title: Cardiodepressive mediators are released after ischemia from an isolated heart: role of coronary endothelial cells.
abstract: OBJECTIVE
  This study was designed to ascertain whether cardiodepressive mediators released after ischemia originate from coronary endothelial cells.
  
  
  BACKGROUND
  Endothelial cells modulate myocardial contractility under physiologic conditions. Few data are available describing the role of coronary endothelial cells on myocardial function after ischemia.
  
  
  METHODS
  Using a model of sequential perfusion of two isolated rat hearts, the effect of the reoxygenated coronary effluent of heart I was investigated on myocardial contractility of heart II. After 40 min of separate perfusion at constant flow (10 ml/min), the two hearts were perfused sequentially with (group I) or without (control group) preceding ischemia (10 min) of heart I. In groups II and III, the coronary endothelium of heart I was functionally removed by Triton X-100 or hyperkalemic infusion before global ischemia. Endothelial damage was confirmed by functional tests and electron microscopy.
  
  
  RESULTS
  Under control conditions no changes were observed in heart II during sequential perfusion. In contrast, after 10 min of ischemia in heart I, a marked reversible decrease in left ventricular pressure, left ventricular dP/dtmax and left ventricular dP/dtmin (-55%, -66% and -70%, respectively) was observed in heart II. Heart rate and coronary perfusion pressure did not change significantly. Selective endothelial damage of heart I before ischemia did not modify the negative inotropic effect observed in heart II.
  
  
  CONCLUSIONS
  Cardiodepressive mediators are released after ischemia during reperfusion from an isolated heart and induce a reversible negative inotropic effect in a sequentially perfused heart. It is unlikely that these agents are derived from the coronary endothelium.
authors.affiliation: Medizinische Klinik, Institut für Pathologie Rudolf Virchow, Universitätsklinikum Charité, Humboldt-Universität zu Berlin, Germany.
authors.forename: V
authors.initials: V
authors.lastname: Stangl
authors.forename: S B
authors.initials: SB
authors.lastname: Felix
authors.forename: R
authors.initials: R
authors.lastname: Meyer
authors.forename: T
authors.initials: T
authors.lastname: Berndt
authors.forename: R
authors.initials: R
authors.lastname: Kästner
authors.forename: K D
authors.initials: KD
authors.lastname: Wernecke
authors.forename: G
authors.initials: G
authors.lastname: Baumann
mesh_terms: D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects / Q000473:pathology*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D005260:Female; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D017830:Octoxynol / Q000494:pharmacology; D051381:Rats; D013997:Time Factors; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D017830:Octoxynol