TRIGGERED ACTIVITY INDUCED BY COMBINED MILD HYPOXIA AND ACIDOSIS IN GUINEA-PIG PURKINJE-FIBERS

TRIGGERED ACTIVITY INDUCED BY COMBINED MILD HYPOXIA AND ACIDOSIS IN GUINEA-PIG PURKINJE-FIBERS
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DOI:
10.1016/s0022-2828(86)80432-1
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发表时间:
1986-12-01
影响因子:
5
通讯作者:
DUPUIS, BA
DUPUIS, BA
中科院分区:
医学2区
文献类型:
--
作者:
ADAMANTIDIS, MM;CARON, JF;DUPUIS, BA

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长期暴露于复合轻度缺氧的影响(PO2230。+-。20毫米汞柱)和酸中毒(pH:6.8+-)。0.05),对体外灌流的豚鼠左室心肌进行了研究。微电极仅刺穿浦肯野纤维。48.+-后,去极化的浦肯野纤维发生触发活动。9分钟暴露在低氧和酸性条件下,开始于短时间的快速电动驾驶或背景缓慢的浦肯野自动驾驶。当延迟的后除极达到其阈值电位时,触发活动发生,在亚阈值后除极后终止。在暴露于低氧和酸性条件下90到180分钟之前,观察到触发的活动和缓慢的背景自律性之间的相互作用。这些效应通过在标准条件下的替换(PO2510.+-)被逆转。20毫米汞柱;pH 7.35。+-。0.05)。去甲肾上腺素(1次。10~(-6)M)可显著加快触发灶的放电速度,使触发活动持续稳定。细胞外Ca~(2+)浓度的升高加重了轻度缺氧和酸中毒的联合作用,并导致早期后除极的发生,引发触发活动。此外,在没有任何触发动作电位的静态纤维中出现了异常的自律性。利多卡因和维拉帕米抑制亚阈值后除极后的触发活动。它们的影响在被淘汰时发生了逆转。结论是,长期暴露在轻度缺氧和酸中毒的复合环境中,通过与其他情况相同的基本机制诱发触发活动,导致钙超载并表现出这种行为。
The effects of prolonged exposure to combined mild hypoxia (PO2 230 .+-. 20 mmHg) and acidosis (pH: 6.8 .+-. 0.05) were studied in guinea-pig left ventricular myocardium superfused in vitro. Only Purkinje fibers were impaled by microelectrodes. Triggered activity developed in depolarized Purkinje fibers after 48 .+-. 9 min of exposure to hypoxic and acid conditions and was initiated either by short periods of rapid electrical driving or by the backgroud slow Purkinje automaticity. Triggered activity occurred when a delayed afterdepolarization attained its threshold potential and terminated after a subthreshold afterdepolarization. Interaction between triggered activity and slow backgroud automaticity was observed until 90 to 180 min of exposure to hypoxic and acid conditions. These effects were reversed by replacement in standard conditions (PO2 510 .+-. 20 mmHg; pH 7.35 .+-. 0.05). Norepinephrine (1 .times. 10-6 M) significantly accerelated the rate of discharge of triggered foci and led to a stable sustained triggered activity. Increasing extracellular Ca2+ concentration aggravated the effects of combined mild hypoxia and acidosis and led to the occurrence of early afterdepolarizations initiating triggered activity. In addition abnormal automaticity developed in quiescent fibers without any triggering action potential. Lidocaine and verapamil suppressed the triggered activity following a subthreshold after-depolarization. Their effects reversed on wash-out. It is concluded that prolonged exposure to combined mild hypoxia and acidosis induces triggered activity by a basic mechanism common to other situations leading to a calcium overload and showing such behaviour.