Objective: The aim of this study was to investigate the contribution of nitric oxide / prostanoid-independent pathways to endotheliumdependent vasorelaxation in human conduit arteries. Methods: Rings of internal thoracic artery (ITA) and radial artery (RA) taken from patients undergoing coronary artery bypass graft surgery were suspended in 10-ml organ baths and relaxation to carbachol and bradykinin studied in the presence and absence of nitric oxide synthase (NOS) inhibitors and potassium channel blockers. Results: No significant relaxation to carbachol or bradykinin was observed in ITA after NOS inhibition. In contrast, in RA less than 40% attenuation of relaxation 1 to carbachol or bradykinin was achieved with any of the NOS inhibitors. In the presence of 20 mM K relaxation to carbachol and 1 bradykinin was inhibited by 2869% and 4269% while in the presence of L-NAME 200 mM120 mM K relaxation was inhibited by 6666% and 7064% respectively in this artery. Tetraethylammonium, glibenclamide, apamin and iberiotoxin had little effect on relaxation to carbachol but charybdotoxin alone and charybdotoxin plus apamin attenuated relaxation to carbachol by 2364% and 4969% in RA. In the presence of L-NAME 200 mM attenuation of these relaxations were increased to 6064% and 7864%. Conclusion: In ITA relaxations to carbachol and bradykinin were mediated via nitric oxide. In contrast in RA, a conduit vessel of similar diameter, both nitric oxide-dependent and independent pathways appeared to contribute to vascular relaxation. This nitric oxide-independent relaxation 21 involved opening of Ca activated potassium channel(s). The existence of alternative pathways mediating endothelium-independent relaxation could be important under pathological conditions and may contribute to the long term survival of radial artery grafts.

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Background Myocardial hemorrhage after myocardial infarction (MI) usually goes undetected. We investigated the diagnostic accuracy of bright blood T2-weighted cardiac magnetic resonance imaging (MRI) for myocardial hemorrhage in experimental MI. Methods and Results MI was created in swine by occluding the left anterior descending (n=10) or circumflex (n=5) coronary arteries for 90 minutes followed by reperfusion for ≤3 days (n=2), 10 days (n=7) or 60 days (n=6). MRI was performed at 1.5 Tesla using bright blood T2-prepared steady-state free-precession, T2* and early (1 min) and late (10 – 15 min) gadolinium enhancement (EGE, LGE, respectively) MRI. Left ventricular sections and histology were assessed for hemorrhage by an experienced cardiac pathologist blinded to the MRI data. Hypointense regions on T2-weighted and contrast-enhanced MRI were independently determined by 3 cardiologists experienced in MRI who were also blinded to the pathology results. Eighty ventricular pathologic sections were matched with MRI (n=68 for EGE MRI). All sections with evidence of MI (n=63 (79%)) also exhibited hyperintense zones consistent with edema on T2-weighted MRI and infarct on LGE MRI. Myocardial hemorrhage occurred in 49 left ventricular sections (61%) and corresponded with signal voids on 48 T2-weighted (98%) and 26 LGE-MRI (53%). Alternatively, signal voids occurred in the absence of hemorrhage in 3 T2-weighted (90% specificity) and 5 LGE MRI (84% specificity). On EGE MRI, 27/43 cases of early MVO corresponded with hemorrhage (63% sensitivity) while 5/25 defects occurred in the absence of hemorrhage (80% specificity). The positive and negative predictive values for pathological evidence of hemorrhage were 94% & 96% for T2-weighted, 84% & 55% for LGE MRI and 85% & 56% for EGE MRI. Conclusions Bright blood T2-weighted MRI has high diagnostic accuracy for myocardial hemorrhage.