Fukuhiro Y
Department of Thoracic and Cardiovascular Surgery, Kawasaki Medical School, Kurashiki, Japan.
Nihon Kyobu Geka Gakkai Zasshi. 1996 Feb;44(2):130-7.
Although the protective effects of the calcium antagonists on ischemic and reperfused myocardium have been investigated, there have been only a few reports regarding their efficacy in relation to the degree of ischemic myocardium. This study was undertaken to investigate the efficacy of diltiazem, a calcium antagonist, in relation to the degree of ischemic myocardial injury in an isolated working rat heart. Three different models of ischemic injury were designed; Group A: 30 min global ischemia with a single dose infusion of St. Thomas' cardioplegic solution (STS), Group B: 60 min global ischemia with multidose infusion (every 30 min) of STS and Group C: 60 min global ischemia with multidose infusion (every 15 min) of STS. These groups received only STS, while Groups A-D, B-D and C-D (the treated groups) received the same solution with diltiazem (0.5 mumol/l). The recovery of post-ischemic cardiac function and the CPK leakage during reperfusion were evaluated, and the two groups were compared. For 30 min global ischemia, the addition of diltiazem to STS significantly improved the percentage recovery ratio of aortic flow (63.2 +/- 8.6% vs 79.9 +/- 5.9%, control vs. diltiazem, p < 0.01) and reduced CPK leakage during reperfusion (87.5 +/- 35.8 IU/20 min/g dry wt vs. 41.7 +/- 14.5 IU/20 min/g dry wt, control vs. diltiazem, p < 0.05). However, no differences in the post-ischemic functional recovery and CPK leakage were noted between the groups for 60 min global ischemia. In conclusion, for myocardial preservation, the addition of diltizaem to St. Thomas' cardioplegic solution was less effective for the 60 min global ischemia. Regarding severe myocardial ischemia, it was suggested that, inhibitation or suppression of calcium channel by diltizaem might insufficient to obtain additional protection of the St. Thomas' cardioplegic solution. Therefore, it would be necessary to control calcium entry through another pathway during ischemia and reperfusion.
尽管已经对钙拮抗剂对缺血及再灌注心肌的保护作用进行了研究，但关于其与缺血心肌程度相关疗效的报道却为数不多。本研究旨在探讨钙拮抗剂地尔硫䓬对离体工作大鼠心脏缺血性心肌损伤程度的疗效。设计了三种不同的缺血损伤模型；A组：单次输注圣托马斯心脏停搏液（STS）30分钟全心缺血；B组：多次输注（每30分钟一次）STS 60分钟全心缺血；C组：多次输注（每15分钟一次）STS 60分钟全心缺血。这些组仅接受STS，而A-D组、B-D组和C-D组（治疗组）接受含地尔硫䓬（0.5 μmol/l）的相同溶液。评估缺血后心脏功能的恢复及再灌注期间肌酸磷酸激酶（CPK）的漏出情况，并对两组进行比较。对于30分钟全心缺血，在STS中加入地尔硫䓬可显著提高主动脉血流的恢复百分比（对照组与地尔硫䓬组分别为63.2±8.6% vs 79.9±5.9%，p<0.01），并减少再灌注期间CPK的漏出（对照组与地尔硫䓬组分别为87.5±35.8 IU/20分钟/克干重 vs 41.7±14.5 IU/20分钟/克干重，p<0.05）。然而，对于60分钟全心缺血，各治疗组之间在缺血后功能恢复及CPK漏出方面未观察到差异。总之，对于心肌保护，在圣托马斯心脏停搏液中加入地尔硫䓬对60分钟全心缺血的效果较差。对于严重心肌缺血，提示地尔硫䓬抑制或阻断钙通道可能不足以获得圣托马斯心脏停搏液的额外保护作用。因此，在缺血和再灌注期间有必要通过另一条途径控制钙内流。
