W. S. Ring

Regional myocardial blood flow during exercise in dogs with chronic left ventricular hypertrophy.

We compared the response of myocardial blood flow to exercise in normal dogs and in dogs with left ventricular hypertrophy (LVH) produced by banding the ascending aorta at 6-9 weeks of age. Blood flow was measured with 15-fim microspheres after the animals with LVH had reached adulthood when left ventricular:body weight ratios were approximately 80% greater than normal. During resting conditions, left ventricular systolic pressure was 202 ± 18 mm Hg in the dogs with LVH and 119 ± 6 mm Hg in the normal dogs (P < 0.01). Three levels of treadmill exercise which increased heart rates to 190, 230 and 260 beats/min resulted in progressive increases in left ventricular systolic pressure to a maximum of 343 ± 18 mm Hg in the dogs with LVH as compared to 165 ± 10 mm Hg in the control dogs (P < 0.01). Unlike normal dogs which showed a significant transmural perfusion gradient favoring the- subendocardium at rest [mean subendocardial: subepicardial ratio (endo:epi) = 1.25 ± 0.07], subendocardial flow did not significantly exceed subepicardial flow in the animals with LVH (mean endo: epi = 1.10 ± 0.08; P > 0.05 between normal and LVH). Myocardial blood flow increased as a direct linear function of heart rate during exericse in both groups of dogs. Exercise decreased the mean endo: epi ratio in both normal dogs (mean endo: epi = 1.10 ± 0.08 during heavy exercise; P < 0.01) and in the animals with LVH (mean endo:epi = 0.94 ± 0.03; P < 0.05), while the endo:epi ratios remained consistently less in the LVH dogs than in the normal animals (P< 0.05). The relative reduction of subendocardial flow in dogs with LVH was most apparent in the posterior papillary muscle region where the endo:epi ratio fell significantly below unity during heavy exercise (endo:epi = 0.79 ± 0.02; P < 0.01). These data demonstrate that relative blood flow to the subendocardium of the left ventricle is significantly less than normal, both at rest and during exercise, in dogs with LVH produced by supravalvular aortic stenosis. Circ Res 48: 76-87, 1981

Effect of maximal coronary vasodilation on transmural myocardial perfusion during tachycardia in dogs with left ventricular hypertrophy.

We tested the hypothesis that a functional abnormality may contribute to impaired myocardial perfusion during tachycardia in the chronically pressure-overloaded hypertrophied left ventricle. Left ventricular hypertrophy (LVH) was produced by banding the ascending aorta of seven young dogs, 5–6 weeks of age, and studies were carried out after the animals reached adulthood when the mean left ventricular: body weight ratio was 91% greater than in seven control dogs. Myocardial blood flow was measured with radioactive microspheres during ventricular pacing at 100, 200, and 250 beats/min in the presence of normal coronary vasomotor activity and during maximum coronary vasodilation (adenosine, iv). At a heart rate of 100 beats/min, there was no difference in myocardial blood flow between control and LVH dogs either during normal conditions or during adenosine infusion. However, since mean coronary perfusion pressure was higher in the dogs with aortic banding, minimum coronary resistance was greater in the dogs with LVH [22.7 ± 2.5 (mean ± BE)] than in the control dogs (14.5 ± 1.4 mm Hg/min per g per ml; P < 0.05). In the presence of intact coronary vasomotor tone, pacing at 2S0 beats/min resulted in transmural redistribution of perfusion away from the subendocardium in the dogs with LVH [subendocardial: subepicardial blood flow ratio (endoiepi) - 0.68 ± 0.09], but not in the control dogs (endo: epi = 1.05 ± 0.03; P < 0.02). This relative reduction of subendocardial flow In the dogs with LVH resulted from extravascular factors since blood flow to the inner half of the left ventricular wall failed to increase in response to adenosine infusion during pacing at 250 beats/min. Thus, both an anatomic abnormality of coronary perfusion, marked by impaired minimum coronary resistance at a heart rate of 100 beats/min, and a functional abnormality of perfusion resulting in redistribution of blood flow away from the subendocardium at a heart rate of 250 beats/min were demonstrated in this model of LVH.

The deformational characteristics of the left ventricle in the conscious dog.

We studied left ventricular minor and major axis diameters and equatorial wall thickness in eleven conscious dogs with chronically implanted pulse-transit ultrasonic dimension transducers. Left ventricular tranemural pressure was measured with micromanometers. Left ventricular volume was varied by inflation of implanted vena caval or aortic occluders. The geometry of the left ventricle was represented as a three-dimensional ellipsoidal shell. Left ventricular eccentricity was found to be a linear function of ventricular volume during both diastole and ejection. However, the relationship was not the same for diastole and ejection, and during diastole the left ventricle was more spherical at large volumes and more elliptical at small volumes than during ejection. The rearrangements in geometry observed during isovolumic contraction appeared to be transitional stages from the diastolic to the ejection-phase relationship. Thus, during isovolumic contraction, the left ventricle became more elliptical at large volumes and more spherical at small volumes. These relationships were not altered significantly by increased afterload or inotropic interventions. We also observed that the diastolic deformation of the ventricular chamber occurred in a set and predictable manner that seemed to be determined by the three-dimensional mechanical properties of the myocardium. The geometric inter- relationships of the ventricular wall determined the relationship between diastolic transmural pressure and mural stress. These findings probably reflect basic structural characteristics of the myocardium and provide a convenient method for quantitatively representing the dynamic geometry of the left ventricle.

Cardiac beta-adrenergic responsiveness is well preserved in moderate protein calorie malnutrition from semistarvation

Twenty-one dogs underwent instrumentation of the left ventricle with ultrasonic dimension to study the effects of acute protein-calorie malnutrition on the adrenergic responsiveness of the heart. This study allowed a chronic and dynamic measurement of the major cardiac axes and the ventricular wall thickness, which in turn can be used to derive sophisticated measurements of global and intrinsic left ventricular function. Of the 21 dogs, 11 received a protein- and calorie-deficient diet designed to achieve a mean weight loss from a baseline of 20-25% over a 4-week period. The other 10 dogs received a normal diet. Dogs were also randomized to receive either acute propranolol beta-receptor blockade (n = 9) or acute isoproterenol beta-receptor stimulation (n = 12) during their baseline studies. Of the nine dogs given propranolol, five were subsequently malnourished and four served as controls. Of the 12 given isoproterenol, six were rendered malnourished and six were controls. All dogs were studied at both baseline and 4 weeks and received drugs in an identical fashion during both studies. The significant changes with malnutrition consisted of decreases in heart rate, cardiac mass, and left ventricular wall thickness. The degree of change in stroke volume, ejection fraction, cardiac output, dp/dt, and Emax (index of left ventricular contractility), with the administration of propranolol or isoproterenol was unaltered by malnutrition. These data support the contention that moderate protein-calorie malnutrition is well tolerated in instrumented, unstessed dogs and that the left ventricles capacity to respond to beta-stimulation and to tolerate beta-blockade is largely unimpaired.