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Articles in PresS, published online ahead of print November 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01061.2001
Submitted on December 4, 2001
Accepted on October 31, 2002
1 Department of Molecular Cardiology, Johns Hopkins University, Baltimore, MD, USA; Department of Physiology and Cell Biology, Ohio State University, Columbus, OH, USA
2 Department of Molecular Cardiology, Johns Hopkins University, Baltimore, MD, USA
3 Dorothy M. Davis Heart and Lung Institute, Ohio State University, Columbus, OH, USA
* To whom correspondence should be addressed. E-mail: janssen.10{at}osu.edu.
The progression of hypertension to cardiac failure involves systemic changes that may ultimately affect contractility throughout the heart. Spontaneous Hypertensive Heart Failure (SHHF) rats have depressed left ventricular function, but right ventricular dysfunction is less well characterized. Ultrathin (87±5 µm), trabeculae were isolated from end-stage failing SHHF rats and from age-matched controls. Under near-physiological conditions (1 mM Ca2+, 37 °C, 4 Hz), developed force (in mN/mm2) was not significantly different in SHHF LV and RV trabeculae and controls. SHHF LV preparations displayed a negative force-frequency behavior (40±7 vs. 23±4 mN/mm2, 2 vs. 7 Hz); this relationship was positive in SHHF RV preparations (27±5 vs. 40±6), and controls (32±6 vs. 44±9). The response to isoproterenol (10-6 M, 4 Hz) was depressed in SHHF LV preparations. The inotropic response to hypothermia was lost in SHHF LV trabeculae, but preserved in SHHF RV trabeculae. Intracellular calcium measurements revealed impaired calcium handling at higher frequencies in LV preparations. We conclude that in end-stage failing SHHF rats right ventricular function is only marginally affected, whereas a severe contractile dysfunction of left ventricular myocardium in present.
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