Schwartz G G, Xu Y, Greyson C, Cohen J, Lu L
Cardiology Section, Department of Veterans Affairs Medical Center, San Francisco, CA 94121, USA.
Cardiovasc Res. 1996 Dec;32(6):1024-37. doi: 10.1016/s0008-6363(96)00150-2.
Inotropic agents are used clinically to improve ventricular function during ischaemia. The goal of this study was to determine whether inotropic stimulation during moderate left ventricular (LV) ischaemia exacerbated post-ischaemic LV dysfunction.
In 18 open-chest, anesthetized pigs, LV pressure versus subendocardial segment length loops were used to generate regional preload-recruitable stroke work (PRSW) and LV end-diastolic pressure (EDP) versus end-diastolic segment length (EDL) relations. Ischaemia was produced by constant, partial constriction of the mid anterior descending coronary artery for 90 min. Nine pigs received dobutamine (4 micrograms.kg-1.min-1, i.v.) during the final 60 min of ischaemia (Group 2), while 9 other pigs did not (Group 1).
During unstimulated ischaemia, anterior subendocardial blood flow (Group 1, 0.27 +/- .05; Group 2, 0.30 +/- .07 ml.g-1.min.-1, mean +/- s.e.m.) and steady-state PRSW (Group 1, 30 +/- 4%; Group 2, 27 +/- 5% of baseline) were similar in both groups. Dobutamine stimulation during ischaemia increased heart rate, mean arterial pressure, subendocardial blood flow, oxygen consumption and steady-state PRSW of the ischaemia zone, but not lactate release. After 60 min reperfusion, steady-state ischaemic zone PRSW remained markedly and nearly equally reduced in both groups (Group 1, 28 +/- 4%; Group 2, 23 +/- 5% of baseline). Reduced PRSW after reperfusion was due primarily to persistent rightward shift of the PRSW intercept with only a modest contribution from reduced PRSW slope.
Low-dose inotropic stimulation during moderate regional LV ischaemia increases aerobic, but not anaerobic energy metabolism, and does not worsen post-ischaemic dysfunction.
临床上使用正性肌力药物来改善缺血期间的心室功能。本研究的目的是确定中度左心室（LV）缺血期间的正性肌力刺激是否会加重缺血后左心室功能障碍。
在18只开胸麻醉猪中，利用左心室压力与心内膜下节段长度环来生成局部可募集前负荷搏功（PRSW）以及左心室舒张末期压力（EDP）与舒张末期节段长度（EDL）的关系。通过持续部分结扎冠状动脉前降支中段90分钟来制造缺血。9只猪在缺血的最后60分钟接受多巴酚丁胺（4微克·千克⁻¹·分钟⁻¹，静脉注射）（第2组），而另外9只猪未接受（第1组）。
在未刺激的缺血期间，两组的心内膜下前部血流（第1组，0.27±0.05；第2组，0.30±0.07毫升·克⁻¹·分钟⁻¹，平均值±标准误）和稳态PRSW（第1组，30±4%；第2组，为基线的27±5%）相似。缺血期间的多巴酚丁胺刺激增加了心率、平均动脉压、心内膜下血流、氧耗量以及缺血区的稳态PRSW，但未增加乳酸释放。再灌注60分钟后，两组的缺血区稳态PRSW仍显著且几乎同等程度降低（第1组，为基线的28±4%；第2组，为基线的23±5%）。再灌注后PRSW降低主要是由于PRSW截距持续右移，而PRSW斜率降低的贡献较小。
中度局部左心室缺血期间的低剂量正性肌力刺激增加有氧能量代谢，但不增加无氧能量代谢，且不会加重缺血后功能障碍。
