Effect of NO on transmural distribution of blood flow in hypertrophied left ventricle during exercise

When exercise in the presence of a coronary artery stenosis results in sube ndocardial ischemia, administration of a nitric oxide (NO) donor increases subendocardial blood flow, whereas NO synthesis blockade worsens subendocar dial hypoperfusion. Because left ventricular hypertrophy (LVH) is also asso ciated with subendocardial hypoperfusion during exercise, this study tested the hypothesis that alterations of NO availability can similarly influence subendocardial blood flow in the hypertrophied heart. Studies were perform ed in seven dogs in which ascending aortic banding resulted in an 80% incre ase in LV weight. Myocardial blood flow was measured with microspheres duri ng treadmill exercise that increased heart rates to 216 +/- 8 beats/min. Du ring control exercise, mean myocardial blood flow in animals with LVH was s imilar to that in historic controls, but the ratio of subendocardial to sub epicardial blood flow was lower in animals with hypertrophy (0.88 +/- 0.07) than in controls (1.36 +/- 0.08; P < 0.05). Blockade of NO synthesis with N-G-nitro-Larginine (L-NNA; 1.5 mg/kg ic) caused no change in heart rate or LV systolic pressure during exercise. Furthermore, LNNA did not worsen sub endocardial hypoperfusion during exercise. Intracoronary infusion of nitrog lycerin (0.4 mu g . kg(-1) min(-1)) did not significantly alter either mean blood flow or the transmural distribution of perfusion during exercise in the hypertrophied hearts. Thus, unlike the subendocardial underperfusion th at occurs when a stenosis limits coronary blood flow alterations of NO avai lability did not alter subendocardial hypoperfusion in the hypertrophied he arts.