Gebhard M M, Gersing E, Brockhoff C J, Schnabel P A, Bretschneider H J
Thorac Cardiovasc Surg. 1987 Feb;35(1):26-32. doi: 10.1055/s-2007-1020192.
During myocardial ischemia the phase angle phi of the complex electric impedance of myocardial tissue at 5 kHz AC exhibits a characteristic behaviour, the progress of which depends on the cardioplegic method applied. By extending the frequency range to 200 Hz and 10 MHz and by analyzing in addition to phase and magnitude also real and imaginary part of the impedance it was possible to elucidate which ischemic changes in the myocardium are responsible for the course of phi (5 kHz). This method we call impedance spectroscopy. Canine hearts were cardioplegically perfused with either the standard solution HTK[4] or the solution HTK[4] + 50 mumol/l Ca++. During the following ischemia at 25 degrees C energy-rich phosphate level, the ultrastructure, the real part, imaginary part and phase angle of the impedance between 200 Hz and 10 MHz were analyzed.
phi (5 kHz) displays very similar characteristics during the ischemic period to those of the real part of the impedance at 200 Hz, Re (200 Hz). Re (200 Hz) increases, when--according to electron microscopic findings--an intracellular myocardial edema begins to develop. The changes of Re(200 Hz) are always smaller, however, than those of phi (5 kHz). This indicates that phi (5 kHz) increases in the course of ischemia not only as a consequence of confinement of the extracellular space by myocardial cellular edema but also because of changes of passive electrical characteristics of the myocardial cell membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
在心肌缺血期间,心肌组织在5kHz交流电下复电阻抗的相位角φ呈现出特征性行为,其变化进程取决于所采用的心脏停搏方法。通过将频率范围扩展至200Hz和10MHz,并除了分析相位和幅值之外还分析阻抗的实部和虚部,得以阐明心肌中的哪些缺血性变化导致了φ(5kHz)的变化过程。我们将这种方法称为阻抗谱法。用标准溶液HTK[4]或溶液HTK[4]+50μmol/L Ca++对犬心进行心脏停搏灌注。在随后25℃的缺血期间,分析富含能量的磷酸盐水平、超微结构以及200Hz至10MHz之间阻抗的实部、虚部和相位角。
在缺血期间,φ(5kHz)呈现出与200Hz时阻抗实部Re(200Hz)非常相似的特征。当根据电子显微镜观察结果细胞内开始出现心肌水肿时,Re(200Hz)增加。然而,Re(200Hz)的变化始终小于φ(5kHz)的变化。这表明在缺血过程中,φ(5kHz)增加不仅是由于心肌细胞水肿导致细胞外间隙受限,还因为心肌细胞膜被动电学特性的改变。(摘要截断于250字)