Mechanism of beneficial effects of nitroglycerin on pacing induced regional myocardial ischemia in dogs

The mechanism whereby nitroglycerin (TNG) improves myocardial ischemia is unclear. Thirteen anesthetized dogs had a flow-limiting coronary stenosis applied to the left anterior descending coronary artery (LAD). Ischemia was induced during two separate 15 minute periods of atrial pacing. Six dogs received intravenous infusions of TNG at a rate sufficient to lower mean arterial pressure (MAP) 10 mm Hg during the second pacing period while 7 dogs received an infusion of saline. Mean LAD flow (LADF) was measured by electromagnetic flow probe, regional myocardial blood flow (MBF) by 7-10μ radioactive microspheres and intramyocardial electrograms by plunge electrode. Control heart rate was 150 beats/min, increasing to 210 ±6 (SEM) beats/min with pacing. The change in mean left atrial pressure (LAP) from 3.4 ± 1.0 to 2.2 ± 1.0 mm Hg with TNG was not significant. LADF did not change with pacing alone but fell from 10±2.4 to 8.6±1.9 ml/min with TNG (P<.05). MBF decreased from 104±12 to 89±12 ml/min/100 gm in LAD endocardium during TNG (P<.05) and from 106±13 to 91±12 ml/min/100 gm in LAD endocardium during TNG (P<.05) and from 106 ± 13 to 91 ± 12 ml/min/100gm in LAD epicardium during TNG (P<.05). The change in endocardial (ST) segment elevation (ΔST) with pacing decreased from 2.3±0.4 to 1.2±0.3 mv with TNG (P<.05). Epicardial ΔST with pacing was not altered by TNG. There were no significant differences in MAP, LAP, LADF, MBF, or ΔST between the first and second pacing periods in untreated dogs. These data suggest that TNG can improve pacing-induced subendocardial ischemia by reducing afterload, without either increasing or redistributing transmural myocardial blood flow.