title: Severe neutrophil depletion by leucocyte filters or cytotoxic drug does not improve recovery of contractile function in stunned porcine myocardium.
abstract: OBJECTIVE
  The contribution of neutrophils to myocardial injury during stunning remains controversial because of conflicting results in neutropenic animals. The goal of this study was to compare the recovery of function in stunned myocardium using two distinct methods for inducing neutropenia in pigs.
  
  
  METHODS
  Three groups of pigs were studied: control (n = 6), and made neutropenic by either Leukopak blood filters (n = 7), or cyclophosphamide (n = 7, 50 mg.kg-1 intravenously 4 d prior to study). In anaesthetised open chest pigs, with the heart paced at 110 beats.min-1, the left anterior descending coronary artery was perfused with an extracorporeal circuit at controlled coronary pressure (CP) and the regional coronary blood flow was measured. Systolic wall thickening was determined by sonomicrometry in the left anterior descending and circumflex coronary artery regions. The protocol consisted of 15 min of low flow ischaemia (CP = 40 mm Hg), followed by a staged reperfusion over 10 min back to baseline (CP = 90 mm Hg), and continued for 2 h. Blood filtration was initiated prior to ischaemia and stopped after 90 min reperfusion.
  
  
  RESULTS
  In both treated groups during ischaemia and the initial 60 min of reperfusion the neutrophil count was severely depleted to < 5% compared to the control group. Aortic pressure, coronary blood flow during ischaemia, area at risk, and systolic wall thickening in the circumflex region were similar between groups. Recovery of systolic wall thickening in the left anterior descending region after reperfusion was equivalent in all three groups. In the filter group, arrhythmias during ischaemia and reperfusion were significantly less.
  
  
  CONCLUSIONS
  As assessed in the pig model of myocardial stunning and using two different methods, severe neutropenia does not reduce the depression of contractile function.
authors.affiliation: Department of Veterans Affairs, Medical Center, Research Service, La Jolla, CA 92161.
authors.forename: C F
authors.initials: CF
authors.lastname: Juneau
authors.forename: B R
authors.initials: BR
authors.lastname: Ito
authors.forename: U
authors.initials: U
authors.lastname: del Balzo
authors.forename: R L
authors.initials: RL
authors.lastname: Engler
mesh_terms: D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D004195:Disease Models, Animal; D005260:Female; D007958:Leukocyte Count; D008297:Male; D008851:Micropore Filters; D009200:Myocardial Contraction / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000473:pathology; D009503:Neutropenia / Q000139:chemically induced; D009504:Neutrophils / Q000473:pathology / Q000502:physiology*; D013552:Swine
chemical_list: D003520:Cyclophosphamide