title: Hemodynamic, left ventricular structural and hormonal changes after discrete myocardial damage in the dog.
abstract: Transmyocardial direct-current (DC) shock produces localized left ventricular myocardial necrosis without obstruction to coronary blood flow. In 43 dogs sequential measurements of hemodynamic, neuroendocrine and myocardial structural changes were made at baseline and for 16 weeks after DC shock. Six dogs (14%) died in the peri-shock period. By 1 week after shock, left ventricular mass, as measured by nuclear magnetic resonance imaging, had increased from a mean value +/- SD of 67.9 +/- 10.1 to 82.5 +/- 12.9 g (p = 0.0001). Left ventricular end-diastolic volume was unchanged at 1 week but increased at 16 weeks from 56.1 +/- 10.3 to 70.3 +/- 10.7 ml (p = 0.0003). Left ventricular mass demonstrated a further increase at 12 months (107.8 +/- 14.8 g). Rest cardiac output was significantly decreased at 4 months (3.67 +/- 1.23 to 3.18 +/- 0.81 liters/min, p less than 0.01) as was stroke volume (43 +/- 9 to 37 +/- 7 ml, p less than or equal to 0.01). Left ventricular ejection fraction decreased progressively from 73% to 38% at 1 year. At 4 months there were increases in mean pulmonary artery pressure (18 +/- 4 to 23 +/- 4 mm Hg, p less than 0.01), pulmonary capillary wedge pressure (9 +/- 3 to 15 +/- 3 mm Hg, p less than 0.01) and right atrial pressure (5 +/- 4 to 9 +/- 3 mm Hg, p less than 0.01). Plasma norepinephrine was increased at 4 months (318 +/- 190 to 523 +/- 221 pg/ml, p = 0.0003), whereas plasma renin activity was not significantly changed (4.3 +/- 2.6 vs. 5.2 +/- 3.4 ng/ml per h). Microsphere regional blood flow studies demonstrated a 50% reduction in skeletal muscle blood flow at 4 months (0.06 +/- 0.06 ml/min per g compared with 0.12 +/- 0.09 in normal dogs, p = 0.05), and a reduction in the endocardial/epicardial blood flow ratio (1.11 +/- 0.13 compared with 1.24 +/- 0.13 in normal dogs, p = 0.02). Therefore, in this model of acute left ventricular damage, left ventricular hypertrophy precedes progressive left ventricular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, University of Minnesota Medical School, Minneapolis.
authors.forename: K M
authors.initials: KM
authors.lastname: McDonald
authors.forename: G S
authors.initials: GS
authors.lastname: Francis
authors.forename: P F
authors.initials: PF
authors.lastname: Carlyle
authors.forename: K
authors.initials: K
authors.lastname: Hauer
authors.forename: J
authors.initials: J
authors.lastname: Matthews
authors.forename: D W
authors.initials: DW
authors.lastname: Hunter
authors.forename: J N
authors.initials: JN
authors.lastname: Cohn
mesh_terms: D000818:Animals; D004285:Dogs; D004556:Electric Injuries / Q000150:complications; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology*; D006335:Heart Injuries / Q000209:etiology; D006439:Hemodynamics / Q000502:physiology*; D009203:Myocardial Infarction / Q000150:complications*; D009206:Myocardium / Q000473:pathology; D009638:Norepinephrine / Q000097:blood; D012083:Renin / Q000097:blood; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D012083:Renin; D009638:Norepinephrine