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Research Article Free access | 10.1172/JCI109139
Department of Medicine (Cardiology), Veterans Administration Hospital, Durham, North Carolina 27705
Department of Surgery, Veterans Administration Hospital, Durham, North Carolina 27705
Duke University Medical Center, Durham, North Carolina 27710
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Department of Medicine (Cardiology), Veterans Administration Hospital, Durham, North Carolina 27705
Department of Surgery, Veterans Administration Hospital, Durham, North Carolina 27705
Duke University Medical Center, Durham, North Carolina 27710
Find articles by Kleinman, L. in: JCI | PubMed | Google Scholar
Department of Medicine (Cardiology), Veterans Administration Hospital, Durham, North Carolina 27705
Department of Surgery, Veterans Administration Hospital, Durham, North Carolina 27705
Duke University Medical Center, Durham, North Carolina 27710
Find articles by Fedor, J. in: JCI | PubMed | Google Scholar
Department of Medicine (Cardiology), Veterans Administration Hospital, Durham, North Carolina 27705
Department of Surgery, Veterans Administration Hospital, Durham, North Carolina 27705
Duke University Medical Center, Durham, North Carolina 27710
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Department of Medicine (Cardiology), Veterans Administration Hospital, Durham, North Carolina 27705
Department of Surgery, Veterans Administration Hospital, Durham, North Carolina 27705
Duke University Medical Center, Durham, North Carolina 27710
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Published August 1, 1978 - More info
Regional myocardial blood flow during both control conditions and ischemia-induced vasodilatation was studied in eight chronically instrumented awake dogs. Seven of these animals had coarctation-banding of the ascending aorta performed at 6 wk of age, and the other dog had congenital subvalvular aortic stenosis. The mean left ventricular weight for the group was 157±7.6 g, and the left ventricular body weight ratio was 8.76±0.47 g/kg. None of the animals exhibited signs of congestive heart failure.
During the control state, the mean left ventricular systolic pressure was 249±12 mm Hg and the left ventricular end-diastolic pressure was 11.5±0.5 mm Hg. The aortic diastolic pressure was 74±6 mm Hg. Mean left circumflex coronary artery blood flow was 71±6 cm3/min. In the animals with coarctation-banding, 52±6% of the flow occurred during systole. In the dog with congenital subvalvular aortic stenosis, 5% of the coronary flow was systolic. Mean transmural blood flow during resting conditions was 0.97±0.08 cm3/min per g, and the ratio of endocardial to epicardial flow (endo/epi) was 0.88±0.07. During reactive hyperemia, the mean transmural blood flow increased to 3.5±0.30 cm3/min per g; however, the endo/epi decreased to 0.52±0.06.
These studies document a difference in transmural blood flow distribution between the normal and the hypertrophied left ventricle: during resting conditions, in the normal ventricle, the highest flow occurs in the endocardial layer, whereas in the hypertrophied ventricle, the highest flow is in the middle layers with the endocardial flow less than the epicardial flow. During ischemia-induced vasodilatation, the abnormal endo/epi becomes accentuated markedly. These data demonstrate that, in situations requiring high flow, the endocardial layer of a heart with marked concentric left ventricular hypertrophy may not be perfused adequately.
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