Systolic Elastance and Resistance in the Regulation of Cardiac Pumping Function in Early Streptozotocin-Diabetic Rats

Abstract

We determined the roles of maximal systolic elastance (Emax) and theoretical maximum flow (Q_max) in the regulation of cardiac pumping function in early streptozotocin (STZ)-diabetic fats. Physically, Emax can reflect the intrinsic contractility of the myocardium as an intact heart, and Q_max has an inverse relation to the systolic resistance of the left ventricle. Rats given STZ 65 mg/kg l.v. (n = 17) were divided into two groups, 1 week and 4 weeks after induction of diabetes, and compared with untreated age-matched controls (n = 15). Left ventricular (LV) pressure and ascending aortic flow signals were recorded to calculate Emax and Q_max, using the elastance-resistance model. After 1 or 4 weeks, STZ-diabetic animals show an increase in effective LV end-diastolic volume (Veed), no significant change in peak iso-volumic pressure (Pisomax), and a decline in effective arterial volume elastance (Ea). The maximal systolic elastance Emax is reduced from 751.5 ± 23.1 mmHg/ml in controls to 514.1 ± 22.4 mmHg/ml in 1- and 538.4 ± 33.8 mmHg/ml in 4-week diabetic rats. Since Emax equals PisomaxVeed, an increase in Veed with unaltered Pisomax may primarily act to diminish Emax so that the intrinsic contractility of the diabetic heart is impaired. By contrast, STZ-diabetic rats have higher theoretical maximum flow Q_max (40.9 ± 2.8 ml/s in 1- and 44.5 ± 3.8 ml/s in 4-week diabetic rats) than do controls (30.7 ± 1.7 ml/s). There exists an inverse relation between Q_max and Ea when a linear regression of Q_max on Ea is performed over all animals studied (r= 0.65, p < 0.01). The enhanced Q_max is indicative of the decline in systolic resistance of the diabetic rat heart. The opposing effects of enhanced Q_max and reduced Emax may negate each other, and then the cardiac pumping function of the early STZ-diabetic rat heart could be preserved before cardiac failure occurs.