Effects of myosin isozyme shift on curvilinearity of the left ventricular end-systolic pressure-volume relation of In situ rat hearts.

Abstract

Recently we have shown that the left ventricular end-systolic pressure-volume relation (ESPVR) of in situ rat hearts is an upward convex curve in contrast to the linear left ventricular ESPVR in dog and human hearts. Within the smaller left ventricular volume range, the left ventricular end-systolic pressure rose steeply with increases in left ventricular volume, but it gradually reached a plateau at the larger left ventricular volumes. In adult rat hearts, the myosin isozyme is V1, unlike V3 in dog and human hearts. To investigate whether myosin isozyme affects the curvilinearity of the left ventricular ESPVR, we evaluated the left ventricular ESPVR in hypothyroid rats in which the left ventricular myosin isozyme had been shifted to V3. In the hypothyroid rats, the left ventricular contractility was depressed and the ESPVR became closer to linear. However, after dobutamine administration the ESPVR returned to curvilinear. In nor-mal rats the curvilinearity of the left ventricular ESPVR was decreased by negative inotropic agents such as adrenergic blockers. These results indicate that the depressed left ventricular contractility in the hypothyroidism make ESPVR linear and that the enhanced left ventricular contractility from dobutamine make it curvilinear. We concluded that the curvilinearity of the rat left ventricular ESPVR is not determined by myosin isozyme per se, but by the left ventricular contractility.