Abstract
Chronic pressure overload can result in ventricular hypertrophy and eventually diastolic dysfunction. In normal myocardium, the time from peak tension to 50% relaxation of isolated cardiac myocardium is not directly determined by the time for calcium decline. This study aims to determine whether the time for calcium decline is altered with a change in preload in early-stage hypertrophied myocardium, and whether this change in time for calcium decline alters the rate of relaxation of the myocardium. Young New Zealand white rabbits underwent a pulmonary artery banding procedure and were euthanized 10 weeks later. Twitch contractions and calibrated bis-fura-2 calcium transients were measured in isolated thin right ventricular trabeculae at optimal length and with the muscle taut. Systolic calcium, calcium transient amplitude, and time from peak tension to 50% relaxation all increased with an increase in preload for both hypertrophied and sham groups. Time for intracellular calcium decline increased both with an increase in preload and an increase in extracellular calcium concentration in hypertrophied myocardium but not in sham, while time from peak tension to 50% relaxation did not significantly change between groups under either condition. Also, time for intracellular calcium decline generally decreased with an increase in extracellular calcium for both hypertrophied and sham groups, while time from peak tension to 50% relaxation generally did not significantly change in either group. Combined, these results indicate that the mild hypertrophy significantly changes calcium handling, but does not impact on the rate of force relaxation. This implies that the rate-limiting step in force relaxation is not directly related to calcium transient decline.
Highlights
Chronic pressure overload can result in ventricular hypertrophy and eventually diastolic dysfunction
This study aims to determine whether the time for calcium decline is altered with a change in preload in the pulmonary artery banding animals when compared to shamoperated animals, and whether a change in time for calcium decline will alter the force-relaxation time of the myocardium, in order to further understand the rate-limiting processes of cardiac relaxation, as they play a large role in cardiac dysfunction
Since the calcium transient is often prolonged in hypertrophy and heart failure (Milani-Nejad and Janssen, 2014), and it has been shown that in normal myocardium force decline is not altered by calcium decline, we investigated whether the time for calcium decline was altered in the pulmonary artery banding model, and whether this would affect the time for force decline
Summary
Chronic pressure overload can result in ventricular hypertrophy and eventually diastolic dysfunction. Hypertrophy and Cardiac Relaxation fully adequate in reducing left ventricular mass (Pokharel et al, 2003). The right ventricle is affected by hypertrophy, as it is subjected to abnormal loading conditions in many patients with congenital heart disease (Faber et al, 2006). Pulmonary artery banding in rabbits has been shown to induce a degree of left ventricular diastolic dysfunction (Kitahori et al, 2009). Diastolic dysfunction can impair ventricular filling, and can be a major contributor to the cardiac dysfunction in heart failure (Grossman, 1990). In a model of rabbit right ventricular hypertrophy we have shown that diastolic dysfunction was observed 10 weeks after banding (Varian et al, 2009). Since calcium handling is known to be altered during hypertrophy, it is currently unclear whether, and to what extent, under near physiological conditions the intracellular calcium transient amplitude and kinetics contribute to the length-dependent increase in force and increase in duration of relaxation under early pathological conditions
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