Age-related changes in pumping mechanical behavior of rat ventricle in terms of systolic elastance and resistance

Citation
Kc. Chang et al., Age-related changes in pumping mechanical behavior of rat ventricle in terms of systolic elastance and resistance, J GERONT A, 55(9), 2000, pp. B440-B447
Citations number
39
Categorie Soggetti
Public Health & Health Care Science","Medical Research General Topics
Journal title
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
ISSN journal
10795006 → ACNP
Volume
55
Issue
9
Year of publication
2000
Pages
B440 - B447
Database
ISI
SICI code
1079-5006(200009)55:9<B440:ACIPMB>2.0.ZU;2-Z
Abstract
Both the maximal systolic elastance (E-max) and the theoretical mauimal flo w ((Q)over dot(max)) can quantify the systolic mechanical behavior of the v entricular pump. Physically, E-max can reflect the intrinsic contractility of the myocardium as an intact heart. The quantity in (Q)over dot(max) is i nversely related to the internal resistance of the left ventricle. How grea t the effects of age are on these E-max and (Q)over dot(max) has never been examined, however. This study was to determine the ventricular pumping mec hanics in terms of the systolic elastance and resistance in male Fischer ra ts at 6, 12, 18, and 24 months of age. We measured left ventricular (LV) pr essure and ascending aortic flow waves using a high-fidelity pressure senso r and an electromagnetic now probe, respectively. Those two parameters that characterize the systolic pumping mechanics of the left ventricle are obta ined by making use of an elastance-resistance model. The basic hemodynamic condition in those animals with different ages is characterized by (i) no s ignificant change in cardiac output and (ii) a decrease in basal heart rate , LV end-systolic pressure, as Hell as effective arterial volume elastance, Changes that take place in the left ventricle with age include a decline i n E-max and an increase in (Q)over dot(max) especially at 24 months. These results demonstrate that the impaired intrinsic contractility of an aging h eart may be compensated to some extent by the diminished ventricular intern al resistance, such compensation in aging rats may maintain normal blood fl ow essential for the metabolic needs of tissues and/or organs before heart dysfunction and failure occur.