We studied the influence of active coronary vasomotion on transmural myocardial perfusion during tachycardia. Regional myocardial blood flow was estimated in chronically prepared awake dogs by injecting radioactive microspheres (7-10 /xm in diameter) into the left atrium. Studies were performed during ventricular pacing at 100, 150, 200, and 250 beats/min under control conditions with intact coronary vasomotor tone, and during maximal coronary vasodilation induced by intravenous infusion of adenosine. During control conditions, mean myocardial blood flow was 1.27 ± 0.12 ml/min per g of myocardium at a heart rate of 100 beats/min, and increased regularly with increasing heart rates. Transmural myocardial perfusion remained essentially uniform as heart rates were increased from 100 to 250 beats/min. During administration of adenosine, mean myocardial blood flow increased to 5.49 ± 0.39 ml/min per g at a heart rate of 100 beats/min, and transmural myocardial perfusion was uniform. As heart rates were increased, flow to the subendocardium decreased as a linear function of heart rate while subepicardial flow was maintained so that the ratio of subendocardial-subepicardial flow fell from 1.00 at a heart rate of 100 beats/min to 0.40 at a heart rate of 250 beats/min. The reduction of subendocardial perfusion with increasing heart rate was most marked in the deepest myocardial layers. This rate-dependent decrease in subendocardial blood flow resulted in a decrease in mean myocardial blood flow with increasing heart rates (mean change at 250 beats/min = -18%; P < 0.05). These data indicate that active coronary vasomotion is necessary for maintenance of uniform transmural myocardial perfusion during tachycardia.
A B S T R A C T Regional myocardial blood flow was measured in nine dogs at rest and during three levels of treadmill exercise by using left atrial injections of 7-10-,um radioactive microspheres. At rest, heart rate was 76±3 beats/min (mean+SEM), mean left ventricular myocardial flow was 0.94±0.09 ml/min/g and endocardial flow (endo) exceeded epicardial flow (epi) in all regions (endo/epi = 1.12-1.33). When treadmill exercise was regulated to increase heart rates from 152±3 to 190±3 to 240±6 beats/min, myocardial blood flow (MBF) to all regions of the left ventricle increased linearly with heart rate (HR) from 1.83±f-0.11 to 2.75± 0.22 to 3.90±0.26 ml/min/g (MBF = 0.0175HR -0.523 ±0.614, r = 0.87). Exercise abolished the gradient of blood flow favoring the left ventricular endocardium at rest, so that the endo/epi flow ratios were not significantly different from 1.00. Right ventricular flows were consistently less than corresponding left ventricular flows, but showed a similar linear increase with heart rate. Right ventricular endo/epi ratios were not different from 1.00 either at rest or during exercise. Thus, exercise resulted in increased myocardial blood flow to all regions of the left and right ventricles with maintenance of subendocardial flow equal to subepicardial flow.
The present study assesses effects of acutely infarcted myocardium on apparent microsphere loss as a function of time, determines effects of apparent microsphere loss on blood flow measurements to ischemic regions, and determines to what extent apparent microsphere loss alters interpretation of serial measurements of collateral blood flow. Studies were performed in 35 awake mongrel dogs chronically instrumented with catheters in the aorta and left atrium and an occluder on the proximal circumflex coronary artery. Myocardial blood flow was measured before and 15 minutes after complete occlusion. Dogs were randomly divided into four groups to be killed at 6 and 24 hours, and 3 and 6 days. In the 3-day group, an additional blood flow measurement was made 24 hours postocclusion. The entire left ventricle was sectioned into 1- to 2-g samples and myocardial blood flow determined. The ratio of preocclusion blood flow in each ischemic sample to mean nonischemic flow was used to calculate apparent microsphere loss and to correct ischemic blood flow in each sample. Significant apparent microsphere loss occurred in epicardial layers at 24 hours and in epi- and endocardial layers at 3 and 6 days; maximum loss at each interval was 22.3, 19.4, and 22.2% respectively. Absolute blood flow corrections for ischemic myocardium were small, range -0.035 to 0.083 ml/min per g. Changes in flow to ischemic regions between 15 minutes and 24 hours were comparable before and after correction for apparent microsphere loss. Although infarction resulted in significant apparent microsphere loss, effects on ischemic blood flow measurements were very small and consequently did not prevent interpretation of serial blood flow measurements after infarction in animals killed at 3 days.
SUMMARY The purpose of this study was to compare the myocardial distribution of thallium-201 and regional myocardial blood flow during ischemia and the physiologic stress of exercise. Studies were carried out in six dogs with chronically implanted catheters in the atrium and aorta and a snare on the circumflex coronary artery distal to the first marginal branch. Regional myocardial blood flow was measured during quiet, resting conditions using 7-10 , of radioisotope-labeled microspheres. Each dog was then exercised on a treadmill at speeds of 5-9 mph at a 50 incline. After 1 minute of exercise the circumflex coronary artery was occluded and thallium-201 and a second label of microspheres were injected. Exercise was continued for 5 minutes. The dogs were then sacrificed and the left ventricle was sectioned into approximately 80 1-2-g samples to compare thallium-201 activity and regional myocardial blood flow.The maximum increase in blood flow ranged from 3.3-7.2 times resting control values. Each dog had myocardial samples in which blood flow was markedly reduced, to less than 0.10 ml/min/g. In each dog there was a close linear relationship between thallium-201 distribution and direct measurements of regional myocardial blood flow. Linear regression analyses demonstrated a correlation coefficient of 0.98 or greater in each dog. These data indicate that during the physiologic stress of exercise, the myocardial distribution of thallium activity is linearly related to regional myocardial blood flow in both the ischemic and nonischemic regions.
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