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J Thorac Cardiovasc Surg 2009;138:141-147
© 2009 The American Association for Thoracic Surgery
Evolving Technology/Basic Science |
a Kids Heart Research, The Children's Hospital at Westmead, Sydney, Australia
b Discipline of Paediatrics and Child Health, Faculty of Medicine, University of Sydney, Sydney, Australia
c Neurogenetics Research Unit and the Institute for Neuromuscular Research, The Children's Hospital at Westmead, Sydney, Australia
d Vascular Biology Group, ANZAC Research Institute, Concord RG Hospital, University of Sydney, Sydney, Australia
e Cardiothoracic Surgery, Adolph Basser Cardiac Research, The Children's Hospital at Westmead, Sydney, Australia
Received for publication August 25, 2008; revisions received November 13, 2008; accepted for publication December 14, 2008. * Address for reprints: David S. Winlaw, MD, FRACS, Kids Heart Research, Locked Bag 4001, Westmead NSW 2145, Australia. (Email: davidw{at}chw.edu.au).
Objectives: Recovery from pediatric cardiac surgery is affected by ischemia–reperfusion injury, cardiac edema, and in some cases a low cardiac output syndrome. Although association has been made between the development of edema and dysfunction, modeling is confounded by intercurrent injurious stimuli that also cause cardiac edema and dysfunction. We tested whether a true causal relationship exists between edema and cardiac dysfunction.
Methods: We induced either ischemia or edema alone in isolated cardiomyocytes and whole Langendorff-perfused hearts. Function was measured as shortening dynamics and developed pressure, respectively.
Results: Ischemic injury impaired function in both cardiomyocytes and whole hearts. Isolated cells showed significant reduction in peak shortening and departure and relaxation velocities. Whole hearts displayed severely reduced developed pressures. Hyposmotic solution forced cardiomyocytes to swell to 7% greater than their normal size. No significant effect on shortening was seen. Similarly, Langendorff-perfused hearts were induced to take on 3% more water than control-perfused hearts and 9% more water than nonperfused hearts. This additional water was associated with mild dysfunction.
Conclusions: We demonstrate the capacity of the heart to tolerate edema greater than that seen in clinical settings without residual effect. Ischemia results in ongoing contractile dysfunction of both isolated cardiomyocytes and whole hearts. We conclude that dysfunction resulting from edema in ex vivo cardiac models is mild and suggest review of the importance given to edema-mediated dysfunction after cardiac surgery.
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