No Impairment of Sympathetic Neurotransmission in Stunned Myocardium

Summary

Reversibly injured myocardium after short periods of ischemia is characterized by a prolonged depression of contractile function which can, however, be enhanced by inotropic interventions. Thus, a lack of inotropic stimulation due to ischemic damage of cardiac sympathetic nerves has been suggested as a mechanism underlying postischemic myocardial dysfunction. We tested this hypothesis in nine anesthetized, vagotomized dogs with left cardiac sympathetic nerve stimulation (CSNS) at 1, 2, 5, 10, and 20 Hz and compared this response to that of intravenous norepinephrine infusion (NE, 0.5–1 μg/kg·min). Regional myocardial wall thickness was measured using sonomicrometry, and mean systolic wall thickening velocity (MSTV) was determined. CSNS was performed before and at 0, 1, 2, 3, 4, 8, 12, 16, 20, and 24 h after release of a 15 min occlusion of a left circumflex coronary artery branch. Before coronary artery occlusion MSTV was increased in a frequency-dependent way from 7.5 ± 2.7 (S.D.) (rest) to 8.1 ± 3.1 (1 Hz), 9.4 ± 3.2 (2Hz), 11.4 ± 2.7 (5Hz), 13.4 ± 2.4 (10Hz), and 16.8 ± 2.1 (20Hz) by CSNS, and to 12.6 ± 3.4 mm/s by NE. Immediately upon reperfusion CSNS increased MSTV from 2.9 ± 2.0 to 2.9 ± 2.8, 4.1 ± 3.0, 5.4 ± 4.6, 6.9 ± 4.5 and 9.4 ± 5.9, and NE increased MSTV to 7.8 ± 1.9 mm/s. Baseline function recovered over 24 h, as did the response to CSNS and NE. Since the recovery of baseline function paralleled the increases in regional contractile function achieved by CSNS or NE, we conclude that there is no impairment of sympathetic neurotransmission in the stunned myocardium.