The cyclooxygenase-2 product prostaglandin E2 modulates cardiac contractile function in adult rat ventricular cardiomyocytes
The cyclooxygenase-2 product prostaglandin E2 modulates cardiac contractile function in adult rat ventricular cardiomyocytes
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DOI：
10.1016/j.phrs.2003.09.002
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发表时间：
2004-02-01
影响因子：
9.3
通讯作者：
Ren, J
中科院分区：
文献类型：
--
作者：
Klein, AL;Wold, LE;Ren, J
前列腺素E-2 （PGE(2)）是环氧化酶-2途径的产物，已被证明可以增加心输出量并调节心脏收缩功能。然而，PGE2的心脏收缩反应是否由于其对单个心室肌细胞的作用尚未阐明。为了评估PGE2在细胞水平上的机械作用，分离成年大鼠心室肌细胞并刺激其在0.5 Hz下收缩。使用IonOptix心肌（(R)）模拟-数字光学检测系统评估机械和细胞内Ca2+特性。收缩和细胞内Ca2+特性评估为峰值缩短（PS），时间到PS (TPS)，时间到90%再延长（TR90），缩短或再延长的最大速度（+/-dL/dt）和Ca2+诱导的细胞内Ca2+荧光释放（CICR），基线细胞内Ca2+水平和细胞内Ca2+衰减率（tau）。PGE(2) (10（-8) ~ 10(-3) M）诱导PS升高，但对TPS、TR90、+/-dL/dt、CICR和tau没有影响。高浓度的PGE(2) （10(-5) M或更高）降低了基线细胞内Ca2+水平。这些数据表明，PGE2的心肌收缩反应可能是由于其在单心室肌细胞水平上的直接心肌收缩作用，可能是通过一种独立于细胞内Ca2+释放的机制。(C) 2003 Elsevier Ltd.版权所有。
Prostaglandin E-2 (PGE(2)), a product of the cyclooxygenase-2 pathway, has been shown to increase cardiac output and modulate cardiac contractile function. However, whether the cardiac contractile response of PGE2 is due to its action on single ventricular myocytes has not been elucidated. To assess the mechanical effect of PGE2 at the cellular level, adult rat ventricular myocytes were isolated and stimulated to contract at 0.5 Hz. Mechanical and intracellular Ca2+ properties were evaluated using an IonOptix Myocam((R)) analog-to-digital optical detection system. Contractile and intracellular Ca2+ properties were evaluated as peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90), maximal velocity of shortening or relengthening (+/-dL/dt) and Ca2+-induced intracellular Ca2+ fluorescence release (CICR), baseline intracellular Ca2+ levels and intracellular Ca2+ decay rate (tau). PGE(2) (10(-8) to 10(-3) M) elicited an augmentation in PS but had no effect on TPS, TR90, +/-dL/dt, CICR and tau. High concentration of PGE(2) (10(-5) M or higher) reduced the baseline intracellular Ca2+ levels. These data indicate that the myocardial contractile response of PGE2 may be due to its direct cardiac contractile action at the single ventricular myocyte level, probably through a mechanism independent of intracellular Ca2+ release. (C) 2003 Elsevier Ltd. All rights reserved.