title: Preinfarction angina: no interference of coronary microembolization with acute ischemic preconditioning.
abstract: Transient episodes of angina preceding acute myocardial infarction may both, protect the myocardium by ischemic preconditioning or damage it when associated with coronary microembolization. We now studied the potential loss of ischemic preconditioning with coronary microembolization. Anesthetized pigs (group 1; n=8) were subjected to 90 min sustained low-flow ischemia. Group 2 (n=8) was subjected to coronary microembolization (i.e. microspheres; 42 microm slashed circle; 3000 per ml min-1 inflow) 35 min before sustained ischemia. In group 3, coronary microembolization was followed 10 min later by one cycle of ischemic preconditioning (10 min ischemia/15 min reperfusion) before subsequent sustained ischemia. Infarct size was determined after 2 h reperfusion by triphenyl tetrazolium chloride staining. Infarct size after sustained ischemia alone (group 1) was 19.4+/-3.4% of the area at risk (mean+/-S.E.M.). With coronary microembolization before sustained ischemia (group 2) infarct size was only slightly larger (23.6+/-4.6%, ns). In group 3 with microembolization followed by ischemic preconditioning, infarct size was reduced to 12.7+/-3.0% (P<0.05 vs. group 2). The relationships between infarct size and transmural blood flow in groups 1 and 3 were not different, giving the impression that ischemic preconditioning failed to protect microembolized myocardium. However, additional coronary microembolization shifted the relationship between infarct size and blood flow upwards to a larger infarct size at any given blood flow. Thus when comparing the relationship of group 3 to its true control (group 2), it was shifted downwards (P<0.05; analysis of covariance (ANCOVA)) indicating persistent protection of microembolized myocardium by ischemic preconditioning. Coronary microembolization induces additional infarction when superimposed on sustained ischemia but does not interfere with the endogenous protection by ischemic preconditioning.
authors.affiliation: Institute of Pathophysiology Center of Internal Medicine, University of Essen Medical School, Essen, Germany.
authors.forename: Andreas
authors.initials: A
authors.lastname: Skyschally
authors.forename: Petra
authors.initials: P
authors.lastname: Gres
authors.forename: Philipp
authors.initials: P
authors.lastname: Heusch
authors.forename: Claus
authors.initials: C
authors.lastname: Martin
authors.forename: Michael
authors.initials: M
authors.lastname: Haude
authors.forename: Raimund
authors.initials: R
authors.lastname: Erbel
authors.forename: Rainer
authors.initials: R
authors.lastname: Schulz
authors.forename: Gerd
authors.initials: G
authors.lastname: Heusch
mesh_terms: D000241:Adenosine / Q000032:analysis; D000789:Angina, Unstable / Q000503:physiopathology*; D000818:Animals; D003326:Coronary Circulation / Q000502:physiology*; D004621:Embolization, Therapeutic; D019194:Ischemic Preconditioning; D013552:Swine
chemical_list: D000241:Adenosine