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首页> 外文期刊>American Journal of Physiology >Negative inotropic drugs alter indexes of cytosolic (Ca(2+))-left ventricular pressure relationships after ischemia.
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Negative inotropic drugs alter indexes of cytosolic (Ca(2+))-left ventricular pressure relationships after ischemia.

机译：负性肌力药物可改变局部缺血后胞质（Ca（2 +））-左心室压力关系的指数。

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摘要

Negative inotropic agents may differentially modulate indexes of cytosolic [Ca(2+)]-left ventricular (LV) pressure (LVP) relationships when given before and after ischemia. We measured and calculated [Ca(2+)], LVP, velocity ratios [[(d[Ca(2+)]/dt(max))/(dLVP/dt(max)); VR(max)] and [(d[Ca(2+)]/dt(min))/(dLVP/dt(min)); VR(min)]], and area ratio (AR; area [Ca(2+)]/area LVP per beat) before and after global ischemia in guinea pig isolated hearts. Ca(2+) transients were recorded by indo 1-AM fluorescence via a fiberoptic probe placed at the LV free wall. [Ca(2+)]-LVP loops were acquired by plotting LVP as a function of [Ca(2+)] at multiple time points during the cardiac cycle. Hearts were perfused with bimakalim, 2,3-butanedione monoxime (BDM), nifedipine, or lidocaine before and after 30 min of ischemia. Before ischemia, each drug depressed LVP, but only nifedipine decreased both LVP and [Ca(2+)] with a downward and leftward shift of the [Ca(2+)]-LVP loop. After ischemia, each drug depressed LVP and [Ca(2+)] with a downward and leftward shift of the [Ca(2+)]-LVP loop. Each drug except BDM decreased d[Ca(2+)]/dt(max); nifedipine decreased d[Ca(2+)]/dt(min), whereas lidocaine increased it, and bimakalim and BDM had no effect on d[Ca(2+)]/dt(min). Each drug except bimakalim increased VR(max) and VR(min) before ischemia; after ischemia, only BDM and nifedipine increased VR(max) and VR(min). Before and after ischemia, BDM and nifedipine increased AR, whereas lidocaine and bimakalim had no effect. At 30 min of reperfusion, control hearts exhibited marked Ca(2+) overload and depressed LVP. In each drug-pretreated group Ca(2+) overload was reduced on reperfusion, but only the group pretreated with nifedipine exhibited both higher LVP and lower [Ca(2+)]. These results show that negative inotropic drugs are less capable of reducing [Ca(2+)] after ischemia so that there is a relatively larger Ca(2+) expenditure for contraction/relaxation after ischemia than before ischemia. Moreover, the differential effects of pretreatment with negative inotropic drugs on [Ca(2+)]-LVP relationships after ischemia suggest that these drugs, especially nifedipine, can elicit cardiac preconditioning.
机译：负性肌力药可能差异调节缺血前和缺血后胞质[Ca（2 +）]-左心室（LV）压力（LVP）关系的指数。我们测量并计算了[Ca（2 +）]，LVP，速度比[[（d [Ca（2 +）] / dt（max））/（dLVP / dt（max））; VR（max）]和[[d [Ca（2 +）] / dt（min））/（dLVP / dt（min））; VR（min）]]和面积比（AR;面积[Ca（2 +）] /每次搏动的LVP面积）在豚鼠离体心脏整体缺血之前和之后。 Ca（2+）瞬态记录是通过放置在LV自由壁上的光纤探针通过印度1-AM荧光记录的。 [Ca（2 +）]-LVP循环是通过在心动周期的多个时间点将LVP绘制为[Ca（2+）]的函数来绘制的。在缺血30分钟之前和之后，用比马卡林，2,3-丁二酮一肟（BDM），硝苯地平或利多卡因灌注心脏。缺血前，每种药物均使LVP降低，但只有硝苯地平降低LVP和[Ca（2+）]的同时使[Ca（2 +）]-LVP环向下和向左移动。缺血后，每种药物均使LVP和[Ca（2+）]下降，[Ca（2 +）]-LVP环向左下方移动。除BDM外，每种药物均降低d [Ca（2 +）] / dt（max）;硝苯地平降低d [Ca（2 +）] / dt（min），而利多卡因增加它，而比马卡林和BDM对d [Ca（2 +）] / dt（min）没有影响。除比马卡林外，每种药物在缺血前均增加VR（max）和VR（min）。缺血后，仅BDM和硝苯地平可增加VR（max）和VR（min）。缺血前后，BDM和硝苯地平会增加AR，而利多卡因和比马卡林则无作用。在再灌注30分钟时，对照心脏表现出明显的Ca（2+）超负荷和LVP降低。在每个药物预处理组中，Ca（2+）的过载在再灌注时均得以减少，但只有用硝苯地平进行预处理的组显示出较高的LVP和较低的[Ca（2+）]。这些结果表明，负性肌力药物在缺血后降低[Ca（2+）]的能力较弱，因此与缺血前相比，缺血后收缩/松弛的Ca（2+）支出相对较大。此外，负性肌力药物预处理对缺血后[Ca（2 +）]-LVP关系的不同影响表明，这些药物，尤其是硝苯地平，可以引起心脏预处理。

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