Effects of low-flow ischemia on the positive inotropic action of angiotensin II in isolated rabbit and rat hearts.
Effects of low-flow ischemia on the positive inotropic action of angiotensin II in isolated rabbit and rat hearts.
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低流量缺血对离体兔和大鼠心脏中血管紧张素 II 正性肌力作用的影响。
DOI：
10.1016/s0008-6363(96)00185-x
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发表时间：
1997
影响因子：
10.8
通讯作者：
Apstein,CS
中科院分区：
文献类型：
--
作者：
Libonati,JR;Eberli,FR;Sesselberg,HW;Apstein,CS
目的：血管紧张素Ⅱ（ANG Ⅱ）可通过碱性化增加肌丝对钙的敏感性，从而增强成年兔心肌细胞的肌力。因此，我们测试的假设，血管紧张素II将有一个更大的变力作用，在缺血条件下比它会在常氧，因为缺血诱导的细胞内酸中毒有助于缺血性收缩抑郁症通过降低肌丝钙sensitivity.Methods：我们研究了血管紧张素II的影响，在隔离，红细胞灌注，等容大鼠和兔心脏在常氧灌注条件下，并在分级降低冠状动脉灌注压（CPP）。在每个灌注水平，ANG II以10 - 11至10 - 5 M的浓度逐渐增加。最大有效ANG II浓度为10− 7 M。结果：我们的研究表明，ANG II在正常灌注和低灌注兔心脏中引起等容左室发展压力的绝对增加相当。然而，由于血管紧张素II给药前缺血性心脏的收缩功能明显抑制，因此在缺血期间对血管紧张素II的相对变力性反应明显大于常氧。同样，血管紧张素II没有积极的变力作用，在大鼠在常氧，但增加收缩力在缺血。为了具体评估ANG II逆转酸中毒负性肌力作用的潜力，用高碳酸酸灌注液（pH = 7.1）灌注含氧量正常的非缺血大鼠心脏。在高碳酸盐灌注期间，当酸中毒抑制收缩时，ANG II [10−7]M使LV发展压力增加19%，+ dP/dt增加27%与正常pH值下无变力作用相比，ANG Ⅱ对缺血大鼠心脏的正性变力作用明显减弱（P< 0.05）（P< 0.001）.结论：在常氧条件下，ANG Ⅱ对家兔和大鼠具有不同的变力作用。在这两个物种中，ANG II的相对变力性反应在低流量缺血期间增强。这些结果与继发于ANG II刺激Na+/H+交换作用的相对细胞内碱化一致。
Objective:Angiotensin II (ANG II) has recently been reported to increase inotropy in adult rabbit myocytes by a mechanism of alkalinization and consequent increased myofilament sensitivity to calcium. Accordingly, we tested the hypothesis that ANG II would have a greater inotropic effect during ischemic conditions than it would during normoxia, since ischemia-induced intracellular acidosis contributes to ischemic contractile depression by decreasing myofilament calcium sensitivity.Methods:We studied the effects of ANG II in isolated, red-blood-cell-perfused, isovolumic rat and rabbit hearts during normoxic perfusion conditions and at graded reductions in coronary perfusion pressure (CPP). At each level of perfusion, ANG II was infused at progressively increasing concentrations ranging from 10−11to 10−5M. The maximal effective ANG II concentration was 10−7M.Results:Our studies show that ANG II caused comparable absolute increases in isovolumic LV developed pressure in normoperfused and hypoperfused rabbit hearts. However, since contractile function was markedly depressed in ischemic hearts prior to ANG II administration, the relative inotropic response to ANG II was significantly greater during ischemia than normoxia. Similarly, ANG II had no positive inotropic effect in the rat during normoxia, but increased contractility during ischemia. To assess specifically the potential of ANG II to reverse the negative inotropy of acidosis, normoxic non-ischemic rat hearts were perfused with a hypercarbic acidotic perfusate (pH = 7.1). During the hypercarbic perfusion when contraction was depressed by acidosis, ANG II [10−7]M increased LV developed pressure by 19% and + dP/dt by 27% (P< 0.05), in contrast to its lack of inotropic effect at a normal pH. The positive inotropic effect observed in rat hearts with ANG II during ischemia was significantly attenuated (P< 0.001) by concomitant infusion with amiloride, 5-(N-ethyl-N-isopropyl) (EIPA), a Na+/H+exchange inhibitor.Conclusions:We conclude that during normoxia, ANG II has a different inotropic potency in rabbits from that in rats. In both species, the relative inotropic responsiveness of ANG II is potentiated during low-flow ischemia. These results are consistent with a relative intracellular alkalinization that occurs secondary to ANG II's action to stimulate Na+/H+exchange.
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DOI：
--
发表时间：
1978
期刊：
European journal of cardiology
影响因子：
--
作者：
J. E. Devlin;H. Mulholland;M. Kelly;S. Webb;G. MacKenzie;A. Adgey
通讯作者：
A. Adgey
心室挛缩和顺应性随整体缺血和再灌注的变化，及其对大鼠冠状动脉阻力的影响。
影响因子：
20.1
作者：
C. Apstein;M. Mueller;W. Hood
通讯作者：
W. Hood
大鼠冠状动脉收缩后不久血管紧张素 II 受体介导的信号转导发生变化。
影响因子：
10.8
作者：
Huang,H;Li,P;Hamby,CV;Reiss,K;Meggs,LG;Anversa,P
通讯作者：
Anversa,P
冠脉流量轻度减少期间的心脏收缩功能障碍是由于大鼠心脏中钙压关系的改变所致。
DOI：
10.1172/jci116054
发表时间：
1992
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Figueredo,VM;Brandes,R;Weiner,MW;Massie,BM;Camacho,SA
通讯作者：
Camacho,SA
禽类血管紧张素 II 心脏受体的表征：与机械活动和磷酸肌醇代谢的耦合。
影响因子：
5
作者：
Kenneth M. Baker;Joseph A. Aceto
通讯作者：
Joseph A. Aceto