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[缺血性心肌的保护]

[Protection of the ischemic myocardium].

作者信息

Zucchi R, Yu G, Ronca-Testoni S, Ronca G, Mariani M

机构信息

Istituto di Cardiologia, Universitá degli Studi, Pisa.

出版信息

Cardiologia. 1993 Dec;38(12 Suppl 1):81-9.

PMID:7912653
Abstract

The Authors review several pharmacological interventions aimed at protecting the ischemic myocardium. Drugs which have been widely used in the treatment of ischemic heart diseases, such as beta-blockers, nitrates and calcium-antagonists, are able to delay the development of ischemic injury if administered before the beginning of ischemia, but their clinical effectiveness is limited. The new drugs which are presently investigated are designed to counteract the molecular mechanisms which mediate irreversible tissue injury, namely cytosolic calcium overload, cellular hyperosmolarity, and free radical production. In particular, interventions able to interfere with the release of calcium from its intracellular stores would be of major importance. In this regards, it is interesting to point out that derivatives of phenylalkylamine calcium-antagonists have been reported to modulate the opening probability of sarcoplasmic reticulum calcium channels.

摘要

作者综述了几种旨在保护缺血心肌的药物干预措施。已广泛用于治疗缺血性心脏病的药物,如β受体阻滞剂、硝酸盐和钙拮抗剂,如果在缺血开始前给药,能够延缓缺血损伤的发展,但其临床疗效有限。目前正在研究的新药旨在对抗介导不可逆组织损伤的分子机制,即胞浆钙超载、细胞高渗和自由基产生。特别是,能够干扰钙从细胞内储存释放的干预措施将具有重要意义。在这方面,有趣的是指出,据报道苯烷基胺钙拮抗剂的衍生物可调节肌浆网钙通道的开放概率。

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1
[Protection of the ischemic myocardium].[缺血性心肌的保护]
Cardiologia. 1993 Dec;38(12 Suppl 1):81-9.
2
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Heat stress improves functional recovery and induces synthesis of 27- and 70-kDa heat shock proteins without preserving sarcoplasmic reticulum function in the ischemic rat heart.热应激可改善缺血大鼠心脏的功能恢复并诱导27 kDa和70 kDa热休克蛋白的合成,但不能维持肌浆网功能。
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