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Recruitment of inotropic reserve in "stunned" myocardium by the cardiotonic agent AR-L 57.

Abstract
Contractile dysfunction of reversibly injured, reperfused myocardium can be enhanced by inotropic interventions. A decrease in the Ca-sensitivity of contractile proteins with slow recovery during reperfusion has been suggested as a potential mechanism underlying this postischemic dysfunction. We therefore tested the effects of the cardiotonic agent AR-L 57 (1 mg/kg i.v.) in six anesthetized, vagotomized dogs during constant atrial pacing at 192 +/- 6 beats/min. Before ischemia, AR-L 57 increased left ventricular pressure from 131 +/- 22 to 138 +/- 21 mm Hg and maximum dP/dt from 3,022 +/- 1,427 to 4,337 +/- 2,608 mm Hg/s. Mean systolic thickening velocity of the posterior myocardium was increased from 8.9 +/- 1.1 to 11.7 +/- 1.1 mm/s. After release of a 15 min LCX-occlusion which caused complete regional akinesia, baseline function in the posterior myocardium was severely depressed and only gradually returned towards control values over 8 h of reperfusion. AR-L 57 increased systolic thickening velocity at 10 min, 4 and 8 h reperfusion to a similar extent as before ischemia. With reference to a purported Ca-sensitizing mechanism underlying the positive inotropic action of AR-L 57, our data suggest no change in the Ca-sensitivity of reperfused myocardium.
AuthorsG Heusch, S Schäfer, K Kröger
JournalBasic research in cardiology (Basic Res Cardiol) 1988 Nov-Dec Vol. 83 Issue 6 Pg. 602-10 ISSN: 0300-8428 [Print] Germany
PMID3223876 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cardiotonic Agents
  • Imidazoles
  • AR-L 57 CL
Topics
  • Animals
  • Cardiotonic Agents (pharmacology)
  • Dogs
  • Female
  • Hemodynamics (drug effects)
  • Imidazoles (pharmacology)
  • Male
  • Myocardial Contraction (drug effects)
  • Myocardial Reperfusion Injury (pathology)
  • Myocardium (pathology)
  • Necrosis

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