title: Independency of myocardial stunning of endothelial stunning?
abstract: OBJECTIVE
  Vascular endothelial cells play an important role in the control of vascular tone. The reasons for coronary endothelial dysfunction are complex and may involve ischemia/reperfusion injury. We investigated whether endothelial, smooth muscle, and myocardial dysfunction are independent phenomena.
  
  
  METHODS
  Rabbit hearts were rapidly excised without intermittent ischemia, connected to a modified Langendorff apparatus, and perfused with a modified Krebs-Henseleit solution containing bovine erythrocytes. Normoxic control hearts (n = 16) were perfused for 125 min. Postischemic hearts (n = 15) were perfused for 45 min, submitted to global ischemia (20 min) and reperfused (60 min). Both the normoxic and the postischemic hearts were divided into three groups that received either 0.9% NaCl (placebo), or 3-morpholinosydnonimine (SIN-1; 100 microM),or substance P (SP; 5 nM).
  
  
  RESULTS
  After SIN-1, CBF in the normoxic hearts was increased by maximum 63% and after SP by 62%. 60 min after the onset of reperfusion, the postischemic hearts of both groups had recovered to 95% LVP(max). In the postischemic hearts, SIN-1 increased CBF still by 58%, while the endothelium-dependent vasomotion was impaired: SP improved CBF by only 9%.
  
  
  CONCLUSIONS
  The particular protocol permitted differentiation between myocardial and vascular stunning. The results show that, while myocardial function has already recovered, endothelial cells are more severely impaired than smooth muscle cells, and that this injury persists beyond myocardial stunning. Thus, endothelial-dependent dysfunction can still impair vasodilatation while ventricular dysfunction has already resolved.
authors.affiliation: Research Group Experimental Surgery, Dept. of Thoracic- and Cardiovascular Surgery, University Hospital Duesseldorf, Düsseldorf, Germany.
authors.forename: Solange C
authors.initials: SC
authors.lastname: Garcia
authors.forename: Valdeci
authors.initials: V
authors.lastname: Pomblum
authors.forename: Emmeran
authors.initials: E
authors.lastname: Gams
authors.forename: Michael R
authors.initials: MR
authors.lastname: Langenbach
authors.forename: Jochen D
authors.initials: JD
authors.lastname: Schipke
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008981:Molsidomine / Q000031:analogs & derivatives / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D017682:Myocardial Stunning / Q000378:metabolism / Q000503:physiopathology*; D011817:Rabbits; D012107:Research Design; D013373:Substance P / Q000378:metabolism; D013997:Time Factors; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology; D016276:Ventricular Function
chemical_list: D014665:Vasodilator Agents; D013373:Substance P; C002385:linsidomine; D008981:Molsidomine