Polymorphonuclear granulocytes induce myocardial dysfunction during ischemia and in later reperfusion of hearts exposed to low-flow ischemia.
Polymorphonuclear granulocytes (PMNs) are known to contribute to reperfusion injury of the heart. However, whether PMNs compromise myocardial function of hearts exposed to a low-flow ischemia has not been determined. Moreover, not much is known about deleterious effects of PMNs at different times during ischemia and reperfusion. Isolated, working guinea pig hearts were subjected to 30 min of low-flow ischemia and reperfusion. Homologous PMNs were applied as 1-min boluses in the presence of thrombin during either ischemia or the first or fifth minute of reperfusion, and postischemic recovery of external heart work (REHW) and intracoronary PMN retention (PMNR) were quantified. In further experiments, the radical scavenger superoxide dismutase (SOD) was added. Compared with controls without PMNs (REHW, 92.4%), application of PMNs led to a significant loss of myocardial function, which was detected at all three examination times. Moreover, intracoronary PMNR increased significantly in comparison with that of controls with hearts not exposed to ischemia or reperfusion. On the other hand, addition of SOD significantly increased REHW. Intracoronary PMNR was not significantly changed by coapplication of SOD. We conclude that thrombin-stimulated PMNs applied at different times during ischemia and reperfusion significantly impaired cardiac function in hearts exposed to a low-flow ischemia.
Seligmann
C
C
Department of Cardiology, University Hospital Benjamin Franklin, Free University of Berlin, D-12200 Berlin, Germany. cseligmann@talknet.de
Bock
A
A
Leitsch
T
T
Schimmer
M
M
Simsek
Y
Y
Schultheiss
H P
HP
D000818:Animals; D003331:Coronary Vessels / Q000276:immunology; D006168:Guinea Pigs; D006321:Heart / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D017202:Myocardial Ischemia / Q000276:immunology*; D015428:Myocardial Reperfusion Injury / Q000276:immunology*; D009206:Myocardium / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D013482:Superoxide Dismutase / Q000276:immunology
D013482:Superoxide Dismutase