title: Influence of leukopenia on collateral flow, reperfusion flow, reflow ventricular fibrillation, and infarct size in dogs.
abstract: Leukocytes contribute to myocardial damage during ischemia and reperfusion. However, the mechanism involved has not been clearly elucidated. The purpose of the present study was to determine whether leukocyte-induced myocardial damage is flow mediated. In open-chest dogs submitted to 2 hours of ischemia, area at risk, infarct size, and regional myocardial blood flow before, during, and after ischemia were measured. Leukopenia was induced by a two-step method (chemotherapy and antineutrophil serum) in a group of 14 dogs as compared to a control group of 18 dogs. The relation of infarct size to the major determinants of infarct size was analyzed by uni- and multilinear regressions. Seven control dogs had ventricular fibrillation at reperfusion compared to one dog with leukopenia. In the group with leukopenia the mean infarct size was smaller (31.1 +/- 5.8% of area at risk) than in the control group (47.7 +/- 2.9, p = 0.02). In addition, the two multiple linear regression equations were significantly different (p = 0.01). Myocardial blood flow to the central ischemic zone did not change significantly between 20 and 120 minutes of ischemia in the control dogs (n = 12; subendocardial = 0.08 +/- 0.03 vs 0.07 +/- 0.03 ml/min/gm; subepicardial = 0.20 +/- 0.07 vs 0.20 +/- 0.05 ml/min/gm) and in the dogs with leukopenia (n = 12; 0.07 +/- 0.02 vs 0.07 +/- 0.02 ml/min/gm and 0.15 +/- 0.004 vs 0.18 +/- 0.04 ml/min/gm). A similar reduction in myocardial blood flow was observed after 6 hours of reperfusion in the control dogs (0.34 +/- 0.07 ml/min/gm vs 1.02 +/- 0.11 at baseline, p less than 0.01) and in the dogs with leukopenia (0.25 +/- 0.04 vs 0.81 +/- 0.08 ml/min/gm, p less than 0.01). It was concluded that the leukocyte-dependent myocardial injury did not appear to be mediated through a flow mechanism during either ischemia or reperfusion.
authors.affiliation: Laboratory of Experimental Pathology, Montreal Heart Institute, Quebec, Canada.
authors.forename: M
authors.initials: M
authors.lastname: de Lorgeril
authors.forename: A
authors.initials: A
authors.lastname: Basmadjian
authors.forename: M
authors.initials: M
authors.lastname: Lavallée
authors.forename: R
authors.initials: R
authors.lastname: Clément
authors.forename: D
authors.initials: D
authors.lastname: Millette
authors.forename: G
authors.initials: G
authors.lastname: Rousseau
authors.forename: J G
authors.initials: JG
authors.lastname: Latour
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation; D004285:Dogs; D005260:Female; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D007958:Leukocyte Count; D007970:Leukopenia / Q000503:physiopathology*; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D015425:Myocardial Reperfusion / Q000379:methods*; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D009504:Neutrophils / Q000502:physiology; D014693:Ventricular Fibrillation / Q000503:physiopathology*