery (LAD) of anesthetized, open-chest dogs (n = 23). The LAD was occluded, and the DV diameter was observed using an intravital microscope with a floating objective system. To evaluate the involvement of G(PTX), the DV was pre-incubated with PTX (100 ng/ml).
  
  
  RESULTS
  The LAD occlusion of the beating heart produced significant dilation of DVs (241 +/- 25 microm) by 10%. The DVs pretreated with PTX (250 +/- 27 microm) did not dilate in response to myocardial ischemia. N(omega)-nitro-L-arginine (100 micromol/l), but not glibenclamide (5 micromol/l), abolished the ischemia-induced DV dilation.
  
  
  CONCLUSIONS
  We have established experimental methods for direct analysis of the interaction between the myocardium and coronary microvessels. We conclude that the ischemic myocardium releases transferable vasodilator signals that are transduced by means of the G(PTX) located in the vascular walls. The nitric oxide pathway is involved in the signal transduction.
authors.affiliation: Department of Cardiovascular Medicine, Tohoku University, Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan.
authors.forename: Kouichi
authors.initials: K
authors.lastname: Sato
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Komaru
authors.forename: Hiroki
authors.initials: H
authors.lastname: Shioiri
authors.forename: Satoru
authors.initials: S
authors.lastname: Takeda
authors.forename: Katsuaki
authors.initials: K
authors.lastname: Takahashi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kanatsuka
authors.forename: Kunio
authors.initials: K
authors.lastname: Shirato
mesh_terms: D000818:Animals; D003331:Coronary Vessels / Q000502:physiology*; D004195:Disease Models, Animal; D019204:GTP-Binding Proteins / Q000187:drug effects / Q000502:physiology*; D006321:Heart / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology*; D037342:Pertussis Toxin; D011817:Rabbits; D020239:Receptor Cross-Talk / Q000502:physiology*; D015398:Signal Transduction; D014664:Vasodilation / Q000502:physiology*; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
chemical_list: D010566:Virulence Factors, Bordetella; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins