High intracellular Na+ preserves myocardial function at low heart rates in isolated myocardium from failing hearts.
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High intracellular Na+ preserves myocardial function at low heart rates in isolated myocardium from failing hearts. / Schillinger, Wolfgang; Teucher, Nils; Christians, Claus; Kohlhaas, Michael; Sossalla, Samuel; Phuc, Van Nguyen; Schmidt, Albrecht G; Schunck, Ortwin; Nebendahl, Klaus; Maier, Lars S; Zeitz, Oliver; Hasenfuss, Gerd.
In: EUR J HEART FAIL, Vol. 8, No. 7, 7, 2006, p. 673-680.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - High intracellular Na+ preserves myocardial function at low heart rates in isolated myocardium from failing hearts.
AU - Schillinger, Wolfgang
AU - Teucher, Nils
AU - Christians, Claus
AU - Kohlhaas, Michael
AU - Sossalla, Samuel
AU - Phuc, Van Nguyen
AU - Schmidt, Albrecht G
AU - Schunck, Ortwin
AU - Nebendahl, Klaus
AU - Maier, Lars S
AU - Zeitz, Oliver
AU - Hasenfuss, Gerd
PY - 2006
Y1 - 2006
N2 - We investigated the hypothesis that increased intracellular [Na+]i in heart failure contributes to preservation of SR Ca2+ load which may become particularly evident at slow heart rates. [Na+]i in SBFI-loaded myocytes from rabbits with pacing-induced heart failure (PHF) was significantly higher at each frequency as compared to Sham-operated animals. Furthermore, PHF rabbits demonstrated reduced SR Ca2+-ATPase protein levels (-37%, p <0.04) but unchanged Na+/Ca2+ exchanger protein levels. At 0.25 Hz, isometric force was similar in cardiac trabeculae from PHF rabbits as compared to control (PHF, 3.6+/-1.3; Sham, 4.4+/-0.6 mN/mm2). Rapid cooling contractures (RCCs) were unchanged indicating preserved SR Ca2+ load at this frequency. In Sham, isometric twitch force increased with rising frequencies to 29.0+/-2.8 mN/mm2 at 3.0 Hz (p <0.05) as compared to 0.25 Hz. RCCs showed a parallel increase by 186+/-47% (p <0.01). In PHF, frequency-dependent increase in force (15.8+/-4.7 mN/mm2 at 3.0 Hz) and RCCs (increase by 70+/-40%) were significantly blunted. Thus, in PHF in rabbits SR Ca2+ load is preserved at low frequencies despite decreased SR Ca2+-ATPase expression. This may result from [Na+]i-dependent changes in Na+/Ca2+ exchanger activity.
AB - We investigated the hypothesis that increased intracellular [Na+]i in heart failure contributes to preservation of SR Ca2+ load which may become particularly evident at slow heart rates. [Na+]i in SBFI-loaded myocytes from rabbits with pacing-induced heart failure (PHF) was significantly higher at each frequency as compared to Sham-operated animals. Furthermore, PHF rabbits demonstrated reduced SR Ca2+-ATPase protein levels (-37%, p <0.04) but unchanged Na+/Ca2+ exchanger protein levels. At 0.25 Hz, isometric force was similar in cardiac trabeculae from PHF rabbits as compared to control (PHF, 3.6+/-1.3; Sham, 4.4+/-0.6 mN/mm2). Rapid cooling contractures (RCCs) were unchanged indicating preserved SR Ca2+ load at this frequency. In Sham, isometric twitch force increased with rising frequencies to 29.0+/-2.8 mN/mm2 at 3.0 Hz (p <0.05) as compared to 0.25 Hz. RCCs showed a parallel increase by 186+/-47% (p <0.01). In PHF, frequency-dependent increase in force (15.8+/-4.7 mN/mm2 at 3.0 Hz) and RCCs (increase by 70+/-40%) were significantly blunted. Thus, in PHF in rabbits SR Ca2+ load is preserved at low frequencies despite decreased SR Ca2+-ATPase expression. This may result from [Na+]i-dependent changes in Na+/Ca2+ exchanger activity.
M3 - SCORING: Zeitschriftenaufsatz
VL - 8
SP - 673
EP - 680
JO - EUR J HEART FAIL
JF - EUR J HEART FAIL
SN - 1388-9842
IS - 7
M1 - 7
ER -
