![]() In this study, we have compared the behavior of the SR from the horse with that of the rabbit. These studies therefore indicate that a slowing in heart rate and accompanying prolongation of APD cannot be simply imposed on the basic EC coupling mechanism without consequences for the electrical and mechanical stability of the heart. With the exception of the rat and mouse, this pacing can lead to diminution of the intracellular Ca 2+ transient and decreased fractional shortening ( 28, 36, 37, 45). Studies on isolated myocardium/myocytes from mammals, including the human, rabbit, and hamster, have shown that a direct imposition of a slow heart rate by pacing at slower than normal (resting) heart rates results in a prolonged APD ( 21, 46, 53). The latter phenomena are also observed in heart failure where APD prolongation is also a consistent electrophysiological observation ( 4, 22, 40, 42).Īnother feature of the equine heart is the slow heart rate experienced at rest (30–40 beats/min). These events activate transient inward currents that increase the probability of triggered arrhythmias ( 25, 29) in particular, early afterdepolarizations, which occur during repolarization, and delayed afterdepolarizations. In smaller mammals, maintained depolarization causes elevated intracellular concentration ( i) and an increased incidence of spontaneous Ca 2+ release ( 2). This value is considerably higher than that from the human, pig, dog, rabbit, and guinea pig, which, despite the wide range of resting heart rates, display comparable APD (0.2–0.35 s) ( 5, 21, 35, 53, 54). The equine action potential duration (APD) anticipated from electrocardiographic measurements would suggest a value of 0.6–1.0 s ( 11, 44) an estimate which is similar to recent in vitro measurements made on equine cardiac tissue ( 16). One important feature of EC coupling is the duration of the ventricular muscle action potential. However, whereas data concerning the details of EC coupling is available for small mammals and human myocardium, only limited data has been reported for larger mammals, including the equine species. The same sequence of events is thought to apply in heart cells across the mammalian species ranging from hearts as small as cells from the mouse to those as large as humans (HR 60–100 beats/min) and horses (HR 30–40 beats/min). This Ca 2+-induced Ca 2+ release ( 14, 15) subsequently leads to myofilament activation and cellular contraction ( 3). The possible reasons for the observed differences in SR Ca 2+ release between the horse and rabbit are discussed.Įxcitation-contraction (EC) coupling within ventricular cardiomyocytes is the process whereby cellular depolarization results in a relatively small influx of Ca 2+ across the sarcolemma that in turn causes a larger release of Ca 2+ from the sarcoplasmic reticulum (SR). Separate measurements of oxalate-supported Ca 2+ uptake into the SR suggest that both horse and rabbit cardiomyocytes have comparable levels SERCA activity. The reason for this disparity in Ca 2+ wave characteristics is unknown. Ca 2+ wave velocity was comparable between the species. ![]() Ca 2+ waves were four times less frequent yet ∼1.5 times greater in amplitude in the horse compared with the rabbit. However, at 550 nM, Ca 2+ waves were produced in both species. ![]() Horse cells failed to produce Ca 2+ waves instead, only local release in the form of Ca 2+ sparks was evident. ![]() Rabbit cardiomyocytes exposed to 260 nM produced spontaneous Ca 2+ release and propagated Ca 2+ waves. Isolated cardiomyocytes from both horse and rabbit hearts were permeabilized, bathed in a mock intracellular solution, and exposed to a specified. In particular, the study focuses on SR Ca 2+ release via the Ca 2+ release channel/ryanodine receptor (RyR2) and Ca 2+ uptake via the sarco(endo)plasmic reticulum Ca 2+-ATPase (SERCA) pump. This study examines and compares the activity of this organelle in the horse with that of the rabbit. The sarcoplasmic reticulum (SR) is one of the main components involved in EC coupling. This would be anticipated to have consequences for excitation-contraction (EC) coupling and require adaptation of the individual processes involved. Both the cardiac action potential duration (APD) (0.6–1 s) and resting heart rate (30–40 beats/min) in the horse are significantly different from humans and smaller mammals, including the rabbit. ![]()
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