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EXPERIMENTAL STUDY

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

^* Department of Cardiovascular Medicine, Tohoku University, Graduate School of Medicine, Sendai, Japan

Manuscript received June 1, 2001; revised manuscript received February 25, 2002, accepted March 11, 2002.

^* Reprint requests and correspondence: Dr. Tatsuya Komaru, Department of Cardiovascular Medicine, Tohoku University, Graduate School of Medicine, 1-1, Seiryo-machi, Aoba-ku, Sendai, 980-8574 Japan.
komaru{at}int1.med.tohoku.ac.jp

OBJECTIVES: 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 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 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 µm) by 10%. The DVs pretreated with PTX (250 ± 27 µm) did not dilate in response to myocardial ischemia. N-nitro-L-arginine (100 µmol/l), but not glibenclamide (5 µmol/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.

Abbreviations and Acronyms   DV   detector vessel   GPTX   pertussis toxin-sensitive G proteins   KATP   adenosine triphosphate-sensitive potassium channels   LAD   left anterior descending coronary artery   L-NNA   N-nitro-L-arginine   LV   left ventricle   NO   nitric oxide   PSS   physiologic saline solution   PTX   pertussis toxin   SNP   sodium nitroprusside

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