TY - JOUR
T1 - Vasodilator signals from the ischemic myocardium are transduced to the coronary vascular wall by pertussis toxin-sensitive G proteins
T2 - A new experimental method for the analysis of the interaction between the myocardium and coronary vessels
AU - Sato, Kouichi
AU - Komaru, Tatsuya
AU - Shioiri, Hiroki
AU - Takeda, Satoru
AU - Takahashi, Katsuaki
AU - Kanatsuka, Hiroshi
AU - Shirato, Kunio
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2002/6/5
Y1 - 2002/6/5
N2 - OBIECTIVES: 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 (GPTX) 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 H2O), 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 GPTX, 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 μm) by 10%. The DVs pretreated with PTX (250 ± 27 μm) did not dilate in response to myocardial ischemia. Nω-nitro-L-arginine (100 μmol/1), but not glibenclamide (5 μmol/1), 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 GPTX located in the vascular walls. The nitric oxide pathway is involved in the signal transduction.
AB - OBIECTIVES: 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 (GPTX) 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 H2O), 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 GPTX, 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 μm) by 10%. The DVs pretreated with PTX (250 ± 27 μm) did not dilate in response to myocardial ischemia. Nω-nitro-L-arginine (100 μmol/1), but not glibenclamide (5 μmol/1), 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 GPTX located in the vascular walls. The nitric oxide pathway is involved in the signal transduction.
UR - http://www.scopus.com/inward/record.url?scp=0037024203&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037024203&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(02)01869-7
DO - 10.1016/S0735-1097(02)01869-7
M3 - Article
C2 - 12039503
AN - SCOPUS:0037024203
VL - 39
SP - 1859
EP - 1865
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 11
ER -