Effect of treadmill exercise on transmural distribution of blood flow in hypertrophied left ventricle.
Pressure-overload left ventricular (LV) hypertrophy (LVH) is associated with increased vulnerability to subendocardial hypoperfusion during exercise. Abnormal perfusion could be the result of failure of the coronary vessels to grow in proportion to the degree of myocyte hypertrophy or could be due to increased extravascular forces acting on the intramural coronary vasculature. This study assessed the contribution of extravascular forces by examining the effect of exercise on the distribution of myocardial blood flow when coronary vasomotor tone was abolished with a maximal vasodilating dose of intracoronary adenosine. One year after ascending aortic banding in six dogs, the LV-to-body weight ratio was 7.80 +/- 0.38 g/kg compared with 4.57 +/- 0.20 g/kg in nine normal dogs (P < 0.01). Under awake resting conditions blood flow in LVH hearts increased from 1.17 +/- 0.27 ml . min-1 . g-1 during basal conditions to 5.78 +/- 1.06 ml . min-1 . g-1 during adenosine (at a coronary pressure of 100 +/- 6 mmHg), whereas in normal dogs blood flow increased from 1.22 +/- 0.17 to 5.26 +/- 0.71 ml . min-1 . g-1 (at a coronary pressure of 62 +/- 4 mmHg). At rest the transmural distribution of blood flow during adenosine was not different between hypertrophied and normal hearts, with subendocardial-to-subepicardial (Endo-to-Epi) blood flow ratios of 1. 01 +/- 0.09 and 1.14 +/- 0.13, respectively (P = not significant). During adenosine infusion, treadmill exercise to produce heart rates of 200-220 beats/min caused redistribution of blood flow away from the subendocardium that was much more marked in LVH (Endo-to-Epi blood flow ratio = 0.35 +/- 0.04) than in normal hearts (Endo-to-Epi blood flow ratio = 0.76 +/- 0.09, P < 0.05 vs. LVH). In comparison with normal, the exaggerated decrease in subendocardial blood flow produced by exercise in LVH hearts resulted from abnormally increased extravascular compressive forces, including a greater decrease in diastolic duration and an increase in LV end-diastolic pressure.
Duncker
D J
DJ
Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.
Ishibashi
Y
Y
Bache
R J
RJ
D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D003971:Diastole; D004285:Dogs; D005080:Exercise Test; D006339:Heart Rate; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D005082:Physical Exertion / Q000502:physiology*; D012039:Regional Blood Flow; D012044:Regression Analysis; D013599:Systole; D014665:Vasodilator Agents / Q000494:pharmacology
D014665:Vasodilator Agents; D000241:Adenosine