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造影剂对培养心室细胞钙瞬变和运动的影响。

Effects of contrast media on calcium transients and motion in cultured ventricular cells.

作者信息

Bell D A, Peeters G A, Davis W L, Kohmoto O, Nelson J A, Barry W H

机构信息

Department of Medicine, University of Utah School of Medicine, Salt Lake City 84132.

出版信息

Invest Radiol. 1988 Nov;23(11):842-6. doi: 10.1097/00004424-198811000-00008.

DOI:10.1097/00004424-198811000-00008
PMID:2850282
Abstract

To investigate the mechanisms of the negative inotropic effects of contrast media, we superfused spontaneously contracting cultured chick embryo ventricular cells with Renografin-76 and iohexol (12% solutions), and hypertonic sucrose during simultaneous measurement of [Ca2+]i transients (indo-1) and motion (video-motion detector system). Exposure to contrast agents caused a significant reduction of contractility, with Renografin-76 having a much greater effect on amplitude of motion than iohexol. Renografin-76 significantly depressed [Ca2+]i transient amplitude, whereas iohexol had no effect. Addition of Ca2+ to correct for calcium binding by Renografin-76 completely reversed its depression of [Ca2+]i transients but only partially reversed the negative inotropic effects. Hypertonic sucrose caused a significant decrease in contraction amplitude, with no significant effects on [Ca2+]i transient amplitude. We conclude that the marked negative inotropic effect of Renografin-76 is caused by both calcium binding and hypertonicity. The less marked depression of contractility produced by iohexol likely is a result of hypertonicity and not caused by alteration of [Ca2+]i.

摘要

为研究造影剂负性肌力作用的机制,我们在用雷奈酸葡胺-76和碘海醇(12%溶液)以及高渗蔗糖对自发收缩的培养鸡胚心室细胞进行灌流的同时,测量[Ca2+]i瞬变(indo-1)和运动(视频运动检测系统)。暴露于造影剂会导致收缩性显著降低,雷奈酸葡胺-76对运动幅度的影响比碘海醇大得多。雷奈酸葡胺-76显著降低[Ca2+]i瞬变幅度,而碘海醇则无影响。添加Ca2+以校正雷奈酸葡胺-76的钙结合作用可完全逆转其对[Ca2+]i瞬变的抑制,但仅部分逆转负性肌力作用。高渗蔗糖导致收缩幅度显著降低,对[Ca2+]i瞬变幅度无显著影响。我们得出结论,雷奈酸葡胺-76明显的负性肌力作用是由钙结合和高渗性共同引起的。碘海醇引起的收缩性降低不太明显,可能是高渗性的结果,而非由[Ca2+]i改变所致。

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引用本文的文献

1
Effects of new intravascular contrast agents on [Ca2+]i transients and contraction in cultured ventricular myocytes.
Heart Vessels. 1992;7(1):42-51. doi: 10.1007/BF01745867.