Poststenotic XXXX induced by peripheral nociceptive stimulation.

@entity296 @entity235 @entity26 @entity3979 @entity158 @entity850 @entity3575
Sympathetic activation increases cardiac performance, and the increased myocardial @entity26 demand is adequately met by an increase in coronary blood flow after metabolic coronary dilation under normal conditions. Distal to a severe @entity3979 , however, activation of cardiac sympathetic nerves induces @entity296 by alpha 2-adrenergic coronary constriction. Activation of cardiac sympathetic nerves is one of the autonomous reactions associated with acute @entity158 . Therefore we investigated the effects of acute @entity158 on regional myocardial function distal to a severe @entity3979 . In 5 anaesthetized, vagotomized @entity235 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 @entity850 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 @entity3575 prevented the deterioration of poststenotic myocardial function during nociceptive stimulation. CONCLUSION: Acute @entity158 can induce @entity296 distal to a severe @entity3979 by activation of cardiac sympathetic nerves. @entity3575 not only prevents the @entity158 sensation but also poststenotic @entity296 .
