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No impairment of sympathetic neurotransmission in stunned myocardium
Insights
This study investigated if cardiac sympathetic nerve damage causes post-ischemic myocardial dysfunction. Results show sympathetic nerve stimulation effectively improved contractile function, indicating no impairment in stunned myocardium.
Area of Science:
- Cardiology
- Physiology
- Myocardial Infarction Research
Background:
- Reversibly injured myocardium exhibits prolonged contractile dysfunction after ischemia.
- Inotropic interventions can enhance function in stunned myocardium.
- Ischemic damage to cardiac sympathetic nerves is a hypothesized cause of post-ischemic dysfunction.
Purpose of the Study:
- To test the hypothesis that impaired sympathetic neurotransmission contributes to post-ischemic myocardial dysfunction.
- To evaluate the functional response of stunned myocardium to direct sympathetic nerve stimulation and norepinephrine infusion.
Main Methods:
- Utilized sonomicrometry in anesthetized dogs to measure regional myocardial wall thickness and mean systolic wall thickening velocity (MSTV).
- Administered cardiac sympathetic nerve stimulation (CSNS) at varying frequencies (1-20 Hz) and intravenous norepinephrine (NE) infusion.
- Assessed responses before and at multiple time points up to 24 hours after a 15-minute coronary artery occlusion and reperfusion.
Main Results:
- CSNS increased MSTV in a frequency-dependent manner before ischemia.
- Immediately after reperfusion, CSNS and NE improved MSTV in stunned myocardium.
- Both baseline function and the response to CSNS and NE recovered over 24 hours.
Conclusions:
- The recovery of contractile function in stunned myocardium paralleled the response to sympathetic stimulation.
- There is no evidence of impaired sympathetic neurotransmission in the stunned myocardium.
- Post-ischemic myocardial dysfunction is not due to a deficit in sympathetic neurotransmission.
Abstract:
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 microgram/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 (2 Hz), 11.4 +/- 2.7 (5 Hz), 13.4 +/- 2.4 (10 Hz), and 16.8 +/- 2.1 (20 Hz) 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.