AJP - Heart and Circulatory Physiology, Vol 256, Issue 2 341-H351, Copyright © 1989 by American Physiological Society
Influence of neutrophil depletion on myocardial function and flow after reversible ischemia
P. G. O'Neill, M. L. Charlat, L. H. Michael, R. Roberts and R. Bolli
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.
We explored the role of polymorphonuclear leukocytes (PMN) in the genesis
of contractile dysfunction (myocardial "stunning") and of vascular
abnormalities after reversible ischemia. Open-chest dogs underwent a 15-min
coronary occlusion and 4 h of reperfusion (REP); treated animals (n = 16)
received intravenous goat antiserum against canine PMN, whereas controls
received nonimmune goat serum (n = 10) or saline (n = 15). In treated dogs,
the average blood PMN levels were 10% of those in saline controls. During
ischemia, collateral flow tended to be higher, and paradoxical systolic
wall thinning tended to be less in neutropenic dogs, but despite this,
recovery of wall thickening after REP was not enhanced in these animals.
Similarly, arrhythmias during ischemia or REP did not differ among the
three groups. Four hours after REP, both resting and minimal coronary
resistance (the latter assessed by adenosine infusion) were higher in the
stunned compared with the nonischemic myocardium; these vascular
derangements, however, were similar in all three groups. Thus profound
neutropenia failed to attenuate mechanical dysfunction, to reduce
arrhythmias, and to prevent vascular abnormalities after a 15-min coronary
occlusion. Although previous studies have suggested that neutrophils
mediate cell death during prolonged ischemia, the present findings suggest
that PMN do not contribute importantly to the damage associated with brief,
reversible ischemia. The duration of flow reduction may be a critical
factor determining whether PMN exacerbate ischemic injury.
