Low-dose inotropic stimulation during left ventricular ischaemia does not worsen post-ischaemic dysfunction.
Low-dose inotropic stimulation during left ventricular ischaemia does not worsen post-ischaemic dysfunction.
复制标题
左心室缺血期间的低剂量正性肌力刺激不会恶化缺血后功能障碍。
DOI：
10.1016/s0008-6363(96)00150-2
复制
发表时间：
1996
影响因子：
10.8
通讯作者：
Lu,L
中科院分区：
文献类型：
--
作者：
Schwartz,GG;Xu,Y;Greyson,C;Cohen,J;Lu,L
ObjectiveInotropic agents are used clinically to improve ventricular function during ischaemia. The goal of this study was to determine whether inotropic stimulationduringmoderate left ventricular (LV) ischaemia exacerbatespost-ischaemicLV dysfunction.Methods: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 μg·kg−1·min−1, i.v.) during the final 60 min of ischaemia (Group 2), while 9 other pigs did not (Group 1).Results: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 ischaemic 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.Conclusions:Low-dose inotropic stimulation during moderate regional LV ischaemia increases aerobic, but not anaerobic energy metabolism, and does not worsen post-ischaemic dysfunction.
