title: L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge.
abstract: Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, "no-reflow" was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on "myocardial stunning." Potential markers for long-term recovery were not affected by L-propionylcarnitine.
authors.affiliation: Laboratory for Experimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, The Netherlands.
authors.forename: L M
authors.initials: LM
authors.lastname: Sassen
authors.forename: K
authors.initials: K
authors.lastname: Bezstarosti
authors.forename: W J
authors.initials: WJ
authors.lastname: Van der Giessen
authors.forename: J M
authors.initials: JM
authors.lastname: Lamers
authors.forename: P D
authors.initials: PD
authors.lastname: Verdouw
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002331:Carnitine / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D004734:Energy Metabolism; D005260:Female; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D010710:Phosphates / Q000378:metabolism; D000099211:Phospholamban
chemical_list: D000255:Adenosine Triphosphate; D002118:Calcium; D002135:Calcium-Binding Proteins; D002331:Carnitine; D010710:Phosphates; D000099211:Phospholamban; C003223:propionylcarnitine