Leukocytic .O2- and cardiac dysfunctions in isolated perfused rat hearts

Superoxide radicals are supposed to contribute to myocardial reperfusion injury. Their origin, however, is still a matter of debate. Polymorphonuclear leukocytes (PMNL) have been discussed as a major postischaemic .O2- source [Lucchesi and Mullane (1986) Ann Rev Pharmacol Toxicol 26: 201-224]. We studied the role of .O2- derived from human polymorphonuclear leukocytes in reperfused and normoxic perfused isolated rat hearts. During reperfusion PMNL exerted deleterious effects on different parameters (e.g. contractility, coronary flow) of isolated rat hearts. Under normoxic perfusion conditions stimulation of PMNL with N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) caused bradycardia and a transient vasoconstriction. Superoxide dismutase (SOD) administration did not influence any of the PMNL effects mentioned, suggesting that leukocytic .O2- was not involved in PMNL-induced cardiac dysfunctions.