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儿茶酚胺损伤的蛙心肌中的无钠挛缩

Sodium-free contractures in frog myocardium damaged by catecholamines.

作者信息

Volkmann R, Carlsten A, Winell S

机构信息

Department of Clinical Physiology, University of Göteborg, Sweden.

出版信息

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1988;89(1):77-81. doi: 10.1016/0742-8413(88)90148-x.

DOI:10.1016/0742-8413(88)90148-x
PMID:2894277
Abstract
  1. Sodium-free contractures were studied in myocardial strips from R. pipiens with extracellular sodium (Na+o) replaced by choline chloride and extracellular calcium (Ca2+o) varied with EGTA-buffer. Normal myocardium was compared with that damaged by adrenaline (ADR) or isoproterenol (ISO). 2. Frog myocardium, damaged by in vivo injections of catecholamines, remained relaxed when exposed to Na+/Ca2+-free solutions. Only in 2 out of 18 experiments were small contractures observed after several hours. 3. Addition of KCN to the Na+/Ca2+-free solution caused small contractures after several hours in 7 out of 10 experiments. 4. The time to maximum Na+-free contractures was correlated to Ca2+o in a dose-dependent manner, but not influenced by catecholamine-induced myocardial damage. 5. Cell injury in the frog heart after in vivo injections of catecholamines does not affect the sarcolemmal Na+/Ca2+-exchange and is not associated with passive leakage of Ca2+ from the extracellular to the intracellular space.
摘要
  1. 用氯化胆碱替代细胞外钠(Na⁺o),并用乙二醇双(2-氨基乙基醚)四乙酸(EGTA)缓冲液改变细胞外钙(Ca²⁺o),研究了豹蛙心肌条的无钠挛缩。将正常心肌与受肾上腺素(ADR)或异丙肾上腺素(ISO)损伤的心肌进行比较。2. 经体内注射儿茶酚胺损伤的蛙心肌,在暴露于无Na⁺/无Ca²⁺溶液时仍保持松弛。18个实验中只有2个在数小时后观察到小的挛缩。3. 在无Na⁺/无Ca²⁺溶液中加入氰化钾(KCN),10个实验中有7个在数小时后引起小的挛缩。4. 最大无钠挛缩的时间与Ca²⁺o呈剂量依赖性相关,但不受儿茶酚胺诱导的心肌损伤影响。5. 体内注射儿茶酚胺后蛙心脏的细胞损伤不影响肌膜Na⁺/Ca²⁺交换,且与Ca²⁺从细胞外被动泄漏到细胞内空间无关。

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Comp Biochem Physiol C Comp Pharmacol Toxicol. 1988;89(1):77-81. doi: 10.1016/0742-8413(88)90148-x.
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J Mol Cell Cardiol. 1989 Sep;21(9):865-75. doi: 10.1016/0022-2828(89)90755-4.