De Jong J W, Harmsen E, De Tombe P P
J Mol Cell Cardiol. 1984 Apr;16(4):363-70. doi: 10.1016/s0022-2828(84)80607-0.
Calcium antagonists potentially prevent ATP breakdown, but literature data on this subject are conflicting. We studied the effect of diltiazem on ATP catabolism in rat heart, perfused according to Langendorff. Administration of the drug took place either before or during ischemia, induced by lowering the perfusion pressure. The reduction in flow without diltiazem was 85%. We observed a significantly (P less than 0.001) lower production of purine nucleosides and oxypurines by the ischemic heart, when we gave diltiazem in a dose range of 1 to 100 microM before ischemia. The highest drug concentration reduced purine release by 85%. Due to ischemia, myocardial adenine nucleotide content decreased by 40% (P less than 0.001); this was partially prevented by 5 microM diltiazem (P = 0.4 v. untreated hearts). The drug also effectively reduced purine release, when applied five minutes after the induction of ischemia, but higher concentrations were needed.
钙拮抗剂有可能防止三磷酸腺苷(ATP)分解,但关于这一主题的文献数据相互矛盾。我们研究了地尔硫䓬对按照Langendorff法灌注的大鼠心脏中ATP分解代谢的影响。药物给药在降低灌注压力诱导的缺血之前或期间进行。无地尔硫䓬时血流减少85%。当我们在缺血前给予1至100微摩尔剂量范围的地尔硫䓬时,观察到缺血心脏产生的嘌呤核苷和氧嘌呤显著减少(P小于0.001)。最高药物浓度使嘌呤释放减少85%。由于缺血,心肌腺嘌呤核苷酸含量下降40%(P小于0.001);5微摩尔地尔硫䓬可部分预防这种情况(与未治疗的心脏相比,P = 0.4)。当在缺血诱导五分钟后应用该药物时,也能有效减少嘌呤释放,但需要更高的浓度。