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Ann Thorac Surg 1994;57:540-545
© 1994 The Society of Thoracic Surgeons

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Articles

Ischemia-dependent efficacy of phosphodiesterase inhibition

Division of Cardiothoracic Surgery, Department of Surgery, New England Deaconess Hospital/Harvard Medical School, Boston, Massachusetts USA

^_* Address reprint requests to Dr Krukenkamp, Division of Cardiothoracic Surgery, New England Deaconess Hospital, 110 Francis St, Suite 2C, Boston, MA 02215.

To evaluate the inotropic efficacy of phosphodiesterase inhibition in hearts with and without ischemic injury, 27 sheep were evaluated sonomicrometrically during incremental volume loading on right heart bypass. Contractility was assessed with the preload recruitable stroke work relationship. Active relaxation rate was estimated using the time constant of isovolumic pressure decay (tau). For nonischemic assessment, groups 1 and 2 (n = 6 each) underwent 45 minutes of vented perfusion after which milrinone was administered to group 1; group 2 served as nonischemic controls. There was no detectable increase in preload recruitable stroke work or decrement in tau after milrinone administration. Groups 3 and 4 underwent 15 minutes of 37 °C ischemia (aortic cross-clamping) followed by 30 minutes of vented reperfusion. Milrinone was then administered to group 3 (n = 7); group 4 (n = 8) served as ischemically injured controls. Inotropic and lusitropic effects were present (group 3 preload recruitable stroke work: 35.4 ± 5.8 mJ · beat^–1 · 100 g^–1 · mL^–1 before milrinone to 49.5 ± 4.4 mJ · beat^–1 · 100 g^–1 · mL^–1 after milrinone [p < 0.05]; group 3 tau: 51.8 ± 5.5 ms before milrinone to 32.2 ± 2.5 ms after milrinone [p < 0.02]). Although milrinone restored contractility and increased the rate of active relaxation in the postischemic hearts, there was no detectable inotropic effect in nonischemic hearts. In this model, milrinone augments contractility and relaxation in postischemic myocardium but offers little inotropic benefit in non-ischemically injured hearts.

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