title: Revascularization for acute regional infarct: superior protection with warm blood cardioplegia.
abstract: Continuous retrograde warm blood cardioplegia was compared with two widely used hypothermic myocardial protection techniques in a canine model of acute regional myocardial ischemia with subsequent revascularization. Animals (n = 30) underwent 45 minutes of left anterior descending coronary artery occlusion then cardioplegic arrest (60 minutes), followed by separation from cardiopulmonary bypass and data collection. The cold oxygenated crystalloid cardioplegia group (CC; n = 8) and the cold blood cardioplegia group (CC; n = 10) had cardiopulmonary bypass at 28 degrees C, antegrade arrest, and intermittent retrograde delivery. The warm blood cardioplegia group (WB; n = 12) had normothermic cardiopulmonary bypass, antegrade arrest, and continuous retrograde delivery. Overall ventricular function (preload recruitable stroke work relationship; ergs x 10(3)/mL) was significantly (p < 0.001) better for WB (WB, 80 +/- 11; CB, 67 +/- 13; CC, 57 +/- 12). Systolic function (maximum elastance relationship; mm Hg/mL) was also significantly (p < 0.001) better for WB (WB, 11.6 +/- 3.6; CB, 8.6 +/- 2.7; CC, 6.2 +/- 1.3). Diastolic function (stress-strain relationship; dynes x 10(3)/cm2) revealed significantly (p < 0.001) decreased compliance for CC (WB, 20 +/- 6; CB, 19 +/- 7; CC, 27 +/- 11). Left anterior descending coronary artery regional adenosine triphosphate/adenosine diphosphate ratios were significantly (p = 0.02) worse for CC (WB, 10.2 +/- 2.3; CB, 9.4 +/- 2.6; CC, 5.6 +/- 1.5). Myocardial edema significantly (p = 0.03) increased over time only in the CC animals (WB, 0.4% +/- 2.3%; CB, -0.3% +/- 3.6%; CC, 5.5% +/- 2.3%). In this model of acute regional myocardial ischemia and revascularization, continuous retrograde warm aerobic blood cardioplegia provided superior myocardial protection compared with cold oxygenated crystalloid cardioplegia with intermediate results for cold blood cardioplegia.
authors.affiliation: Department of Surgery, Emory University School of Medicine, Atlanta, Georgia.
authors.forename: W S
authors.initials: WS
authors.lastname: Horsley
authors.forename: J D
authors.initials: JD
authors.lastname: Whitlark
authors.forename: J D
authors.initials: JD
authors.lastname: Hall
authors.forename: J P
authors.initials: JP
authors.lastname: Gott
authors.lastname: Pan-Chih
authors.forename: A H
authors.initials: AH
authors.lastname: Huang
authors.forename: Y
authors.initials: Y
authors.lastname: Park
authors.forename: D P
authors.initials: DP
authors.lastname: Jones
authors.forename: R A
authors.initials: RA
authors.lastname: Guyton
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology; D003971:Diastole / Q000502:physiology; D004285:Dogs; D004487:Edema / Q000209:etiology; D006324:Heart Arrest, Induced / Q000009:adverse effects / Q000379:methods*; D006439:Hemodynamics / Q000502:physiology; D006358:Hot Temperature; D007036:Hypothermia, Induced / Q000379:methods; D009203:Myocardial Infarction / Q000503:physiopathology / Q000628:therapy*; D009204:Myocardial Revascularization; D009206:Myocardium / Q000378:metabolism; D013312:Stress, Physiological / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D000255:Adenosine Triphosphate