The mechanism through which edema reduces left ventricular compliance has not been defined. Accordingly, diastolic properties of in situ left ventricular swine papillary muscles were studied in three groups: control (n = 6, 4 degrees to 6 degrees C), edematous (150 mOsm/L coronary perfusion, n = 6, 4 degrees to 6 degrees C), and ischemic contracture (n = 8, 28 degrees C). Lagrangian stress (a) and strain (E) were calculated from slow stretch data and approximated by sigma = alpha(e(beta epsilon)- 1). The natural logarithm of stress versus strain was linear over the physiologic range of 0.05 < strain < 0.40. Hypotonic perfusions (1 L x 3) progressively shifted the stress-strain relationship upward and to the left. Compared to baseline, ct increased significantly (p < 0.05) after perfusion 3 (6.7 +/- 2.1 baseline, 12.2 +/- 6.6 perfusion 1, 12.7 +/- 3.5 perfusion 2, and 42.9 +/- 16.3 gm/cm(2) perfusion 3). The constant P did not change significantly (13.0 +/- 1.5 baseline, 13.1 +/- 1.6 perfusion 1, 13.2 +/- 1.6 perfusion 2, and 14.1 +/- 1.4 perfusion 3). Right ventricular water content increased after each perfusion (77.1% +/- 1.4% baseline, 81.6% +/- 1.3%, 84.7% +/- 1.5%, and 86.9% +/- 1.7%, p < 0.05). With ischemic contracture, ct increased from 61.9 +/- 17.8 to 173.1 +/- 61.5 gm/cm(2) (p > 0.05) and beta increased insignificantly from 6.5 +/- 0.6 to 10.6 +/- 1.8 (p = NS). In the control group all variables were unchanged after 210 minutes. We conclude that myocardial stiffness increases, with myocardial edema. This may explain decreased compliance in the edematous left ventricle.