Protective effect of early and late treatment with nifedipine during myocardial infarction in the conscious dog.
Protective effect of early and late treatment with nifedipine during myocardial infarction in the conscious dog.
复制标题
硝苯地平早期和晚期治疗对清醒犬心肌梗死的保护作用。
DOI：
10.1161/01.cir.69.1.131
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发表时间：
1984
期刊：
影响因子：
37.8
通讯作者：
Hutchins,GM
中科院分区：
文献类型：
--
作者：
Melin,JA;Becker,LC;Hutchins,GM
在24只清醒的狗中研究了硝苯地平早期和晚期治疗对侧支血流量和心肌梗死面积的影响。硝苯地平静脉输注5小时开始15分钟（n = 9）和3小时（n = 6）永久性闭塞后回旋支冠状动脉中段，并与早期和延迟的车辆治疗（对照组; n = 9）。滴定硝苯地平剂量（90至168微克/小时），以降低平均动脉压5%至10%。在动物死亡或2至7天后处死后，通过死后冠状动脉造影确定解剖风险区域或闭塞的冠状动脉床。通过左心室横截面称重，测量梗死区和危险区的重量。与对照组相比，硝苯地平早期和晚期治疗组的左心室面积百分比（15.6%和14.6% vs 21.6%）和风险区域百分比（46.7%和41.6% vs 65.7%）均较小（p <0.05）。用放射性微球测量的侧支血流量在硝苯地平治疗5小时期间增加了31%至50%，但平均增加量在统计学上并不大于对照组。当心外膜侧支血流超过0.40 ml/min/g时，硝苯地平的心肌保护作用持续发生，且用药后增加至少0.1 ml/min/g。然而，当血流量小于这些量时，只有大约一半的动物表现出梗死面积减少。结果表明，侧支血流的增加占硝苯地平的有益作用的一部分，但不介导的流动的直接机制也可能作出贡献。
The effect of early and late nifedipine treatment on collateral blood flow and myocardial infarct size was investigated in 24 previously instrumented conscious dogs. Nifedipine was infused intravenously for 5 hr beginning 15 min (n = 9) and 3 hr (n = 6) after permanent occlusion of the midcircumflex coronary artery and compared with early and delayed vehicle treatment (controls; n = 9). Doses of nifedipine (90 to 168 micrograms/hr) were titrated to reduce mean arterial pressure by 5% to 10%. After animals died or were killed 2 to 7 days later, the anatomic risk region, or occluded coronary bed, was defined by postmortem coronary arteriography. The masses of infarct and risk region were measured by planimetry of weighed transverse sections of the left ventricle. Infarct size was smaller (p less than .05) with early and late nifedipine treatment compared with control, both as percent of left ventricle (15.6% and 14.6% vs 21.6%) and as percent of risk region (46.7% and 41.6% vs 65.7%). Collateral blood flow, measured with radioactive microspheres, increased 31% to 50% during 5 hr of nifedipine treatment, but the mean increase was not statistically greater than that seen in controls. Myocardial protection by nifedipine occurred consistently when epicardial collateral flow exceeded 0.40 ml/min/g and the increase after the drug was at least 0.1 ml/min/g. When flows were less than these amounts, however, only about half of the animals demonstrated reduced infarct size. The results suggest that an increase in collateral flow accounts for part of the beneficial effect of nifedipine but that direct mechanisms not mediated by flow may also contribute.