title: The spontaneously hypertensive rat as a model of the transition from compensated left ventricular hypertrophy to failure.
abstract: Studies of hemodynamics and intrinsic left ventricular myocardial function are carried out to investigate the transition from stable hypertrophy to cardiac decompensation in the aging (18-24 months) spontaneously hypertensive rat (SHR). Echocardiographic data in awake animals demonstrate increased end-diastolic and end-systolic volumes and depressed ejection fractions in left ventricles from SHR with failure (SHR-F) as compared to age matched hypertensive (SHR-NF) and non-hypertensive control animals (WKY). Cardiac catheterization data in anesthetized animals demonstrate depression of both systolic pressure and +dP/dt, and elevated end-diastolic pressure in the SHR-F relative to the two control groups. Since loading conditions and altered demand states may contribute to altered ventricular function, studies of isolated perfused hearts were carried out which demonstrate impaired systolic stress development in the SHR-F group under conditions in which loading conditions are controlled; in addition, it is observed that increasing perfusion pressure by 30 mm Hg has little effect on function. Depression of systolic function and increases in passive stiffness of isolated muscle preparations from the SHR-F indicate impairment of systolic and diastolic function at the tissue level. While all of the preparations studied have potential shortcomings, an integration of findings from these complementary approaches supports the conclusion that heart failure develops in the aging SHR. Furthermore, these data suggest that impaired function is due to changes in the intrinsic properties of the myocardium and that the connective tissue response may play an important role. These studies, in conjunction with the findings of others who have studied the aging SHR, provide support for the use of the aging SHR as a model of the transition from compensated hypertrophy to failure.
authors.affiliation: Department of Veterans Affairs Medical Center, Boston, MA 02130, USA.
authors.forename: O H
authors.initials: OH
authors.lastname: Bing
authors.forename: W W
authors.initials: WW
authors.lastname: Brooks
authors.forename: K G
authors.initials: KG
authors.lastname: Robinson
authors.forename: M T
authors.initials: MT
authors.lastname: Slawsky
authors.forename: J A
authors.initials: JA
authors.lastname: Hayes
authors.forename: S E
authors.initials: SE
authors.lastname: Litwin
authors.forename: S
authors.initials: S
authors.lastname: Sen
authors.forename: C H
authors.initials: CH
authors.lastname: Conrad
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004452:Echocardiography; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D006439:Hemodynamics; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology*; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D011921:Rats, Inbred WKY / Q000502:physiology