Effects of diltiazem, a calcium channel inhibitor, in retarding cellular damage produced during early myocardial ischemia in pigs: a morphometric and ultrastructural analysis.
Effects of diltiazem, a calcium channel inhibitor, in retarding cellular damage produced during early myocardial ischemia in pigs: a morphometric and ultrastructural analysis.
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地尔硫卓（一种钙通道抑制剂）在延缓猪早期心肌缺血期间产生的细胞损伤中的作用：形态测量和超微结构分析。
DOI：
10.1016/s0735-1097(84)80281-8
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发表时间：
1984
影响因子：
24
通讯作者：
Schwartz,A
中科院分区：
文献类型：
--
作者：
Fujiwara,H;Ashraf,M;Millard,RW;Sato,S;Schwartz,A
用形态计量学方法观察了静脉注射地尔硫卓对30只猪缺血心脏透壁组织损伤的保护作用。在单独的实验中，通过结扎冠状动脉左前降支远端20、40和120分钟使猪心脏缺血。心率、左室收缩压和体循环舒张压在阻断40分钟内略有下降，然后恢复到对照水平。然而，对照组和地尔硫卓治疗组之间无显著差异。通过微球技术测量，在对照组和地尔硫卓治疗组的心脏中，缺血区域均无血流量。无论缺血持续时间如何，在两组中均观察到紧邻心内膜和心外膜下方的少数细胞层中几乎没有细胞损伤。与对照组相比，暴露于地尔硫卓的心脏在缺血的所有时间段后，在心内膜下、心肌中层和心外膜下检测到较少的细胞损伤。然而，即使在药物治疗的心脏，闭塞2小时后，细胞仍然严重injure.The保护作用的地尔硫对缺血心肌区域的细胞完整性似乎是独立的血流，并可能是一个反映的直接影响地尔硫对心肌细胞。确切的机制尚未解决。然而，在没有明显侧支循环的缺血心脏中，用钙通道阻断药物地尔硫卓预处理导致急性冠状动脉结扎后细胞损伤的延迟发生，并且在长达40分钟的缺血期内细胞损伤较少。
A protective effect of intravenous diltiazem pretreatment on transmural histologic damage in ischemic hearts of 30 pigs was determined morphometrically. The pig hearts were rendered ischemic by ligation of the distal left anterior descending coronary artery for 20, 40 and 120 minutes in separate experiments. Heart rate, left ventricular systolic pressure and systemic diastolic pressure decreased slightly during 40 minutes of occlusion, and then recovered to control levels. However, there were no significant differences between control and diltiazem-treated groups. Blood flow, measured by the microsphere technique, was uniformly absent in the ischemic areas in both control and diltiazem-treated hearts. In the few cell layers immediately beneath the endocardium and epicardium, little cellular damage was observed in either group regardless of the duration of ischemia. In the subendocardial, mid-myocardial and subepicardial layers, less cellular damage was detected after all periods of ischemia in hearts exposed to diltiazem in comparison with that observed in control hearts. However, even in the drug-treated hearts, after 2 hours of occlusion, the cells remained severely injured.The protective effect of diltiazem on the cellular integrity in the ischemic myocardial regions appears to be independent of blood flow and may be a reflection of a direct effect of diltiazem on myocytes. The precise mechanism is unresolved. Nevertheless, in the ischemic heart without a significant collateral circulation, pretreatment with the calcium channel blocking drug, diltiazem, results in a delayed onset of cellular damage after acute coronary artery ligation and less cellular damage at ischemic periods up to 40 minutes' duration.