Siegel G, Rückborn K, Schnalke F, Müller J
Institute of Physiology, Free University of Berlin, Germany.
Eur Heart J. 1993 Nov;14 Suppl I:99-103.
Human coronary arteries were taken from heart transplant patients. Arteriosclerotic arteries were more depolarized and constricted over the whole PO2 range between 535 and 0 mmHg. During oxygen deficiency, control preparations showed a maximal hyperpolarization of delta V = 10.9 mV and a maximal relaxation of delta T = 0.466 g. Arteriosclerotic arteries, however, became hyperpolarized by merely delta V = 7.1 mV and relaxed by delta T = 0.258 g. In normal coronary arteries, indomethacin reduced the hypoxic hyperpolarization and dilatation at 30 mmHg PO2 by about 51%. The reduction was 27% in arteriosclerotic vessels. The complete removal of the endothelium caused a 49% (73% in arteriosclerotic coronaries) restriction of dilatory vascular reactivity. The relationship was quite similar for a carbogen Krebs solution. The hyperpolarizing and dilatory contribution of prostacyclin was 32% in normal and 12% in arteriosclerotic coronary arteries. The remainder could be attributed to the basal release of endothelium-derived hyperpolarizing factor (EDHF). Thus, it may be concluded that in arteriosclerotic blood vessels, prostacyclin (PGI2) synthesis and release are predominantly diminished. Finally, we found that the ratio PGI2/EDHF in the voltage and tension changes strongly shifted to the PGI2 side with a declining oxygen concentration. This is true for normal and arteriosclerotic vessels. In addition, a disturbed transmembrane cation distribution in the arteriosclerotic coronary vessels may be an additional explanation for the depolarized membrane potential and increased muscle tone. [Na+]i of normal arteries amounted to 16.6, of arteriosclerotic arteries to 60.9 mmol.l-1; [K+]i values were 134.6 in normal and 95.0 mmol.l-1 in arteriosclerotic coronaries, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
取自心脏移植患者的人类冠状动脉。在535至0 mmHg的整个氧分压范围内，动脉粥样硬化动脉的去极化程度更高且收缩更明显。在缺氧期间，对照制剂显示最大超极化ΔV = 10.9 mV，最大舒张ΔT = 0.466 g。然而，动脉粥样硬化动脉仅超极化ΔV = 7.1 mV，舒张ΔT = 0.258 g。在正常冠状动脉中，吲哚美辛使30 mmHg氧分压下的缺氧超极化和扩张减少约51%。在动脉粥样硬化血管中减少了27%。完全去除内皮导致血管舒张反应性受限49%（动脉粥样硬化冠状动脉中为73%）。对于加碳的 Krebs 溶液，这种关系非常相似。前列环素的超极化和舒张作用在正常冠状动脉中为32%，在动脉粥样硬化冠状动脉中为12%。其余可归因于内皮衍生超极化因子（EDHF）的基础释放。因此，可以得出结论，在动脉粥样硬化血管中，前列环素（PGI2）的合成和释放主要减少。最后，我们发现随着氧浓度降低，电压和张力变化中PGI2/EDHF的比值强烈向PGI2一侧偏移。正常和动脉粥样硬化血管均如此。此外，动脉粥样硬化冠状动脉中跨膜阳离子分布紊乱可能是膜电位去极化和肌张力增加的另一个原因。正常动脉的[Na+]i为16.6，动脉粥样硬化动脉为60.9 mmol·l-1；正常冠状动脉的[K+]i值为134.6，动脉粥样硬化冠状动脉为95.0 mmol·l-1。（摘要截于250字）
