论文部分内容阅读
有较多的证据表明,冠状动脉痉挛在Prinzmetal变异型心绞痛的发病原理上起重要作用,但其发生机理尚不明了。血管平滑肌收缩依赖于钙离子的数量,后者为肌原纤维ATP酶的激活所必需。生理学上,氢离子具有高度的钙拮抗作用,似与钙离子竞争跨膜钙运转系统和肌原纤维ATP酶上相同的激活部位。因而,如钙离子浓度增加或氢离子浓度减少即发生血管收缩,而钙离子缺乏或氢离子浓度增加则血管扩张。本文研究在变异型心绞痛患者,用过度换气和输注
There is more evidence that coronary spasm plays an important role in the pathogenesis of Prinzmetal variant angina, but its mechanism of action is unknown. The contraction of vascular smooth muscle depends on the amount of calcium ion, which is necessary for the activation of myofibrillar ATPase. Physiologically, hydrogen ions have a high calcium antagonistic effect and appear to compete with calcium ions for the same activation site on the transmembrane calcium system and myofibrillar ATPase. Thus, vasoconstriction occurs as the concentration of calcium ions increases or as the concentration of hydrogen ions decreases, while vasodilatation occurs as a result of lack of calcium ions or increased concentrations of hydrogen ions. This article studies patients with variant angina with hyperventilation and infusion