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Cardiovascular Research 1995 30(1):113-121; doi:10.1016/S0008-6363(95)00018-6
© 1995 by European Society of Cardiology
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Copyright © 1995, European Society of Cardiology

Cardiac hypertrophy impairs recovery from ischaemia because there is a reduced reactive hyperaemic response

Aileen M. McAinsha, Mark A. Turnera, Danny O'Harec, Ratnam Nithythyananthanb, Desmond G. Johnstonb, Daniel J. O'Gormana and Desmond J. Sheridana,*

aAcademic Cardiology Unit, St. Mary's Hospital Medical School, 10th Floor, Queen Elizabeth the Queen Mother Wing, South Wharf Road, London W2 1NY, UK
bDepartment of Metabolic Medicine, St. Mary's Hospital Medical School, 10th Floor, Queen Elizabeth the Queen Mother Wing, South Wharf Road, London W2 1NY, UK
cPFSU, Imperial College of Science, Technology and Medicine, London, SW7, UK

* Corresponding author.

Objective: The aim was to investigate whether impaired coronary flow reserve associated with cardiac hypertrophy could significantly limit the flow debt repayment following short periods of coronary occlusion and exacerbate or prolong episodes of myocardial ischaemia. Methods: Left ventricular hypertrophy was induced in guinea pigs by aortic constriction and the hearts were isolated six weeks later for Langendorff perfusion. Sham operated animals served as controls. The reactive hyperaemic response was studied following various lengths of occlusion of flow and the extent of aerobic and anaerobic metabolism was assessed in each group. Results: Heart weight /body weight ratio was increased by approximately 25% (P < 0.001) with aortic constriction. The reactive hyperaemic flow response in isolated hearts was impaired by hypertrophy in both magnitude (P < 0.05) and duration. The repayment of flow debt was also significantly reduced, suggesting an inadequate recovery of the myocardium following the occlusion. The total amount of O2 consumed by the heart throughout the duration of hyperaemia was less in hypertrophy than in sham operated controls, suggesting a decrease in aerobic metabolism. Total lactate discharge expressed as a ratio of O2 consumed, which provides an estimation of the degree of anaerobic in relation to aerobic metabolism, was greater in hypertrophy than in sham operated controls. Conclusions: The hypertrophied heart is more vulnerable to brief periods of ischaemia because of an impaired reactive hyperaemic response which results in delayed metabolic recovery. These abnormalities may contribute to the Increased morbidity associated with cardiac hypertrophy.

KEYWORDS Hypertrophy; Reactive hyperemia; Myocardial ischemia; Cardiac metabolism; Guinea pig heart; Coronary blood flow


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