title: 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 (E(max)) and theoretical maximum flow ((max)) in the regulation of cardiac pumping function in early streptozotocin (STZ)-diabetic rats. Physically, E(max) can reflect the intrinsic contractility of the myocardium as an intact heart, and (max) has an inverse relation to the systolic resistance of the left ventricle. Rats given STZ 65 mg/kg i.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 E(max) and (max), using the elastance-resistance model. After 1 or 4 weeks, STZ-diabetic animals show an increase in effective LV end-diastolic volume (V(eed)), no significant change in peak isovolumic pressure (P(iso)(max)), and a decline in effective arterial volume elastance (E(a)). The maximal systolic elastance E(max) 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 E(max) equals P(iso)(max)/V(eed), an increase in V(eed) with unaltered P(iso)(max) may primarily act to diminish E(max) so that the intrinsic contractility of the diabetic heart is impaired. By contrast, STZ-diabetic rats have higher theoretical maximum flow (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 (max) and E(a) when a linear regression of (max) on E(a) is performed over all animals studied (r = 0.65, p < 0.01). The enhanced (max) is indicative of the decline in systolic resistance of the diabetic rat heart. The opposing effects of enhanced (max) and reduced E(max) may negate each other, and then the cardiac pumping function of the early STZ-diabetic rat heart could be preserved before cardiac failure occurs.
authors.affiliation: Department of Physiology and Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan. kcchang@ha.mc.ntu.edu.tw
authors.forename: Kuo-Chu
authors.initials: KC
authors.lastname: Chang
authors.forename: Huey-Ming
authors.initials: HM
authors.lastname: Lo
authors.forename: Yung-Zu
authors.initials: YZ
authors.lastname: Tseng
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006334:Heart Function Tests; D007328:Insulin / Q000008:administration & dosage; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin; D013599:Systole / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology*
chemical_list: D007328:Insulin; D013311:Streptozocin