Temperature-dependent postextrasystolic potentiation and Ca²⁺ recirculation fraction in canine hearts

Abstract

. Temperature-dependent postextrasystolic potentiation and Ca 2ϩ recirculation fraction in canine hearts. Am J Physiol Heart Circ Physiol 282: H403-H413, 2002; 10.1152/ajpheart.00427.2000.-We have found that cardiac temperature proportionally changes O2 cost of contractility, defined as O2 consumption for myocardial total Ca 2ϩ handling normalized to contractility in terms of the end-systolic pressure-volume ratio (maximal elastance, Emax), in the canine left ventricle (temperature sensitivity, Q10 ϭ 2). We have separately found that a decrease in the recirculation fraction (RF) of Ca 2ϩ within myocardial cells underlies an increased O2 cost of Emax in stunned hearts. We therefore hypothesized that a similar change in RF would underlie the Q10 of O2 cost of Emax. We tested this hypothesis by analyzing RF calculated from an exponential decay component of the transiently alternating postextrasystolic potentiation in the canine left ventricle. RF decreased from 0.7 to 0.5 as cardiac temperature increased from 33 to 38°C with Q10 of 0.5, reciprocal to that of O2 cost of Emax. We conclude that Q10 of ATP-consuming reactions involved in Ca 2ϩ handling and Emax response to it could reasonably account for the reciprocal Q10 of RF and O2 cost of Emax. excitation-contraction coupling; calcium handling; ventricular contractility; sarcoplasmic reticulum MYOCARDIAL Ca 2ϩ handling in excitation-contraction (E-C) coupling determines not only cardiac contractility but also O 2 consumption for the Ca 2ϩ handling (30). To quantify the O 2 consumption for Ca 2ϩ handling relative to left ventricular contractility in terms of end-systolic pressure-volume ratio (maximum elastance, E max ), we had proposed the O 2 cost of E max (30). We defined it as the ratio of O 2 consumption for total Ca 2ϩ handling, namely, other than contraction and basal metabolism, to E max (30).We have attributed an increased O 2 cost of E max to a decrease in the recirculation fraction (RF) of Ca 2ϩ within myocardial cells as well as a decrease in the response of E max to total released Ca 2ϩ (E max reactivity, R) in canine failing (e.g., stunned and ryanodinetreated) hearts (3, 10, 13, 27). We have separately found that cardiac cooling from 40 to 30°C considerably decreased the O 2 cost of E max with a temperature sensitivity (Q 10 ) of ϳ2 in canine hearts (18). However, the underlying mechanisms in the temperature-dependent O 2 cost of E max remain to be elucidated (18,24,31).Therefore, in the present study, we hypothesized that cardiac temperature would also change either RF or E max reactivity or both, and thereby change the O 2 cost of E max . We tested this hypothesis in the canine heart. We used our recently developed method to obtain RF by extracting an exponential decay component from the transient alternans decay of postextrasystolic potentiation (PESP) (3,10,13,16,19,(26)(27)(28). We obtained interesting results to support that the temperature-dependent ATP-consuming activities in Ca 2ϩ -handling processes could largely account for the temperatur...

Load Independence of Temperature-Dependent Ca2+ Recirculation Fraction in Canine Heart

“…We obtained RF at 33°C, 36°C, and 38°C while eliminating the temperature-dependent changes in peak isovolumic LVP of the regular beats by adjusting LVV. The present results yielded essentially the same temperature dependence of RF as the previous study [14], i.e., whether or not we changed LVV to compensate for the temperature-dependent LVP. The present results validated our present hypothesis.…”

“…Therefore, it remains unknown whether the temperature-dependently decreased LVP at a constant LVV affected the temperature-dependent RF. Based on our previous results [13,14], we hypothesized that the temperature-dependent RF would primarily be due to the temperature effect per se rather than the simultaneously changed peak LVP.…”

“…The present results indicated a similar temperature dependence of RF and its Q 10 to those we observed previously without equalizing peak LVP. Thus, the temperature-dependent RF is indepenunchanged despite increasing LV volume (LVV) at normothermia [13], but it decreases with increasing temperature from 33°C to 38°C at a constant LVV [14]. However, increasing temperature simultaneously decreased ventricular contractility and thus peak isovolumic LV pressure (LVP) at a constant LVV because of the negative inotropism of warming [15][16][17][18][19][20][21][22].…”

Exponential Fitting of Postextrasystolic Potentiation May Underestimate the Cardiac Ca2+ Recirculation Fraction: A Theoretical Analysis

“…At these physiological beat intervals, RF increases as the beat interval shortens [17] in contrast to the constant RF independent of beat intervals longer than the period of full mechanical restitution [20,21,27,28]. At present, we are not interested in such relatively long beat intervals because we have to obtain RF at the shorter beat intervals we consistently observe in our cardiac mechanoenergetics experiments [7][8][9][10][11][12]22].…”

“…Here, we used aϭ0.5, e ϭ2, and s ϭ0.8 as the representative values for regular beat intervals of 400-600 ms and extrasystolic beat intervals of 300-400 ms in our previous observations [11,12,17]. Furthermore, we increased b from 0 in steps of 0.1 and stopped it at 0.5 (ϭa) although our previous observations have shown that alternans PESPs obviously have bՆa [11,12,17]. In other words, PESPs with bϾa appeared so obvious that no one would dare to fit an exponential curve to it.…”