Cardiac contractile dysfunction during mild coronary flow reductions is due to an altered calcium-pressure relationship in rat hearts.
Cardiac contractile dysfunction during mild coronary flow reductions is due to an altered calcium-pressure relationship in rat hearts.
复制标题
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
复制
发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Camacho,SA
中科院分区：
文献类型：
--
作者：
Figueredo,VM;Brandes,R;Weiner,MW;Massie,BM;Camacho,SA
冠状动脉狭窄或闭塞会导致冠脉流量减少和心肌收缩抑制。在严重的血流量减少时，增加的无机磷(PI)和细胞内酸中毒明显地在收缩抑制中起作用。然而，在较温和的流量减少期间，收缩抑制的机制(S)不太清楚。先前的心脏灌流研究表明，在轻度血流减少期间，PI或pH没有变化，这表明血管内压的变化(花园软管效应)可能是这种收缩抑制的中介。其他人报道了关于另一种可能的收缩介质--胞浆游离钙(CaI)--的相互矛盾的结果。为了研究CaI、PI、pH和血管压力在轻度血流减少时调节收缩性能中的作用，我们在Langendorff灌流的大鼠心脏上进行了Indo-1钙荧光和31P磁共振波谱测量。在血流减少到对照组的50%的过程中，血管紧张素转换酶和舒张期钙水平没有变化。等电点与开发压力关系密切，在流量降低25%的情况下，PI从2.5+/-0.3升至4.2+/-0.4摩尔/克干重。PH值保持不变，直到流量降低50%。血管内压升高到超生理水平后，发育压进一步升高，而CaI无明显变化。这些发现与以下假设相一致，即在轻度冠状动脉流量减少时，收缩抑制是通过改变血管紧张素转换酶与压力之间的关系而不是通过减少血管紧张素转换酶来调节的。此外，PI升高和血管内压降低可能是轻度冠脉流量减少时钙-压关系改变的原因。
Coronary artery stenosis or occlusion results in reduced coronary flow and myocardial contractile depression. At severe flow reductions, increased inorganic phosphate (Pi) and intracellular acidosis clearly play a role in contractile depression. However, during milder flow reductions the mechanism(s) underlying contractile depression are less clear. Previous perfused heart studies demonstrated no change of Pi or pH during mild flow reductions, suggesting that changes of intravascular pressure (garden hose effect) may be the mediator of this contractile depression. Others have reported conflicting results regarding another possible mediator of contractility, the cytosolic free calcium (Cai). To examine the respective roles of Cai, Pi, pH, and vascular pressure in regulating contractility during mild flow reductions, Indo-1 calcium fluorescence and 31P magnetic resonance spectroscopy measurements were performed on Langendorff-perfused rat hearts. Cai and diastolic calcium levels did not change during flow reductions to 50% of control. Pi demonstrated a close relationship with developed pressure and significantly increased from 2.5 +/- 0.3 to 4.2 +/- 0.4 mumol/g dry weight during a 25% flow reduction. pH was unchanged until a 50% flow reduction. Increasing vascular pressure to superphysiological levels resulted in further increases of developed pressure, with no change in Cai. These findings are consistent with the hypothesis that during mild coronary flow reductions, contractile depression is mediated by an altered relationship between Cai and pressure, rather than by decreased Cai. Furthermore, increased Pi and decreased intravascular pressure may be responsible for this altered calcium-pressure relationship during mild coronary flow reductions.