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  • Title: Poststenotic ischaemic myocardial dysfunction induced by peripheral nociceptive stimulation.
    Author: Kröger K, Schipke J, Thämer V, Heusch G.
    Journal: Eur Heart J; 1989 Nov; 10 Suppl F():179-82. PubMed ID: 2620687.
    Abstract:
    UNLABELLED: Sympathetic activation increases cardiac performance, and the increased myocardial oxygen demand is adequately met by an increase in coronary blood flow after metabolic coronary dilation under normal conditions. Distal to a severe coronary stenosis, however, activation of cardiac sympathetic nerves induces myocardial ischaemia by alpha 2-adrenergic coronary constriction. Activation of cardiac sympathetic nerves is one of the autonomous reactions associated with acute somatic pain. Therefore we investigated the effects of acute somatic pain on regional myocardial function distal to a severe coronary stenosis. In 5 anaesthetized, vagotomized dogs activation of cardiac sympathetic nerves was achieved by electrical stimulation of the nervus peronaeus superficialis. To analyse regional myocardial function, myocardial wall thickness was continuously measured by sonomicrometry in the circumflex-perfused posterior and in the anterior (control) myocardium. Under control conditions, nociceptive stimulation increased systolic wall thickening of the posterior myocardium from 10.9 +/- 3.9% to 13.6 +/- 5.0%. With a severe stenosis on the left circumflex coronary artery, systolic wall thickening was reduced to 7.0 +/- 2.5% and further decreased to 4.6 +/- 2.3% during nociceptive stimulation. Intravenous injection of 27 micrograms/kg fentanyl prevented the deterioration of poststenotic myocardial function during nociceptive stimulation. CONCLUSION: Acute somatic pain can induce ischaemic myocardial dysfunction distal to a severe coronary stenosis by activation of cardiac sympathetic nerves. Fentanyl not only prevents the pain sensation but also poststenotic ischaemic myocardial dysfunction.
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