He M X, Wang S, Downey H F
Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, 76107, USA.
Am J Physiol. 1997 Mar;272(3 Pt 2):H1333-41. doi: 10.1152/ajpheart.1997.272.3.H1333.
To test the role of inorganic phosphate (Pi) in downregulation of myocardial contractile force at the onset of ischemia, Pi of rat hearts was determined with 31P nuclear magnetic resonance spectroscopy. Forty cycles of brief hypoperfusion (30% of baseline flow for 33 s) were used to achieve a time resolution of 0.512 s for comparing dynamic changes in Pi and contractile force. Initial control values of left ventricular developed pressure (LVP), heart rate, and oxygen consumption were 136 +/- 11 mmHg, 236 +/- 4 beats/min, and 95 +/- 3 microl O2 x min(-1) x g(-1); these values were unchanged at the end of the experiment. During the first 10 s of hypoperfusion, Pi increased at a rate (percentage of the total observed change) faster than the decrease in LVP; Pi and LVP then changed at the same rate during the remainder of the hypoperfusion. ADP did not change in advance of LVP. Intracellular pH did not change. The results indicate that Pi plays an important role in initiating the downregulation of myocardial contractile force at the onset of ischemia. Perfusion pressure also declined faster than LVP at the onset of ischemia, indicating potential importance of vascular collapse in contractile downregulation during early ischemia.
为了测试无机磷酸盐(Pi)在缺血开始时心肌收缩力下调中的作用,采用31P核磁共振波谱法测定大鼠心脏的Pi。使用40个周期的短暂低灌注(为基线血流的30%,持续33秒),以实现0.512秒的时间分辨率,用于比较Pi和收缩力的动态变化。左心室舒张末期压力(LVP)、心率和耗氧量的初始对照值分别为136±11 mmHg、236±4次/分钟和95±3微升O2×分钟-1×克-1;这些值在实验结束时未发生变化。在低灌注的前10秒内,Pi的增加速率(占观察到的总变化的百分比)比LVP的降低速率更快;在低灌注的其余时间里,Pi和LVP以相同的速率变化。ADP在LVP之前没有变化。细胞内pH值没有变化。结果表明,Pi在缺血开始时启动心肌收缩力下调中起重要作用。在缺血开始时,灌注压也比LVP下降得更快,表明血管塌陷在早期缺血期间收缩力下调中具有潜在重要性。