915-79 Nitric Oxide is a Preferential Subendocardial Vasodilator

The effects of nitric oxide (NO) on myocardial blood flow (MBF) have been studied previously by observing responses to agents that stimulate or block endogenous NO release. To study the direct in vivo effects of endoluminally administered NO on transmural myocardial perfusion, we studied 4 anesthetized dogs using a new method for intracoronary NO administration. NO gas was bubbled through deoxygenated saline to achieve the saturation constant (2–3 mM). During ventricular pacing at 100 beats/min, the solution was infused into the left main coronary artery at doses of 0.2 and 16  μ mol/min, Transmural myocardial perfusion and coronary blood flow were measured with radioactive microspheres after 2 minutes of infusion. Changes in MFB (ml/gm/min) induced from continuous NO infusion were compared to endothelially mediated NO release induced by intracoronary administration of acetylcholine (Ach 2,0  μ mol/min) and non-NO mediated vasodilitation by intracoronary adenosine (AD 1.2  μ mol/min). Results: Basal NO 0.2 NO 16 Ach AD MBF(mean) 0.8 ± 0.03 1.4 ± 0.10 * 1.6 ± 0.08 * 1.6 ± 0.06 * 2.5 ± 0.11 * ED MFB 0.7 ± 0.03 1.4 ± 1.4 * 1.8 ± 0.12 * 1.8 ± 0.08 * 2.7 ± 0.13 * EDIEP 0.7 ± 0.02 1.0 ± 0.06 * 1.3 ± 0.07 * 1.2 ± 0.05 * 1.3 ± 0.07 * mean ± sem * p l 001 vs. basal ED/EP = endocardial to epicardial blood flow ratio High dose NO (16  μ mol/min) caused an increase in endocardial and total myocardial blood flow which was similar to that produced by acetylcholine. Conclusions Nitric oxide causes dose dependent increases in myocardial blood flow and the endocardial to epicardial blood flow ratio. High dose endoluminal NO infusion causes changes in myocardial blood flow and transmural myocardial perfusion which are equivalent to that caused byendothelial derived NO, Moreover, whether administered exogenously or released endogenously, NO is a preferential sub-endocardial vasodilator.