Korean anti-inflammatory compound allergina enhances cardiac contractile function in isolated ventricular cardiomyocytes.

OBJECTIVES: The herbal compound Allergina has a long history in the clinical treatment of allergic inflammatory diseases in some countries including Korea. However, the direct effect of Allergina on ventricular contractile function has not been defined. DESIGN: This study was designed to investigate the impact of Allergina on ventricular contractile function. SETTINGS: Ventricular contractile function was examined in single isolated left ventricular cardiomyocytes. SUBJECTS/INTERVENTIONS: Isolated cardiomyocytes from adult male Sprague-Dawley rats were electrically stimulated to contract at 0.5 Hz. OUTCOME MEASURES: Mechanical and intracellular Ca2+ transients properties of cardiomyocytes were evaluated using an IonOptix Myocam (IonOptix Inc., Milton, MA) system and fura-2 fluorescent dye. Contractile properties analyzed included peak shortening (PS), time-to-peak shortening (TPS), time-to-90% relengthening (TR90), and maximal velocity of shortening/relengthening (+/- dL/dt). Intracellular Ca2+ transients were evaluated as the fura-fluorescence intensity change (DeltaFFI) and fluorescence decay time. RESULTS: Allergina (10(-7) - 10(-3) mg/mL) significantly augmented PS in a dose-dependent manner with a maximal response of 50.4%. Allergina did not elicit any effect on TPS, TR(90), and +/-dL/dt. Intracellular Ca2+ transients displayed consistent findings in that Allergina enhanced the electrically-stimulated increase in change of intracellular Ca2+ transients (DeltaFFI) and slowed intracellular Ca2+ fluorescence decay without affect the resting intracellular Ca2+ levels. CONCLUSIONS: Collectively, these data demonstrated a direct cardiac stimulatory property of Allergina on cardiac contraction and intracellular Ca2+ transients in isolated left ventricular cardiomyocytes.

Impact of estrogen replacement on ventricular myocyte contractile function and protein kinase B/Akt activation.

Women with functional ovaries have a lower cardiovascular risk than men and postmenopausal women. However, estrogen replacement therapy remains controversial. This study examined the effect of ovarian hormone deficiency and estrogen replacement on ventricular myocyte contractile function and PKB/Akt activation. Nulliparous female rats were subjected to bilateral ovariectomy (Ovx) or sham operation (sham). A subgroup of Ovx rats received estrogen (E(2)) replacement (40 microg. kg(-1). day(-1)) for 8 weeks. Mechanical and intracellular Ca(2+) properties were evaluated including peak shortening (PS), time to PS (TPS), time to 90% relengthening (TR(90)), maximal velocity of shortening/relengthening (+/-dL/dt), fura 2 fluorescence intensity (FFI), and decay rate. Levels of sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a), phospholamban (PLB), and Akt were assessed by Western blot. Ovx promoted body weight gain associated with reduced serum E(2) and uterine weight, all of which were abolished by E(2). Ovx depressed PS and +/-dL/dt, prolonged TPS, TR(90), and decay rate, and enhanced resting FFI, all of which, with the exception of TPS, were restored by E(2). Ovx did not alter the levels of SERCA2a, PLB, and total Akt, but significantly reduced Akt activation [phosphorylated Akt (pAkt)], pAkt/Akt, and the SERCA2a-to-PLB ratio. These alterations in protein expression were restored by E(2). E(2) enhanced PS and +dL/dt in vitro, which was abolished by the E(2) receptor antagonist ICI-182780. Ovx reduced myocyte Ca(2+) responsiveness and lessened stimulating frequency-induced decline in PS, both ablated by E(2). These data suggest that mechanical and protein functions of ventricular myocytes are directly regulated by E(2).