Blake K, Clusin W T
Eur J Pharmacol. 1986 Aug 15;127(3):261-5. doi: 10.1016/0014-2999(86)90372-9.
Diltiazem retards ischemic arrhythmias and reduces cellular depolarization, as inferred from recordings of T-Q segment depression (delta T-Q). To explore this further, we correlated delta T-Q with the extracellular K+ electrode potential (delta EK) during serial ischemic trials. delta T-Q and delta EK were uniform in control trials, but decreased markedly in trials that immediately followed diltiazem infusion (0.5 mg/kg). delta EK at 2 min of ischemia was reduced from 11.8 +/- 1.3 to 7.4 +/- 1.2 mV; while delta T-Q was reduced from 7.2 +/- 0.5 to 4.4 +/- 0.7 mV. The effect of diltiazem on ischemic depolarization is largely, but not entirely explained by reduction of delta EK.
从T-Q段压低（ΔT-Q）的记录推断，地尔硫䓬可延缓缺血性心律失常并减少细胞去极化。为进一步探究此现象，我们在系列缺血试验中，将ΔT-Q与细胞外钾电极电位（ΔEK）进行了关联分析。在对照试验中，ΔT-Q和ΔEK是一致的，但在紧接着输注地尔硫䓬（0.5mg/kg）后的试验中，二者均显著降低。缺血2分钟时，ΔEK从11.8±1.3mV降至7.4±1.2mV；而ΔT-Q从7.2±0.5mV降至4.4±0.7mV。地尔硫䓬对缺血性去极化的作用在很大程度上，但并非完全由ΔEK的降低所解释。
