Lang T W, Meerbaum S, Corday E, Davidson R M, Hashimoto K, Farcot J C, Osher J
Am J Cardiol. 1976 Mar 31;37(4):523-43. doi: 10.1016/0002-9149(76)90393-3.
The consequences of sublingual and intravenous nitroglycerin treatment after acute coronary occlusion were studied in 18 closed chest dogs. Intravenous (0.1 mg/min) or sublingual (0.4 mg/15 min) nitroglycerin therapy was instituted 1 hour after occlusion and the effects were observed over a period of 2 hours. Hemodynamics and global and regional cardiac function were measured in both the coronary occluded and nonoccluded segments of the left ventricle before and during coronary occlusion, and after administration of nitroglycerin. A similar nine dog control series was used to establish the significance of the measured effects of nitroglycerin. Intravenous nitroglycerin therapy after 1 hour of occlusion resulted in a marked increase in heart rate (37 +/- 12 [mean +/- standard error of the mean] percent), reduction of systolic blood pressure (9 +/- 3%), decrease in left ventricular end-diastolic and end-systolic volumes (32 +/- 5% and 34 +/- 5%), increase in coronary sinus flow (64 +/- 24%) and decrease in left ventricular stroke work (29 +/- 8%). Sublingually administered nitroglycerin produced similar trends but much less pronounced effects. However, intravenous or sublingual administration of nitroglycerin provided no improvement or caused further deterioration in ischemic region lactate extraction and potassium loss. The left ventricular ejection fraction, which was severly depressed after 1 hour of occlusion, changed minimally after administration of nitroglycerin, and there was no evidence of any correction of regional left ventricular akinesia or dyskinesia. Whereas mean systemic vascular resistance changed minimally as a result of nitroglycerin therapy, it increased 19 +/- 8% during a corresponding period of an untreated coronary occlusion series suggesting that nitroglycerin prevented an anticipated increase. Postocclusion S-T segment elevation in the electrocardiogram persisted after treatment. Our data corroborated that nitroglycerin reduced left ventricular volumes and increased coronary sinus flow; however, these improvements were accompanied by persisting metabolic and mechanical derangements in the ischemic region.
在18只开胸犬身上研究了急性冠状动脉闭塞后舌下含服和静脉注射硝酸甘油治疗的后果。闭塞1小时后开始静脉（0.1毫克/分钟）或舌下（0.4毫克/15分钟）硝酸甘油治疗，并在2小时内观察效果。在冠状动脉闭塞前、闭塞期间以及给予硝酸甘油后，测量左心室冠状动脉闭塞段和非闭塞段的血流动力学、整体和局部心脏功能。使用类似的9只犬的对照系列来确定硝酸甘油所测效果的显著性。闭塞1小时后静脉注射硝酸甘油治疗导致心率显著增加（37±12[平均值±平均标准误差]%），收缩压降低（9±3%），左心室舒张末期和收缩末期容积减小（32±5%和34±5%），冠状窦血流量增加（64±24%），左心室每搏功降低（29±8%）。舌下含服硝酸甘油产生了类似趋势，但效果要小得多。然而，静脉或舌下给予硝酸甘油并未改善缺血区域的乳酸摄取和钾丢失，或导致其进一步恶化。闭塞1小时后严重降低的左心室射血分数在给予硝酸甘油后变化极小，并且没有证据表明局部左心室运动不能或运动障碍得到任何纠正。虽然硝酸甘油治疗使平均体循环血管阻力变化极小，但在未治疗的冠状动脉闭塞系列的相应时间段内其增加了19±8%，这表明硝酸甘油阻止了预期的增加。治疗后心电图中的闭塞后ST段抬高持续存在。我们的数据证实，硝酸甘油减少了左心室容积并增加了冠状窦血流量；然而，这些改善伴随着缺血区域持续的代谢和机械紊乱。
