Modulation of nitric oxide affects myocardial perfusion–contraction matching in anaesthetized dogs with recurrent no-flow ischaemia

Authors

  • J. G. Kingma Jr,

    1. Coronary Physiology Research Group, Institut universitaire de cardiologie et pneumologie de Québec, Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada G1K 7P4
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  • D. Simard,

    1. Coronary Physiology Research Group, Institut universitaire de cardiologie et pneumologie de Québec, Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada G1K 7P4
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  • J. R. Rouleau

    1. Coronary Physiology Research Group, Institut universitaire de cardiologie et pneumologie de Québec, Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada G1K 7P4
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J. G. Kingma Jr: Institut universitaire de cardiologie et pneumologie de Québec, 2725 Chemin Ste-Foy, Québec, Quebec, Canada G1V 4G5.  Email: john.kingma@fmed.ulaval.ca

Abstract

Myocardial perfusion and contraction are closely coupled; however, the effect of recurrent no-flow ischaemia on perfusion–contraction matching remains to be established. In the present studies, we examined the influence of modulating nitric oxide availability on perfusion–contraction matching after recurrent no-flow ischaemia in acute open-chest, anaesthetized dogs. The following three groups were studied: (1) saline; (2) l-NAME (10 mg kg−1i.v.); and (3) enalaprilat (1.5 mg kg−1i.v.). Regional myocardial blood flow was measured with microspheres and contractile function with piezoelectric crystals to determine systolic wall thickening. Dogs underwent four cycles of 5 min acute ischaemia and 5 min coronary reperfusion; area at risk was similar for all groups. In all dogs, ischaemic zone contractile function was depressed after recurrent no-flow ischaemia despite increased myocardial blood flow during reperfusion; contractile function was further depressed during l-NAME and was partly restored with enalaprilat. Within the ischaemic region, blood flow in subendocardial and subepicardial layers increased significantly compared with baseline during each reperfusion period independently of treatment. Our findings suggest that reduced NO availability can significantly impair myocardial perfusion–contraction matching, which is partly restored by administration of an NO donor.

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