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蛙心由钠钙交换介导的缓慢无钠挛缩

Slow sodium-free contractures in the frog heart mediated by the sodium-calcium exchange.

作者信息

Volkmann R, Winell S, Pettersson A 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):71-5. doi: 10.1016/0742-8413(88)90147-8.

Abstract
  1. Sodium-free contractures were studied in myocardial strips from R. pipiens when extracellular sodium (Na+o) was replaced by choline chloride and extracellular free calcium (Ca2+o) was defined with EGTA-buffer. 2. Resting membrane potentials (RMP) were normal in sodium-free solutions with Ca2+o calculated below 1.0 x 10(-9) mol/l. 3. When Ca2+o was subsequently increased from zero to 1.0 x 10(-3) mol/l Na+-free contractures developed slowly with unchanged RMP even at maximum contracture, at which the intracellular ultrastructure is grossly altered. 4. The contractures developed significantly faster in the presence of 3 x 10(-6) mol/l ouabain. 5. In sodium-free solutions La3+ did not influence Ca2+-dependent contractures, apart from causing an increase in time to maximum contracture. 6. It is concluded that sarcolemmal integrity is maintained in frog myocardium treated initially with Na+/Ca2+-free solutions and then with Na+-free medium containing 1 mmol/l Ca2+. 7. Our experiments indicate that sodium-free, Ca2+o-dependent contractures are mediated by the Na+/Ca2+-exchange, operation at higher rates when Na+i is increased. La3+ (1 mmol/l) probably does not compete with Ca2+ at extracellular binding sites of the exchanger. 8. The Na+/Ca2+-exchange may under certain experimental conditions be able to increase Ca2+i to cytotoxic concentrations.
摘要
  1. 当用氯化胆碱替代细胞外钠(Na⁺ₒ)并用乙二醇双四乙酸(EGTA)缓冲液确定细胞外游离钙(Ca²⁺ₒ)时,对豹蛙心肌条的无钠挛缩进行了研究。2. 在Ca²⁺ₒ计算值低于1.0×10⁻⁹mol/L的无钠溶液中,静息膜电位(RMP)正常。3. 随后当Ca²⁺ₒ从零增加到1.0×10⁻³mol/L时,即使在最大挛缩时RMP不变,无钠挛缩也缓慢发展,此时细胞内超微结构发生严重改变。4. 在存在3×10⁻⁶mol/L哇巴因的情况下,挛缩发展明显加快。5. 在无钠溶液中,除了导致达到最大挛缩的时间增加外,镧离子(La³⁺)不影响钙依赖性挛缩。6. 得出的结论是,在用无钠/无钙溶液初始处理,然后用含1mmol/L钙的无钠培养基处理的青蛙心肌中,肌膜完整性得以维持。7. 我们的实验表明,无钠、Ca²⁺ₒ依赖性挛缩由钠/钙交换介导,当细胞内钠(Na⁺ᵢ)增加时以更高速率运转。镧离子(1mmol/L)可能不在交换体的细胞外结合位点与钙竞争。8. 在某些实验条件下,钠/钙交换可能能够将细胞内钙(Ca²⁺ᵢ)增加到细胞毒性浓度。

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