Abstract
Long‐term systemic arterial hypertension, and its associated compensatory response of left‐ventricular hypertrophy, is fatal. This disease leads to cardiac failure and culminates in death. The spontaneously hypertensive rat (SHR) is an excellent animal model for studying this pathology, suffering from ventricular failure beginning at about 18 months of age. In this study, we isolated left‐ventricular trabeculae from SHR‐F hearts and contrasted their mechanoenergetic performance with those from nonfailing SHR (SHR‐NF) and normotensive Wistar rats. Our results show that, whereas the performance of the SHR‐F differed little from that of the SHR‐NF, both SHR groups performed less stress‐length work than that of Wistar trabeculae. Their lower work output arose from reduced ability to produce sufficient force and shortening. Neither their heat production nor their enthalpy output (the sum of work and heat), particularly the energy cost of Ca2+ cycling, differed from that of the Wistar controls. Consequently, mechanical efficiency (the ratio of work to change of enthalpy) of both SHR groups was lower than that of the Wistar trabeculae. Our data suggest that in hypertension‐induced left‐ventricular hypertrophy, the mechanical performance of the tissue is compromised such that myocardial efficiency is reduced.
Highlights
Systemic hypertension is known to be associated with pathologic left-ventricular hypertrophy
Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society
This study examines the mechanoenergetic performance of the spontaneously hypertensive rat (SHR) at end-stage hypertrophy-induced left-ventricular failure (SHR-F)
Summary
Systemic hypertension is known to be associated with pathologic left-ventricular hypertrophy. Long-term effects of this disease are fatal as they lead to cardiac failure, culminating in death. In patients with hypertensive-hypertrophy, reduced myocardial efficiency at the whole-organ level has consistently been reported (Ishibashi et al 1996; Laine et al 1999; Akinboboye et al 2004; de las Fuentes et al 2006). Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
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