title: Myocardial segment shrinkage during coronary reperfusion in situ. Relation to hypercontracture and myocardial necrosis.
abstract: We have investigated the changes in myocardial segment length induced by reperfusion, and their relation to myocyte hypercontracture and contraction band necrosis. Regional wall function was monitored by ultrasonic gauges in 39 pigs submitted to 48-min occlusion of the left anterior descending coronary artery (LAD) and 6h of reperfusion. Infarct size (triphenyltetrazolium reaction), the extent of contraction band necrosis (quantitative histology) and myocardial water content (desiccation) were measured. Reperfusion induced a marked reduction in end-diastolic length of the LAD segment in all animals, maximal within 15 min after reflow. After 30 min of reperfusion, end-diastolic length of the LAD segment remained below the basal value in 15 animals. The 15 animals that showed shrinkage of the reperfused segment did not differ from the remaining animals in heart rate, aortic pressure, or control segment variables, but had larger infarcts (mean +/- SEM: 32.1 +/- 5.4 vs 12.1 +/- 3.2% of the area at risk, P = 0.003). There was an inverse correlation between end-diastolic length of the LAD segment after 30 min of reperfusion and infarct percentage (r = -0.72) or the extent of contraction band necrosis (r = -0.71). End-diastolic length reduction was more pronounced in larger infarcts despite a more severe myocardial oedema. Neither systolic shortening of the LAD segment nor end-diastolic length or systolic shortening of the control segment, or haemodynamic variables after 30 min of reperfusion correlated to infarct percentage or to the extent of contraction band necrosis. It is concluded that myocardial segment shrinkage during reperfusion reflects myocyte hypercontracture leading to contraction band necrosis.
authors.affiliation: Servicio de Cardiología, Hospital General Universitario Vall d'Hebron, Barcelona, Spain.
authors.forename: J A
authors.initials: JA
authors.lastname: Barrabés
authors.forename: D
authors.initials: D
authors.lastname: Garcia-Dorado
authors.forename: M
authors.initials: M
authors.lastname: Ruiz-Meana
authors.forename: H M
authors.initials: HM
authors.lastname: Piper
authors.forename: J
authors.initials: J
authors.lastname: Solares
authors.forename: M A
authors.initials: MA
authors.lastname: González
authors.forename: J
authors.initials: J
authors.lastname: Oliveras
authors.forename: M P
authors.initials: MP
authors.lastname: Herrejón
authors.forename: J
authors.initials: J
authors.lastname: Soler Soler
mesh_terms: D000818:Animals; D004489:Edema, Cardiac / Q000503:physiopathology; D006321:Heart / Q000502:physiology; D006331:Heart Diseases / Q000503:physiopathology; D006439:Hemodynamics; D006470:Hemorrhage / Q000503:physiopathology; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000502:physiology*; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000166:cytology* / Q000473:pathology*; D009336:Necrosis; D013552:Swine; D013997:Time Factors